Autolus Therapeutics plc

EX-99.1 · ex991autoluannualreporta.htm

EX-99.1
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 ex991autoluannualreporta.htm
 EX-99.1

 Registered	Number	11185179	(England	&	Wales) Annual	Report	and	financial	statements for	the	year	ended	31	December	2025 for Autolus	Therapeutics	plc

 Introduction	and	Contents Autolus	Therapeutics	plc	(the	“Company”,	“Group”	or	“Parent	Company”)	is	a	public	limited	company	incorporated	under the	laws	of	England	and	Wales	and	is	listed	on	the	Nasdaq	Global	Select	Market	(“NASDAQ”).	The	Company	is	a	“quoted company”	for	the	purposes	of	the	Companies	Act	2006	(the	“Companies	Act”).	This	document	(the	“Annual	Report	and financial	statements”)	is	comprised	of	the	reports	and	consolidated	financial	statements	listed	below. Company	Information ...................................................................................................................................................... 3 Strategic	Report ............................................................................................................................................................... 4 Directors’	Report .............................................................................................................................................................. 33 Directors’	Remuneration	Report ..................................................................................................................................... 38 Independent	auditor’s	report	to	the	members	of	Autolus	Therapeutics	plc ................................................................ 68 Consolidated	Income	Statement	and	Other	Comprehensive	Loss ................................................................................ 77 Consolidated	Balance	Sheet ............................................................................................................................................ 78 Consolidated	Statement	of	Changes	in	Equity ............................................................................................................... 79 Consolidated	Cash	Flow	Statement ................................................................................................................................ 80 Notes	to	the	Consolidated	Financial	Statements ........................................................................................................... 81 Parent	Company	Balance	Sheet ...................................................................................................................................... 137 Parent	Company	Statement	of	Changes	in	Equity .......................................................................................................... 138 Notes	to	the	Parent	Company	Financial	Statements ..................................................................................................... 139 AUTOLUS	THERAPEUTICS	PLC 2

 Company	Information Directors Michael	Bonney, Chair	of	the	Board	of	Directors Christian	Itin,	Executive	Director	and	CEO Robert	Azelby Linda	Bain John	Berriman Cynthia	Butitta Robert	Iannone Elisabeth	Leiderman Ravi	Rao Ryan	Richardson William	Young Company	Secretary Alex	Driggs Registered	Office The	MediaWorks 191	Wood	Lane London W12	7FP United	Kingdom Registered	Number 11185179 Auditors Ernst	&	Young	LLP R+ Blagrave	Street Reading RG1	1AZ United	Kingdom Bankers Barclays	Bank 1	Church	Street Peterborough PE1	1XE United	Kingdom Solicitors Cooley	(UK)	LLP 22	Bishopsgate London EC2N	4BQ United	Kingdom AUTOLUS	THERAPEUTICS	PLC 3

 Introduction Autolus	Therapeutics	plc (the	"Company") is	a	public limited	company incorporated in	England	and	Wales	and	has the following	wholly	owned	subsidiaries:	Autolus	Limited,	Autolus Inc.,	Autolus	GmbH,	Autolus	Switzerland	AG	and	Autolus Holdings	(UK)	Limited. In	this	Annual	Report	and	financial	statements,	unless	the	context	otherwise	indicates,	references to	the	“Group”,	“Autolus”,	“we”,	“us”	or	“our”	include	the	Company	and	its	wholly-owned	subsidiaries. Autolus	Therapeutics	plc	is	required	to	produce	a	strategic	report	complying	with	the	requirements	of	the	Companies	Act 2006	(Strategic	Report	and	Directors’	Report)	Regulations	2013	and	the	Companies	(Miscellaneous	Reporting)	Regulations 2018	(the	“Regulations”).	The	board	of	directors	(the	“Board”,	“Directors”	or	“Board	of	Directors”)	present	their	strategic report on the affairs of the	Group (the “Strategic	Report”), together	with the financial statements for the year ended 31	December	2025. Development	of	the	Group Autolus	Therapeutics	plc	is	a	public	limited	company	under	the	laws	of	England	and	Wales,	originally	incorporated	under the laws of England and Wales in February 2018 as a private limited company called Autolus Therapeutics Limited. Autolus	Limited	was	originally	incorporated	under	the	laws	of	England	and	Wales	in	July	2014.	Pursuant	to	the	terms	of our	corporate	reorganisation,	the	shareholders	of	Autolus	Limited	exchanged	each	of	the	shares	held	by	them	in	Autolus Limited	for	the	same	number	and	class	of	newly	issued	shares	of	Autolus	Therapeutics	Limited	and,	as	a	result,	Autolus Limited became a wholly owned subsidiary of Autolus Therapeutics Limited. On 18 June 2018, Autolus Therapeutics Limited re-registered as a public limited company and	was renamed Autolus Therapeutics plc. On 22 June 2018, our outstanding	preferred	and	ordinary shares	were	converted into	a single	class	of	ordinary shares	and	various	classes	of deferred	shares,	and	we	completed	our	initial	public	offering	of	American	Depositary	Shares	(“ADS’”),	each	representing one	of	our	ordinary	shares,	on	NASDAQ. Principal	Activity We	are	an	early	commercial-stage	biopharmaceutical	company	developing,	manufacturing	and	delivering	next-generation T cell therapies and candidates for the treatment of cancer and autoimmune diseases. Using our broad suite of proprietary and	modular T cell programming technologies,	we	are	engineering	precisely targeted	and controlled	T cell therapies	that	are	designed	to	better	recognise	target	cells,	break	down	their	defence	mechanisms	and	eliminate	target cells.	We	believe	our	programmed	T	cell therapies	have the	potential to	be	best-in-class	and	offer	patients substantial benefits over the existing standard of care, including the potential for cure in some patients. In	November 2024, the United States Food and Drug Administration (the “FDA”) approved our biologics license application (“BLA”) for the marketing	of	AUCATZYL	(obecabtagene	autoleucel,	also	known	as	obe-cel)	in	the	United	States	for	the	treatment	of	adult patients	(18	years	and	older)	with	relapsed	or	refractory	B-cell	precursor	acute	lymphoblastic	leukaemia	(“r/r	B-ALL”).	The commercial launch and first sale of AUCATZYL in the United States occurred in January 2025. The United Kingdom Medicines	and	Healthcare	products	Regulatory	Agency	(“MHRA”)	granted	AUCATZYL	conditional	marketing	authorization in	April	2025.	In	November	2025,	the	National	Institute	for	Health	and	Care	Excellence	(“NICE”)	recommended	AUCATZYL for	use	in	the	National	Health	Service	(“NHS”)	in	England	and	Wales	as	a	treatment	option	for	adult	patients	(age	26	and older)	with	r/r	B-ALL.	We	launched	AUCATZYL	in	the	United	Kingdom	in	January	2026,	and	it	is	available	through	routine commissioning	by	the	NHS.	In	July	2025,	the	European	Commission	(“EC”)	granted	marketing	authorization	for	AUCATZYL in adult patients (age 26 and older) with r/r B-ALL. Evaluation of potential pricing and feasibility of market entry opportunities in	certain	European	Union	(“EU”)	countries is	ongoing;	however,	at	this	time, launch	in	the	EU	is	on	hold and	we	do	not	anticipate	any	EU	sales	of	AUCATZYL	in	2026. AUCATZYL is a B-lymphocyte antigen CD19 (“CD19”) chimeric antigen receptor (“CAR”) T cell therapy. AUCATZYL is designed	with	a	fast	target	binding	off-rate	to	minimize	excessive	activation	of	the	programmed	T	cells.	Adult	r/r	B-	ALL	is an	extremely	aggressive type	of	blood	cancer	with	a	high	unmet	medical	need in the treatment	of	patients	once they relapse,	where	historically	patients	suffer	from	poor	outcomes.	AUCATZYL	is	manufactured	at	our	dedicated	commercial manufacturing site, the	Nucleus, in Stevenage,	U.K.	We intend for the	Nucleus to	meet the global supply demands	of AUCATZYL,	with	Cardinal	Health	105,	LLC	serving	as	our	commercial	distribution	partner	in	the	US. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 4

 In addition to AUCATZYL/obe-cel for the treatment of adult r/r B-ALL, we are advancing obe-cel in other oncology indications	including	paediatric	B-ALL	and	B-NHL.	Data	from	the	Phase	1b	cohort	of	the	ongoing	Phase	1b/2	CATULUS	trial evaluating the safety and efficacy of obe-cel in paediatric B-ALL and B-NHL patients was presented at the American Society	of	Haematology	(“ASH”)	Annual	Meeting	in	December	2025.	Data	show	the	safety	profile	of	obe-cel	in	paediatric patients is consistent	with that previously reported in adults,	with low rates of high-grade cytokine release syndrome (“CRS”)	and	immune	effector	cell-associated	neurotoxicity	syndrome	(“ICANS”).	Overall	response	rate	(“ORR”)	was	high	at 95%,	and	nearly	90%	of	responders	had	ongoing	remission	at	data	cut-off.	Enrolment	into	the	Phase	2	cohort	is	ongoing, and	in	October	2025,	the	FDA	granted	regenerative	medicine	advanced	therapy	(“RMAT”)	designation	to	obe-cel	for	the treatment	of	paediatric	patients	with	r/r	B-ALL.	We	expect	to	have	Phase	2	cohort	of	the	trial	fully	enrolled	in	the	first	half of	2027. Obe-cel is	also	being	developed for the treatment	of	autoimmune indications,	and	we	have initiated	a	Phase	1 trial in patients	with severe, refractory systemic lupus erythematosus (“SLE”). Data from the ongoing Phase 1 CARLYSLE trial evaluating obe-cel in patients	with severe refractory systemic lupus erythematosus	was presented at the ASH	Annual Meeting	in	December	2025.	The	data	showed	deep,	durable	responses	in	patients	receiving	the	50	million	obe-cel	CAR	t- cell	dose	level,	and	initial	data	suggest	substantial	early	improvement	in	three	patients	dosed	with	obe-cel	at	100	million dose level. All patients show deep B-cell depletion after infusion, suggesting an immune reset. Nine patients were evaluable	for	safety,	and	no	ICANS	or	high-grade	CRS	were	observed.	The	Company	has	advanced	obe-cel	into	a	Phase	2 potentially	pivotal	study	known	as	LUMINA	in	patients	with	severe,	refractory lupus	nephritis	(“LN”).	We	are	advancing obe-cel into	clinical	development in	progressive	multiple	sclerosis	(“MS”)	and	in	October	2025,	we	have	dosed	our	first patients	in	a	Phase	1	dose	escalation	clinical	trial,	with	initial	data	expected	to	be	reported	at	the	end	of	2026. Our	T	cell	programming	technologies	allow	us	to	tailor	our	therapies	to	address	the	specific	disease	we	are	targeting	and introduce	new	programming	modules	into	a	patient’s	T	cells	to	give	those	T	cells	improved	properties	to	better	recognise target	cells	and	overcome	fundamental	disease	defence	mechanisms.	Cancers	in	particular	thrive	on	their	ability	to	fend off	T	cells	by	evading	recognition	by	T	cells	and	by	establishing	other	defence	mechanisms,	such	as	checkpoint	inhibition, and	creating	a	hostile	microenvironment.	We	believe	our leadership in	T	cell	programming	technologies	will	provide	us with	a	competitive	advantage	as	we	look	to	develop	future	generations	of	T	cell	therapies	targeting	both	haematological cancers, solid tumours and autoimmune	diseases, including potential products that could have a sufficient tolerability profile	to	enable	use	in	outpatient	settings. Our	Pipeline Our current clinical-stage	pipeline comprises four	programs	being	developed in	eight	haematological and solid tumour indications	and	two	autoimmune	indications.	Our	current	pipeline	is	below: AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 5

 Our	product	pipeline	is	built	on	our	core	principles	of	modular	innovation	with	protein-based	cell	programming	focused on advanced targeting, pharmacological control and enhancement of activity. After identifying a target,	we select the suite	of	programming	modules	that	we	believe	is	best	suited	to	target	that	particular	disease	based	on	the	latest	clinical data and the results of our research. The particular modules selected may vary, and not every product candidate, including our current product candidates, contain all categories of modules. A viral vector is then used to introduce combinations	of	these	modules	into	the	DNA	of	the	T	cells. The	diagram	below	shows	how	our	programming	modules	relate	to	our	product	candidates. Our	programs	have	been	highly	tailored	and	specifically	engineered	via	our	proprietary	modules,	and	have	the	potential to	be	truly	differentiated	assets	that	could	address	limitations	of	current	treatments	and	provide	innovative	options	for patients. Our	Strategy Our	strategic	priorities	include: • Continue	building	upon	United	States	and	United	Kingdom	commercialization	of	AUCATZYL	for	adult	r/r	B-ALL. • Optimize our manufacturing operations to improve gross margin, and innovate on a next-generation manufacturing	platform. • Evaluate	the	potential	pricing	and	feasibility	of	market	entry	opportunities	in	certain	EU	countries. • Develop	obe-cel	for	treatment	of	potential	additional	indications,	including	paediatric	r/r	B-ALL,	LN	and	MS. Programmed	T	Cell	Therapies Chimeric	Antigen	Receptors	(“CARs”) We	use	CARs	to	reprogram	our	T	cell	product	candidates.	These	receptors	combine	the	antigen	recognition	domain	of	an antibody	with	the	activation	and	costimulatory	domains	from	the	T	cell	receptor	to	rearm	a	patient’s	T	cells	to	recognise and	kill	target	cells. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 6

 CAR	T	Cell	Production We	have	developed	our own	proprietary viral vector and semi-automated cell	manufacturing processes to engineer a patient's T cells with the CAR and other programming modules. We believe that this autologous approach has the potential	to	be	both	the	safest	and	most	therapeutically	effective	approach	to	manufacturing	CAR	T	cells. Our	technological	approach	is	the	development	of	advanced	T	cell	engineering	components	designed	to	directly	address clinical	challenges.	A	focus	in	our	early-stage	pipeline	is	incorporation	of	multiple	components	in	a	single	product. Programmed	T	Cell	Therapies	for	the	Treatment	of	Cancers Cancers	originate	from	individual	cells	that	have	developed	mutations	in	essential	cellular	programs,	driving	increased	cell division	and	growth.	A	key	control	mechanism	to	detect	and	eliminate	such	cells	is	the	patient’s	own	T	cells.	T	cells	are	a type of white blood cells used by the human immune system to defend the body against infectious pathogens and cancerous cells. Using their T cell receptor like a	molecular scanner, T cells are able to discriminate between normal human	cells	and	ones	that	contain	a	mutation	that	alters	their	function.	If	the	T	cell	recognises	an	altered	cell,	it	becomes activated and kills that particular cell. For a cancer to grow to the detriment of the patient, cancer cells evolve mechanisms	to	evade	recognition	by,	or	establish	other	defences	against,	T	cells. In recent years	we have seen the emergence of cancer immunotherapy, in	which treatments harness the power of a patient’s	immune	system	to	combat	their	disease. Cancer	immunotherapy	treatment	requires	the	activation	and	expansion	of	cancer-specific	T	cells,	which	kill	cancer	cells by	recognizing	antigen	targets	expressed	on	cancer	cells.	Studies	have	shown	that	tumours	develop	escape	mechanisms that	prevent	T	cell-mediated	destruction	through	immune	checkpoint	proteins,	which	shut	down	antitumour immunity. Clinical trials have shown that treatment with immune checkpoint inhibitors can restore T cell activity and results in durable clinical responses. Several anti-PD1	and	anti-PD-L1 antibodies are approved for the treatment	of various solid tumours,	and	Pembrolizumab	is	also	approved	in	relapsed/refractory	classical	Hodgkin’s	disease	or	primary	mediastinal	B- cell lymphoma. However, none of the immune checkpoint inhibitors are currently approved in other haematologic indications.	While these approaches collectively represented	major advances in cancer treatment, they all lack active redirection	of	the	patient’s	T	cells	to	the	cancer,	eventually	limiting	clinical	activity. More recently, redirected	T cell therapies that	are	designed to	give the	patient’s T cells a	new	specificity to recognise cancer cells have been developed. The first approved product of this class is a  bi-specific  T cell engager called blinatumomab	(Blincyto®)	from	Amgen	Inc.	Blinatumomab	targets	the	CD19	antigen	on	the	surface	of	B	cells	and	cancers derived	from	B	cells.	Blinatumomab	is	approved	for	the	treatment	of B-ALL. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 7

 More	recently,	genetically	programmed	redirected	T	cell	therapies	have	been	approved.	These	include	the	CD19	targeting  therapies	Kymriah®,	Yescarta®,	Tecartus®,	and	Breyanzi®,	developed	by	Novartis	AG,	Kite	Pharma,	Inc.	and	Bristol	Myers Squibb	Inc.,	respectively,	for	the	treatments	of	B-ALL	and	B-NHL.	All	four	of	these	therapies	showed	high	response	rates and,	in	a	subset	of	patients,	prolonged	treatment	effects.	For	those	patients	experiencing	a	relapse,	the	common	causes for	relapse	are	insufficient	survival	of	the	programmed	T	cells,	loss	of	the	CD19	target	on	the	cancer	cells	and	upregulation of	checkpoint	inhibitor PD-L1 on	the	cancer	cells. In	view	of	the	limitations	of	current	therapies,	there	remains	a	critical	unmet	medical	need	for	improved	T	cell	therapies. We	believe	that improving	efficacy	and	durability	over	the	products	currently	on	the	market	or in	development	for	the treatment	of	cancers	requires	addressing	target	antigen	loss,	countering	checkpoint	inhibition	and	adding	novel	targets	to expand	the	range	of indications	amenable to	programmed	T	cell therapy.	We	believe	our	commercial	product	and	our clinical-stage	product	candidates	and	our	approach	to	T	cell	programming	have	the	potential	to	address	these	limitations. Existing T cell immunotherapies, including CAR T therapies, have shown significant efficacy in haematological malignancies;	however,	the	extent	and	duration	of	the	treatment	effects	and	disease	remission	are	yet	to	be	fully	defined. Optimizing	the	targeting	module	of	a	programmed	T	cell	may	enhance	its	effect	and	safety.	Also,	in	response	to	targeted therapies,	cancer	cells	often	mutate	and	cease	to	express	the	antigen	the	therapy	was	designed	to	recognise. This	loss	of	target	antigen	leads	to	patient	relapse.	Additionally,	numerous	challenges,	including	lack	of	T	cell	persistence and	upregulation	of	checkpoint	inhibitors,	represent	significant	hurdles	that	need	to	be	addressed	by	new	therapies.	T	cell immunotherapies	also	have	the	capacity	to	elicit	toxicities	including	CRS,	neurologic	toxicity	and	the	elimination	of	normal cells	via	on-target	off	tumour	recognition.	Further,	manufacturing	T	cells	can	be	prohibitively	costly	if	the	manufacturing process	is	not	appropriately	designed	to	support	parallel	processing	and	automation.	Finally,	realization	of	the	potential of	this	approach	across	a	broad	range	of	solid	tumour	types	will	require	multiple	technology	solutions	in	order	to	address limitations	of	the	current	generation	of	therapies. Emerging	Promise	of	T	Cell	Immunotherapies	for	the	Treatment	of	Autoimmune	Diseases Autoimmune	diseases	are	the	result	of	an	immune	system	that	is	overactive,	causing	it	to	attack	and	damage	the	patient’s own	tissues.	Autoimmune	diseases	can	affect	multiple	organs	throughout	the	body	and	can	be	life	threatening	in	some cases.	The	presence	of	autoreactive	B	cells	that	produce	autoreactive	antibodies--antibodies	that	attack	the	body’s	own tissues--are	a common feature	of these	diseases.	As such, therapeutic	approaches that	deplete	B cells	have	had some clinical	success.	These	B	cell	depletion	approaches,	such	as	the	antibodies	that	target	CD20	(Rituximab,	Ocrelizumab	and Ofatumumab)	and	BAFF	(Belimumab)	are	approved	for	the	treatment	of	autoimmune	diseases	including	systemic	lupus erythematosus and	multiple sclerosis. These antibody-based approaches	have shown limited	efficacy, typically limiting the	progression	of	the	autoimmune	disease	rather	than	ameliorating	the	disease	completely.	These	therapies	also	require long-term	administration	and	can	have	serious	side	effects. Recently a small academic clinical trial conducted by Mackensen and colleagues from the University of Erlangen in Germany	has	shown	that	targeting	CD19	with	CAR	T	therapies	can	profoundly	improve	outcomes	for	patients	with	lupus and	other	autoimmune	diseases.	CD19	is	a	B	cell	specific	antigen	that	is	highly	expressed	on	B	cells	including	malignant	B cells that cause	cancers like	B-ALL	and	autoreactive	B	cells that	are	a common feature	of	autoimmune	disease. In this academic	clinical	trial,	treatment	of	15	autoimmune	disease	patients	with	a	single	dose	of	autologous	CD19	CAR	T	cells resulted in rapid and durable responses in patients. These patients all had advanced disease, with multi-organ involvement	and	were	refractory	to	current	therapies.	The	treatment	showed	potential	transformational	clinical	benefit, with	all	patients	in	remission	or	with	major	reductions	in	symptoms	with	a	median	follow	up	of	15	months.	Toxic	effects were	manageable	and	mostly	mild. CD19 CAR T cell therapy shows the potential for superior efficacy compared to B cell depleting antibodies. It	may be possible	that	CD19	is	a	better	target	than	CD20	or	BAFF,	as	it	is	expressed	more	broadly	on	the	autoreactive	plasma	cells and	plasma	blasts	as	well	as	B	cells.	Additionally,	CAR	T	cells	may	be	better	at	depleting	the	B	cells	than	the	antibodies,	as they	can	penetrate	into	all	tissues,	including	some	that	antibodies	cannot	reach. The	future	promise	of	CAR	T	cell	therapy	for	autoimmune	diseases	will	be	driven	by	efficacy,	safety	and	cost	effectiveness. Existing	CD19	CAR	T	cell	therapies	are	effective	at	treating	B-cell	malignancies;	however,	the	extent	and	duration	of	the treatment	effects	and	disease	remission	as	well	as	the	potential	for	toxicities	including	CRS	and	neurologic	toxicity	varies considerably	between	the	different	approved	treatments.	Differences	in	efficacy	and	safety	are	likely	to	be	seen	between different	CD19	CAR	T	cell	therapy	approaches	for	autoimmune	diseases,	and	optimizing	the	CD19	targeting	module	may be important for enhancing efficacy and safety. Further, manufacturing T cells can be prohibitively costly if the manufacturing	process	is	not	appropriately	designed	to	support	parallel	processing	and	automation. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 8

 Our	Solution:	Advanced	T	Cell	Programming Our	technological	approach	is	the	development	of	advanced	T	cell	engineering	components	designed	to	directly	address clinical	challenges.	A	focus	in	our	early-stage	pipeline	is	incorporation	of	multiple	components	in	a	single	product. Advanced	Targeting	Technologies We	have	developed	advanced	antigen	targeting	technologies	to	improve	the	ability	of	our	programmed	T	cell	therapies	to selectively identify and target cancer cells and to deliver a sustained antitumour effect. These targeting technologies include	fast	off-rate	CARs,	novel	targets,	high	avidity	spacers,	dual-targeting	and	pattern	recognition. Fast	Off-Rate	CARs We	have	designed	programmed	T	cells	with	fast	off-rate	binders.	These	fast	off-rate	kinetics	are	similar	to	the	behaviour of	naturally	occurring	T	cells.	Obe-cel	has	this	enhanced	kinetic	profile,	which,	when	compared	to	data	reported	for	other CAR	T	cell	product	candidates	in	clinical	development	for	ALL	that	use	high	affinity	binders,	appears	to	result	in	reduced Cytokine	Release	Syndrome	and	in	increased	T	cell	engraftment.	We	use	Fast	Off-Rate	CARs	targeting	CD19	in	our	obe-cel, AUTO1/22	and	AUTO8	programs. Dual-Targeting	CARs Relapse	due	to	target	antigen	loss	or	down	regulation	is	a	major	cause	of	treatment	failure	in	CAR	T	cell	therapy.	We	have developed product candidates that target two antigens on a cancer cell and are designed to reduce the chances for relapse	due	to	antigen	escape.	Evidence	suggests	that	it	may	also	improve	a	response	in	those	patients	with	low	levels	of expression	of	a	target	antigen	on	their	cancer	cells.	We	use	Dual	Targeting	CARs	in	our	AUTO1/22	and	AUTO8	programs. Pharmacological	Control	of	T	Cell	Activity Management	of	toxicity	is	a	critical	step	in	the	successful	application	of	programmed	T	cell	therapies.	We	have	developed multiple	technologies	designed	to	pharmacologically	control	T	cell	activity in	the	event	a	patient	suffers	certain	serious adverse	events	related	to	the	T	cell	therapy.	Safety	switches	are	designed	to	selectively	eliminate	the	programmed	T	cells following	administration	of	a	pharmacological	agent,	whilst	tuneable	or	controllable	CAR	T	cells	allow	the	activity	of	T	cell therapy	to	be	dialled	down	following	administration	of	a	pharmacological	agent. Rituximab	Safety	Switch	(RQR8) The RQR8 safety switch is designed to selectively eliminate the programmed T cells by the administration of the commercially available monoclonal antibody rituximab. Once administered, rituximab binds to the engineered CD20 epitopes	on	the	surface	of	the	programmed	T	cell	and	triggers	cell	death.	We	use	the	RQR8	safety	switch	in	our	AUTO4, AUTO5	and	AUTO6NG	programs. Rapamycin	Safety	Switch	(RapaCasp9) The	RapaCasp9 safety switch is designed to selectively eliminate the	programmed	T cells by the administration	of the commercially	available	drug rapamycin.	Once	administered, rapamycin	heterodimerises	caspase	9	via	FRB	and	FKBP to activate	a	cell	death	cascade	and	selectively	eliminate	the	programmed	T	cells. Tetracycline	Controllable	CAR	(TetCAR) TetCAR	is	a	controllable	CAR	T	cell	system	designed	to	reversibly	dampen	the	activity	of	the	programmed	T	cells	by	the administration of the commercially available antibiotic tetracycline to a patient. Once administered, tetracycline temporarily	dislocates	the	CAR	signalling	domain	from	the	cancer	antigen	binding	domain	leading	to	deactivation	of	the	T cell	therapy.	Activity	is	then	restored	on	clearance	of	the	pharmacological	agent	from	the	patient. Tumour	Microenvironment	Shielding Tumour cells and other cells in the tumour	microenvironment can debilitate antitumour immune responses. Proteins expressed on tumour cells can trigger inhibitory receptors on T cells to block their ability to eliminate the tumour. Secretion of TGFβ by the tumour and other cells can shut down the activity of a T cell therapy.	We have developed technologies	designed	to	shield	our	programmed	T	cells	from	these	immunosuppressive	pathways. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 9

 Checkpoint	Shielding	(dSHP2) Immune checkpoint receptors act through a common signalling pathway inside the T cell that prevents normal T cell activation.	We	have	developed	a	modified	version	of	an	adaptor	protein,	SHP2,	that	in	preclinical	studies	has	been	shown to	efficiently	counteract	the	inhibition	of	T	cells	resulting	from	the	PD-L1/PD-1	interaction. In	addition, it is	designed	to simultaneously disarm multiple inhibitory receptors on the cancer cell. We use the dSHP shielding module in our AUTO6NG	program. Enhanced	Activity One	of	the	challenges	of	targeting	some	solid	tumours	is	the	lack	of	such	easily	accessible	stimulation	for	programmed	T cells, leading to poor persistence and a weak antitumour activity. Co-administration with cytokines can boost T cell activity	and	persistence.	Certain	cytokines	can	potentiate	the	antitumour	of	the	T	cell	therapy	by	recruiting	and	activating other	immune	cells	to	kill	the	tumour. However,	systemic	or	local	administration	of	cytokines	can	be	toxic,	therefore	we	have	developed	programming	modules that	are	designed	to	harness	the	enhanced	activity	of	cytokines	whilst	avoiding	the	potential	for	toxicities. Chimeric	Cytokine	Receptors	(CCRs) The CCR is a programming module that is designed to deliver a cytokine signal directly inside T cells without administration	or	secretion	of	cytokines	themselves.	We	use	proteins	from	an	antibody	structure	to	stably	heterodimerize two	cytokine	signalling	domains	together	to	deliver	a	proliferative	and	survival	signal	into	our	T	cells.	Preclinical	data	has demonstrated the potential for the CCR to improve the persistence and activity of CAR T cell therapy against solid tumours.	We	use	the	CCR	enhanced	activity	module	in	AUTO6NG. Host	Immune	System	Recruitment	(ssIL12) IL-12	is	a	potent	antitumour	cytokine	that	mediates	the	activity	of	many	different	antitumour	immune	cells.	The	majority of	clinical	studies	involving	treatment	of	patients	with	IL-12	were	associated	with	severe	systemic	side	effects	mediated by	high	levels	of	IFNγ.	Our	ssIL12	module	is	designed	to	secrete	very	low	levels	of	IL-12	from	our	T	cells	and	our	preclinical data	demonstrates	the	potential	for	ssIL12	to	provide	antitumour	activity	without	systemic	toxicity. Engineering	survival	signal	(Fas-TNFR) CAR	T	cells	have	shown	remarkable	efficacy	against	haematological	cancers,	but	their	effectiveness	in	solid	tumours	has been limited	by inhibitory factors expressed	by the tumour	or its	microenvironment.	One such inhibitory factor is Fas ligand	(“FasL”),	which	binds	to	the	Fas	receptor	(CD95)	on	the	surface	of	an	activated	T	cell	and	triggers	the	CAR	T	cell	to die by apoptosis. Our Fas chimeras consist of the extracellular domain of Fas fused to the intracellular domain from different TNF receptor superfamily	members. Expression of these chimeras in a CAR T cell not only blocks apoptosis triggered	by	FasL,	but	results	in	co-stimulation,	which	promotes	CAR	T	cell	survival	and	proliferation. Business	Review Our	Commercial	Product:	AUCATZYL	for	Adult	r/r	B-ALL AUCATZYL/obe-cel, formerly known as AUTO1, is a gene therapy product consisting of autologous T cells that are transduced with a lentiviral vector to express a novel anti-CD19 Chimeric Antigen Receptor (CD19 (CAT) CAR). The transduced T cells express second-generation CARs in which the CD19 CAR construct uses 41BB-ζ and CD3- ζ endodomains. CD19	is	an	ideal	target	for	a	CAR	T	cell	therapy	as	it	is	a	cell	surface	marker	for	B-precursor	cells	and	B-lymphocytes	that	is present	on	most	B	cell	malignancies.	CD19	is	also	a	cell	surface	marker	expressed	broadly	on	the	autoreactive	B-cells	and plasma	cells that	are	associated	with	autoimmune	diseases	such	as lupus. Upon	CD19	directed	CAR	T	cell therapies, it also leads to	B-cell aplasia	which can	be	used as a pharmacodynamic	marker. CD19	CAR	T cell therapies have	proven effective in treating	B-cell leukaemias,	B-cell lymphoma	and	early	evidence	suggest they	are	effective in treating	b-cell mediated	autoimmune	diseases.	Efficacy	is	dependent	on	engraftment	and	expansion	of	the	CAR	T	cells.	However,	rapid activation and expansion of CAR T cells can result in CRS and/or ICANS,	which in some cases can be life-threatening, particularly for elderly patients and patients with comorbidities that have a poor tolerance for toxicity. Furthermore, excessive activation of CAR T cells can lead to cell exhaustion and limit their engraftment and expansion,	which	may impact	the	initial	efficacy	and	durability	of	therapeutic	effect.	Obe-cel	is	an	autologous	therapy	in	which	a	patient’s	T	cells are	genetically	modified	to	express	a	novel	CD19-specific	binder	designed	to	reduce	side	effects	observed	with	this	class of	therapeutics. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 10

 AUCATZYL/obe-cel recognises and interacts with the CD19 target with a fast off-rate enabled by the novel CAT scFv binding domain. This property allows the AUCATZYL/obe-cel cells to efficiently recognise target cells, inject cytotoxic proteins	to	initiate	the	natural	self-destruction	process	present	in	all	human	cells	and	then	rapidly	disengage	from	them	in order	to	engage	the	next	target	cell,	a	process	also	known	as	serial	killing.	Rapid	disengagement	from	the	target	antigen	is expected to minimize excessive activation of the programmed T cells, reduce toxicity and may also reduce T cell exhaustion. Clinical	Development	of	Obe-cel	in	Adult	ALL Background	of	Adult	ALL According to the	American	Cancer	Society, adult	ALL	was	predicted to	affect	approximately	6,500	adults in the	United States in 2023. Combination chemotherapy enables 90% of adult patients to experience complete remission (“CR”). However,	the	majority	of	these	remissions	are	not	long-lasting	in	adult	patients.	Despite	this	initial	CR,	and	in	contrast	to paediatric	ALL,	the	prognosis	of	adult	ALL	is	still	poor	and	has	not	changed	significantly	during	the	last	two	decades,	with long-term	remission	rates	limited	to	30-40%.	Approximately	50%	of	all	adult	ALL	patients	will	relapse,	and	data	from	the Medical Research	Council’s	UKALL12/ECOG	2993 study, published in 2007, found that five-year	overall survival (“OS”), rate	in	adults	who	relapse	following	standard	multi-agent	chemotherapy	is	7%.	In	a	published	2016	retrospective	analysis conducted	by	the	Group	for	Research	on	Adult	Acute	Lymphoblastic	Leukaemia	on	adult	patients	(age	18-63)	in	France, Belgium	and	Switzerland relapsing after first-line	paediatric-inspired therapy, the	overall survival at 2 and	5 years	was 19.3% (14–24%) and 13.3% (8–18%), respectively. The only curative option for relapsed or refractory ALL consists of achieving a second CR by salvage therapy followed by an allogeneic hematopoietic stem cell transplant (“allo-HSCT”). Without allo-HSCT, a subsequent relapse occurs in nearly all patients. However, less than half of patients achieve a second CR, and therefore only a subset	will be eligible for this procedure. Even then, less than one-third of patients receiving the transplant are expected to sustain long-term disease-free survival. Further, allo-HSCT is associated	with severe morbidity and significant mortality. Many patients with relapsed or refractory ALL will have been maximally treated	with	chemotherapy,	and	often	do	not	achieve	a	second	CR	in	order	to	be	eligible	for	allo-HSCT. Two	targeted	monoclonal	based	therapies	have	been	approved	in	a	number	of	jurisdictions,	including	the	United	States and	the	EU,	for	the	treatment	of	adult	ALL:	blinatumomab	and	inotuzumab	ozogamicin.	Both	of	these	therapies	achieve high	CR	rates,	but	durability	is	limited.	In	a	randomized	Phase	3	clinical	trial	of	blinatumomab	in	heavily	pretreated	B-cell precursor	ALL,	the	blinatumomab	arm	achieved	a	CR	rate	of	44%,	of	which	76%	also	achieved	MRD-negative	CR,	and	the median	duration	of	remission	was	7.3	months.	The	median	OS	in	those	patients,	though	significantly	improved	compared to chemotherapy, was still only 7.7 months. Similarly, in a Phase 3 clinical trial of inotuzumab ozogamicin, a higher percentage of patients achieved MRD-negative CR when treated with inotuzumab compared to standard-of-care chemotherapy,	but	the	median	duration	of	remission	was	4.6	months	and	median	OS	was	equally	short	with	7.7	months. On	October	1,	2021	the	FDA	approved	the	use	of	the	CAR	T	cell	therapy	brexucabtagene	autoleucel	(“Tecartus”)	for	adults with	B-cell	precursor	ALL	that	has	not	responded	to	treatment	(refractory)	or	has	returned	after	treatment	(relapsed).	The European	Commission	approved	Tecartus	for	adults	aged	26	and	over	with	relapsed	or	refractory	B-cell	precursor	ALL	in September	2022. On	November	8,	2024	the	FDA	approved	the	use	of	obe-cel	for	the	treatment	of	adults	with	r/r	B-ALL. Obe-cel	Phase	1b/2	Clinical	Trial	in	Adult	ALL	(FELIX	Trial) We	initiated	the	FELIX	study,	a	Phase	1b/2	clinical trial	of	obe-cel for	the	treatment	of	adult	r/r	B-Acute	Lymphoblastic Leukaemia,	in	2020. The	data	were	published	in	the	New	England	Journal	of	Medicine	in	December	2024. The	published	data	were	from	a	pooled	analysis	of	data	from	all	patients	across	all	cohorts	in	the	FELIX	Phase	1b/2	study. Of the	153 r/r	B-ALL	patients	enrolled in the	FELIX study,	127 (83.0%) received	at least	one	obe-cel infusion	and	were evaluable.	Eligible	patients	underwent	leukapheresis,	and	bridging	therapy,	except	blinatumomab,	was	permitted	at	the investigator’s discretion. Obe-cel was administered in a bone marrow (“BM”) burden adjusted split dose following lymphodepletion,	with	a	BM	mandated	prior	to	lymphodepletion	to	guide	dosing.	The	second	obe-cel	dose	was	given	in the	absence	of	severe/unresolved	toxicity. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 11

 The	primary	end	point	was	overall	remission	(“CR/CRi”).	In	the	pivotal	cohort	of	patients,	(cohort	IIA	(n=94)),	the	CR/CRi for	patients	who	received	at	least	one	infusion	of	obe-cel	was	76.6%.	Across	all infused	patients	(n=127),	of	the	91/127 with	≥5%	BM	blasts	pre-lymphodepletion,	the	CR/CRi	was	74.7%.	Median	response	duration	for	all	infused	patients	was 21.2	months.	Median	event-free	survival	(EFS)	was	11.9	months	and	the	estimated	6-	and	12-month	event-free	survival rates	were	65.4%	and	49.5%,	respectively.	BM	burden	pre-lymphodepletion	correlated	with	median	event-free	survival; patients	with low (<5%	BM	blasts), intermediate (≥5–≤75%	blasts), and high (>75%	blasts) BM	burden had event-free survival	rates	at	12	months	of	68.0%,	54.9%	and	25.0%,	respectively. Median	overall survival (“OS”)	was	15.6	months	and	estimated	6-	and	12-month	overall survival rates	were	80.3%	and 61.1%, respectively. BM	burden	pre-lymphodepletion correlated	with	overall survival; patients	with low, intermediate, and high BM burden had an overall survival rate at 12	months of 71.5%, 58.7% and 55.0%, respectively. BM burden before	enrolment	also	influenced	event-free	and	overall	survival. Of the 127 patients infused (pooled across all study cohorts), 99 patients responded. Of the responders, 18 patients (18.2%) proceeded to allo-Stem Cell Transplant (“allo-SCT”) while in remission at a median of 101 days post-obe-cel infusion.	In	6/18	(33.3%),	this	was	a	second	allo-SCT. Median	duration	of	CAR	T	persistence	by	droplet	digital	PCR	(ddPCR)	in	peripheral	blood	was	17.8	months. Obe-cel	was	associated	with	minimal	immunotoxicity.	CRS	and	ICANS	rates	(Grade	≥3)	were	2.4%	and	7.1%,	respectively. Overall, 87 (68.5%) patients developed CRS, and 29 (22.8) developed ICANS. Severe ICANS post-obe-cel	were seen as largely limited to patients with high BM burden pre-lymphodepletion. Intensive care unit admissions occurred in 20 (15.7%) patients for a median of 5.5 days (range: 1−37) of which 7 of the 20 patients were admitted due to immunotoxicity	management	(5	ICANS,	2	CRS). Most recently	at the	European	Haematology	Association	annual	meeting in	2025, longer term	follow	up	data from	the FELIX study	were presented. At the updated	median follow	up of 32.8	months, 38.4%	of responders	were in ongoing remission	without	consolidative	allo-SCT	or	other therapies.	The	24-month	probability	of	Event	Free	Survival	was	43%, and	for	Overall	Survival	was	46%,	with	an	emerging	long-term	plateau	observed.	A	substantial	subset	of	patients	benefit from standalone treatment	with	obe-cel, achieving long-term remission.	No	new safety signals	or	Grade	≥3 secondary malignancies	were	observed	at	the	extended	follow-up.	These	results	suggest	that	obe-cel	may	be	a	definitive	treatment for	some	patients	with	r/r	B-ALL. Obe-cel	Phase	1	Clinical	Trial	in	Adult	ALL	(ALLCAR19	Trial) In the first	quarter	of	2018,	our	academic	partner	University	College	London	(“UCL”) initiated	a	single-arm,	open label, multicentre	Phase	1 clinical trial of obe-cel, named the	ALLCAR19 trial, in patients aged	16 to 65 years	with	high-risk, relapsed	or	refractory	CD19	positive	B-lineage	ALL.	The	clinical	trial	was	conducted	at	sites in	the	United	Kingdom.	The trial	enrolled	patients	with	a	high	tumour	burden;	45%	of	treated	patients	had	50%	or	greater	bone	marrow	blasts.	In	the trial, 20 patients received obe-cel; product for 14 of those patients	was	manufactured using a semi-automated, fully- enclosed	process.	The	therapy	was	well tolerated,	with	no	patients	experiencing	Grade	3	or	higher	CRS.	Three	patients (15%), all of whom had high leukaemia burden (>50% blasts), experienced Grade 3 ICANS that resolved swiftly with steroids. Of the 20 patients evaluable for efficacy, 17 patients (85%) achieved minimum residual disease (“MRD”)- negative	CR	at	one	month. A	pooled	analysis	of long-term follow-up	data from	ALLCAR19	and	FELIX	Phase	1b	Studies	were	presented	at the	ASH, meeting in December 2023. Data from the pooled analysis of r/r B-ALL patients (n=36) treated with obe-cel in the ALLCAR19	and	FELIX	Phase	1b	studies	showed	high	remission	rates	of	81%	(29/36).	After	a	median	follow-up	of	3	years and without subsequent transplant, 41% of patients continued in complete remission. The estimated EFS rate with censoring	of	subsequent	transplant	or	new	treatment	was	45%	at	36	months;	all	patients	in	ongoing	remission	were	MRD negative	at	last	assessment	and	median	duration	of	response	was	not	reached. Regulatory	Status	and	Plans The US FDA granted	marketing approval for obe-cel on November 8, 2024 under the brand name AUCATZYL for the treatment of r/r B-ALL. The approval is based on data from the Phase 2 cohort of FELIX study. The MHRA granted AUCATZYL	conditional	marketing	authorization	in	April	2025	for	Adult	Patients	(≥	18	years)	with	r/r	B-ALL. In	November 2025,	NICE	recommended	AUCATZYL	for	use	in	the	National	Health	Service	(“NHS”)	in	England	and	Wales	as	a	treatment option	for	adult	patients	(≥26	years)	with	r/r	B-ALL.	We	launched	AUCATZYL	in	the	United	Kingdom	in	January	2026,	and	it is available through routine commissioning by the NHS. On 17 July 2025, the European Commission (“EC”) granted marketing	authorization	for	AUCATZYL	in	adult	patients	(age	26	and	older)	with	r/r	B-ALL.	Evaluation	of	potential	pricing and	feasibility	of	market	entry	opportunities	in	certain	European	Union	(“EU”)	countries	is	ongoing;	however,	at	this	time, launch	in	the	EU	is	on	hold	and	the	Company	does	not	anticipate	any	EU	sales	of	AUCATZYL	in	2026. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 12

 Commercialization	Strategy	for	AUCATZYL We have retained worldwide commercial rights for AUCATZYL. We plan to expand our global commercialization capabilities	over	time	such	that	we	are	able	to	commercialize	any	product	candidate in	a	broader	number	of	countries over	time,	but	with	a	focus	on	achieving	an	early	presence	in	the	US	and	the	U.K.	We	may	pursue	strategic	collaborations with	third	parties	in	order	to	maximize	the	commercial	potential	of	AUCATZYL. Having	achieved	marketing	approval	for	AUCATZYL	for	the	treatment	of	patients	with	r/r	B-ALL	in	the	US,	U.K	and	parts	of Europe,	we	are	expanding	upon	our	commercial	launch	in	those	countries.	In	addition	to	the	standard	sales	&	marketing elements	and	medical	affairs	activities required	to	successfully	commercialize	an	oncology/haematology	product, there are several additional requirements needed for effectively commercializing CAR-T cell therapies, including bespoke processes for distribution, patient scheduling, centre engagement and a dedicated treatment centre service hub. The product	may be administered only by authorized centres that are specialized in haematology and have the necessary infrastructure	and	capabilities	for	administering	CAR-T	therapies. In	December 2024,	AUCATZYL	was added to the	National Comprehensive	Cancer	Network&reg;, (“NCCN”) Clinical Practice Guidelines	in	Oncology,	(“NCCN	Guidelines&reg;”),	for	the	treatment	of	adult	r/r	B-ALL.	The	NCCN	is	a	not-for-profit	alliance	of 30 leading	cancer	centres	devoted	to	patient	care,	research,	and	education.	The	NCCN	Guidelines	are	a	comprehensive set	of	guidelines	detailing	the	sequential	management	decisions	and	interventions	that	currently	apply	to	97%	of	cancers affecting	patients in the	US	and	are intended	to	ensure	that	all	patients receive	preventive,	diagnostic, treatment,	and supportive	services	that	reflect	the	latest	evidence	in	oncological	patient	care. Our	Manufacturing	and	Logistics	Capabilities We	are	devoting significant resources to process development and	manufacturing in order to ensure	high	quality and reliable product supply to patients, as well as to reduce our per unit manufacturing costs and time to market for AUCATZYL	and	any	of	our	programmed	T	cell	product	candidates	for	which	we	obtain	regulatory	approval. The manufacture and delivery of programmed T cell therapies to patients involves complex, integrated processes, including harvesting T cells from patients, manufacturing viral vectors with nucleic acid content encoded with our programming	modules,	manufacturing	programmed	T	cells	using	the	viral	vectors	ex	vivo,	multiplying	the	T	cells	to	obtain the	desired	dose,	and	ultimately	infusing	the	T	cells	back	into	a	patient’s	body. Commercial success in T cell therapies requires a	manufacturing	process that is reliable, scalable and economical.	We have	established	a	manufacturing	process that is scalable	and	serves	as	a	manufacturing	platform	designed	to	support rapid development of our programmed T cell therapy product candidates through clinical trial phases and regulatory approval	processes.	We	are	using	a	semi-automated,	fully	enclosed	system	for	cell	manufacturing,	which	is	designed	to provide	a common	platform	suitable for	manufacturing	all of	our	product candidates. This	platform	allows for	parallel processing	having	the	ability	to	scale	for	commercial	supply	in	a	controlled	environment	at	an	economical	cost.	We	have established reliable and consistent viral vector production and viral transduction processes further, also a key to our process	reproducibility	and	reliability. Our	manufacturing	and	logistics	process	is	designed	to	ensure	that	product	integrity	is	maintained	during	shipment	along with	accurate	tracking	and	tracing	of	shipments.	We	are	expanding	internal	manufacturing	and	supply	capabilities	as	well as	the	use	of	expert	service	providers	on	maturing	our	vein-to-vein	logistics	in	support	of	commercial	operations.	Chain	of identity	and	chain	of	custody	electronic	systems	are	in	place	to	ensure	transport	and	processing	reliability. Our	manufacturing	and	commercialization	strategy	requires	a	fully	integrated	vein-to-vein	product	delivery	cycle.	Having established	manufacturing	processes	suitable	for	commercialization	early in	the	development	of	AUCATZYL	has	allowed us	to	focus	on	expanding	manufacturing	capacity	during	our	commercial	launch.	Our	purpose-built	facility,	the	Nucleus,	is located	in	Stevenage,	U.K	and	covers	70,000	square	feet.	This	facility,	which	has	a	global	reach,	can	meet	our	near	and mid-term	clinical	and	commercial	needs	allowing	ample	time	for	expanding	our	manufacturing	footprint	when	needed.	In March 2024, the Nucleus facility obtained a Manufacturer’s Importation Authorization (MIA) together with the accompanying Good Manufacturing Practice (“GMP”) certificate. These licenses enable us to manufacture both commercial and clinical autologous drug products in the facility. The	Nucleus provides	multiple clean rooms,	QC labs, warehouse	and	administrative	space	and	is	being	fitted	out	in	a	phased	manner	as	demand	requires.	At	full	capacity,	we expect the	Nucleus facility to	provide	manufacturing	capacity for	approximately	2,500	batches	annually.	Our	plan is to establish our manufacturing infrastructure in a manner that would minimize logistical complexities and costs for all regions	going	forward. We believe our scalable closed-system manufacturing process, along with our proprietary and modular T cell programming	technologies,	would	be	challenging	and	costly	for	potential	competitors	to	replicate. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 13

 Our	Manufacture	and	Delivery	Performance Data	on	manufacturing	and	delivery	performance	for	obe-cel	in	the	FELIX	clinical	trial	were	published	in	the	New	England Journal of Medicine in December 2024. The FELIX study successfully demonstrated the robust operability of obe-cel manufacturing,	QC	and	logistics	processes,	meeting	target	V2C	(time	from	leukapheresis	to	quality	release)	and	V2D	(time from	leukapheresis	to	delivery	of	product	to	the	hospital).	Median	V2C	and	V2D	times	were	21	and	24	days,	respectively. All apheresis starting	material	was successfully	processed	despite the	multitude	of constraints	posed	by the	COVID-19 pandemic. In total, 96%	of	manufactured obe-cel batches reached their target dose of 410 x 106 CAR T cells. Further optimization and improvements made during the study increased reliability, consistency, and precision of the manufacturing	process, and supported the	development	of the	Nucleus	manufacturing facility	with	greater	production capacity.	Commercially	in	2025	we	achieved	≥90%	manufacturing	success	rate. Manufacturing	Agreements	with	Third	Parties We	obtain	viral	vector	for	commercial	supply	of	AUCATZYL	and	for	late	stage	clinical	trials	from	our	partner	AGC	Biologics. We also have	manufacturing agreements	with other contract	manufacturing and development organizations for early phase	vector	manufacturing.	All	vector	manufacturing is	done in	accordance	with	current	Good	Manufacturing	Practice (“cGMP”) in compliant manufacturing facilities. The manufacturing agreements governing the external supply arrangements	also	provide for	access to services including	quality	management systems,	qualified	persons for	product release,	office	space,	frozen	storage	and	warehousing	services. In	March	2018,	we	entered	into	a	strategic,	long-term	supply	agreement	with	Miltenyi	Biotec	GmbH	(“Miltenyi”),	for	the supply	of	Miltenyi’s	CliniMACS	Prodigy	instruments,	reagents	and	disposables	for	the	manufacture	of	our	programmed	T cell therapies, including for pre-clinical, clinical and commercial production of AUCATZYL, as well as the provision of related	support	services.	We	amended	the	supply	agreement	most	recently in	September	2023.	The	supply	agreement sets forth procedures to ensure continuity of supply to us of	Miltenyi’s products, both during the clinical phase and commercial	phases	of	our	product	candidates.	After the initial ten-year term	of the	agreement,	we	have two	separate options to renew the agreement, each for an additional five-year term. The supply agreement contains customary termination	provisions, allowing for termination	by a	party	upon the	other	party’s uncured	material breach, upon the other	party’s bankruptcy	or insolvency	or	upon the	other	party	being subject to an	extended	period	of force	majeure events. We may also terminate the supply agreement upon advance written notice, if we decide to suspend or discontinue	the	development	or	commercialization	of	our	product	candidates.	The	supply	agreement	is	governed	under the	laws	of	Germany. Competition There	are	two	direct	in	class	competitors	to	AUCATZYL	approved	for	the	treatment	of	adult	patients	with	r/r	B-ALL:	the autologous	CAR	therapies	Tecartus	and	Kymriah.	Tecartus	is	approved	for	use	in	adult	B-ALL	and	Kymriah	is	approved	for use	in	adolescents	and	young	adults	(i.e.,	patients	up	to	the	age	of	25).	We	believe	AUCATZYL	has	a	differentiated	safety profile	and	shows	potential	for	longer	term	outcomes	when	compared	to	these	current	approved	therapies. In addition, it is possible that companies could take other autologous CAR T cell products forward in adult ALL or allogeneic “off-the-shelf” CAR T cell therapies could be developed which would be considered direct competitors. Allogeneic	products	are	in	early	development	in	indications	other	than	B-ALL,	and,	because	these	products	are	not	made from the	patient's	own	cells, they	might	be	more convenient to	deliver,	without the	need to	wait for	a	product to	be manufactured (typical manufacturing times for autologous products are currently 18-25 days). However, this class of product	has	not	shown	the	same	levels	of	durable	activity	and	the	products	in	clinical	trials	are	therefore	likely	to	require periodic repeat dosing as opposed to autologous products, which allow for the therapy to be given as a one-time treatment. Our	Product	Candidates	for	the	Treatment	of	Haematological	Cancers	and	Autoimmune	Diseases Our	clinical-stage	product	candidates	targeting	haematological	cancers	are	obe-cel,	AUTO1/22	and	AUTO8. Additionally, obe-cel	is	also	being	explored	as	a	potential	therapeutic	approach	targeting	certain	autoimmune	diseases. Obe-cel for	the	Treatment	of	Paediatric	ALL,	B-NHL	and	other	B-cell	malignancies In addition to AUCATZYL/obe-cel for the treatment of adult r/r B-ALL, we are advancing obe-cel in other oncology indications	including	paediatric	B-ALL	and	B-NHL,	for	which	we	have	initiated	the	Phase	1b/2	CATULUS	trial. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 14

 Background	of	Paediatric	ALL According	to	the	American	Cancer	Society,	B-ALL	is	most	common	in	childhood,	peaking	between	two	and	four	years	of age. As per the National Cancer Institute Surveillance, Epidemiology and End Results statistics database, there are approximately	3,400	new	cases	of	paediatric	B-ALL	diagnosed	in	the	United	States	each	year. The current standard of care for both paediatric and adult B-ALL patients is a standard regimen of combination chemotherapy.	Paediatric	patients	typically	respond	well	to	the	complex	first-line	chemotherapy	treatment.	According	to the	American	Cancer	Society,	the	five-year	survival	rate	for	children	with	B-cell	ALL	is	more	than	85%	overall.	In	paediatric populations,	blinatumomab	has	demonstrated	efficacy	both	in	patients	with	relapsed	or	refractory	disease,	as	well	as	a component	of frontline	combination therapy for	newly	diagnosed	patients.	The recently	published	COG	AALL1731 trial was a randomized phase 3 trial evaluating the benefit of the addition of blinatumomab to standard chemotherapy in patients	with	National	Cancer	Institute	(NCI)	standard-risk	B-ALL.	With	a	median	follow-up	of	2.5	years,	3-year	DFS	was 96.0%	&plusmn;	1.2%	among	patients	randomized	to	receive	blinatumomab	with	chemotherapy,	compared	with	87.9%	&plusmn;	2.1%	in the	chemotherapy-alone	group	(Gupta	et	al.,	NEJM	2025). However,	10	to	20%	of	paediatric	B-cell	ALL	patients	relapse	with	chemotherapy-resistant	disease.	These	patients	are	re- treated	with intensive	chemotherapy,	and	those	that	respond	may	proceed	to	receive	an	allogenic	stem	cell transplant (“SCT”). However, SCT can be associated	with significant long-term	morbidity due to the risk of treatment associated developmental	impairments,	developing	graft-versus-host	disease,	and	transplant-related	mortality,	although	the	risk	of death	have	declined	with	better	post-transplant	management. A	phase	3	trial	conducted in	Europe	enrolled	children	with	high	risk first relapse	of	B-ALL (relapse	at	<18	months	after diagnosis	or	marrow	relapse	at	≥18	months	from	diagnosis	but	<6	months	after	completion	of	therapy).	Those	achieving an	M1	(<5%	blasts)	or	M2	(≥5	but	<25%	blasts)	marrow	after	reinduction	therapy	were	treated	with	2	cycles	of	standard consolidation	chemotherapy	and	were	then	randomized	to	receive	either	blinatumomab	or	consolidation	chemotherapy before	planned	allogeneic	HSCT.	In	total,	108	patients	were	randomized	before	early	termination	of	enrolment	because	of meeting	prespecified	criteria	finding	benefit	of	blinatumomab	(Locatelli	et	al.,	JAMA	2021;325;(9):843-854.	doi:10.1001/ jama.2021.0987).	With	a	median	follow-up	of	44	months,	blinatumomab	demonstrated	improved	EFS	across	subgroups and	improved	OS	(HR,	0.34;	95%	CI,	0.17-0.69)	(Locatelli	et	al..,	Leukaemia	37,	222–225	(2023).	https://doi.org/10.1038/ s41375-022-01770-3).	In	parallel,	the	COG	performed	a	similar	randomized	AALL1331	phase	3	study	in	patients	with	high- risk (marrow relapse	<	36	months after initial diagnosis	or isolated	EMD relapse	<18	months after initial diagnosis) or intermediate	risk	first	relapse.	As	in	the	European	trial,	randomization	was	terminated	early	because	of	the	combination of findings	of	higher	disease-free	survival (DFS),	OS,	and	MRD	clearance,	as	well	as lower	toxicity in the	blinatumomab arm compared with the chemotherapy arm (Hall AG and Rau RE, Blood Adv 2025; https://doi.org/10.1182/ bloodadvances.2024014043).	With	a	median	follow-up	of	2.9	years,	2-year	DFS	in	the	blinatumomab	arm	was	54.4%	vs 39.0%	in	the	chemotherapy	arm	(HR,	0.7;	95%	CI,	0.47-1.03)	and	OS	in	the	blinatumomab	arm	was	71.3%	vs	58.4%	in	the chemotherapy arm (HR, 0.62; 95% CI, 0.39-0.98) (Brown PA et al., JAMA 2021;325;(9):833-842. doi:10.1001/ jama.2021.0669). Patients	with	high-risk	clinical	or	genetic	features	including	gene	abnormalities,	as	well	as	those	who	have	an	inadequate response to initial chemotherapy,	may	not respond	well	with the	current	available treatments for	B-cell	ALL (including SCT),	some	of	these	patients	will	have	a	five-year	OS	rate	of	approximately	15%.	Additionally,	long-term	survival	rates	are only approximately 10 to 20% among patients receiving a second SCT and negligible in those unable to proceed to a second	transplant. There	is	still	a	significant	unmet	medical	need	in	paediatric	patients	with	high-risk	relapsed	or	refractory	B-cell	ALL.	CD19 CAR	T	cell	therapies	have	been	developed	for	these	patients.	The	CD19	CAR	T	therapy,	Kymriah,	however,	is	not	approved in	patients	with	first	relapse.	In	the	approved	indication	in	refractory	patients	or	patients	up	to	25	years	of	age	in	second or later relapse,	Kymriah	has shown	approximately	80%	of complete	molecular response rate.	However,	at six	months after	treatment,	approximately	40%	of	the	patients	relapsed	and	the	majority	of	the	relapses	were	CD19	negative	disease, with	approximately	two-thirds	of	relapses	determined	to	have	been	due	to	loss	of	CD19	on	the	target	cells	in	one	study. CD19	CAR	T	cell therapies	have	been tested in	paediatric	B-ALL	patients	and	have shown	sustained responses	without allo-HSCT.	In	adult	ALL,	however,	one	of	the	major	challenges	has	been	severe	toxicity,	including	death	due	to	CAR	T	cell- mediated	toxicity	observed	in	the	clinical	trials	of	these	products.	Obe-cel	has	been	designed	to	reduce	toxicity	but	still sustain	durable	CRs Obe-cel	Phase	1b	Clinical	Trial	in	Paediatric	B-ALL In December 2023, Autolus initiated the Phase 1b CATULUS trial to evaluate the safety and efficacy of obe-cel in paediatric	patients	with	r/r	B-ALL	and	r/r	B-NHL.	This	is	a	single-arm,	open	label,	multicentre	trial	enrolling	patients	aged 18	and	younger. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 15

 The	CATULUS	trial	is	a	single-arm,	open-label,	multicentre	Phase	1	study	enrolling	high-risk	patients	under	age	18	with	r/r B-ALL that is primary refractory, in high-risk first relapse, or in second	or later relapse. At the	ASH annual	meeting in December 2025 initial data from the study were presented. The safety profile of obe-cel in paediatric patients was consistent with that previously reported in adults, with low rates of high-grade CRS and ICANS (both 8.7%). Twenty patients	were in	ongoing remission at data cut-off	with a	median follow-up	of 8.8	months. These	preliminary findings support	further	exploration	of	obe-cel	in	paediatric	R/R	B-ALL.Currently,	the	Phase	2	pivotal	expansion	cohort	is	open	for enrolment	in	the	US,	UK	and	Spain. In	October	2025,	FDA	granted	regenerative	medicine	advanced	therapy	(RMAT)	designation	to	obe-cel	for	the	treatment of	paediatric	patients	with r/r	B-ALL.	The	RMAT	designation is	a	program	created	under the	21st	Century	Cures	Act to accelerate	development	and	regulatory	review	of	regenerative	medicine	therapies, including	cell	therapies, intended	to treat	serious	or	life-threatening	diseases. The	data	reported	from	the	CATULUS	trial	are	consistent	with	previous	data	reported	in	the	academic	UCL-led	CARPALL trial	in	patients	aged	24	years	or	younger	with	high-risk	relapsed	or	refractory	CD19	positive	B-ALL,	which	were	published in	the	journal	Nature	Medicine	in	2019. Obe-cel	Phase	1	Clinical	Trial	in	other	B-cell	malignancies	(ALLCAR19	and	CAROUSEL	Trials) The	ALLCAR19	clinical	trial	has	also	been	expanded	to	include	three	additional	cohorts	with	a	total	of	40	patients: • 10	patients	with	r/r	DLBCL	(including	transformed	FL,	but	not	Richter’s	transformation); • 10	patients	with	relapsed	or	refractory	B-cell	CLL	/	small	lymphocytic	leukaemia;	and • 20	patients	with	relapsed	or	refractory	indolent	B-NHL	(either	FL,	MCL	or	marginal	zone	lymphoma). Our collaborators at UCL have submitted a full manuscript of all 40 patients treated in the extension cohorts to the journal	Blood	in	January	2026.	The	abstract	of	this	manuscript	states	the	following: • 40 received obe-cel (10 patients per disease group). No patients experienced ≥grade 3 cytokine release syndrome	and	1/40	(3%)	experienced	grade	3	neurotoxicity.	Overall	response	rate	was	36/39	(92%).	PFS	at	6	and 12 months was 87% (95% confidence interval [CI], 72–94) and 76% (95% CI, 60–87), respectively. Excellent expansion (geometric mean Cmax: 113,047 copies/&micro;g genomic DNA) and CAR T persistence were observed (19/23	patients	alive	and	progression-free	at last follow-up).	Obe-cel	has	a	good	safety	profile,	high remission rates and durable responses in r/r adult B-cell cancers beyond B-ALL. Preliminary data support further development	of	obe-cel	for	these	indications. • The	median	follow-up	of	the	entire	extension	cohorts	was	24.2	months	(range,	1.3–48.4). • The	median	follow-up	for	the	different	cohorts	was	as	follows: ◦ DLBCL:	Median	observed	follow-up	post-infusion	was	36.1	months	(range,	1.4-39.4). ◦ FL:	Median	follow-up	from	infusion	was	47.8	months	(range,	18.2-48.4). ◦ MCL:	Median	follow-up	from	infusion	was	18.8	months	(range,	3.9-48.0). ◦ CLL/SLL:	Median	observed	follow-up	from	infusion	was	15.1	months	(range,	1.3-36.5). UCL	has	also initiated	a	Phase	1	exploratory trial (CAROUSEL)	of	obe-cel in	patients	with relapsed	or refractory	PCNSL. CAROUSEL	is	evaluating	the	feasibility	of	generating	obe-cel	and	safety	of	administration	in	this	patient	population.	UCL presented initial	data	at the	EHA	meeting in June	2022.	Expansion	of	obe-cel	was	observed in the	peripheral	blood	by qPCR,	with	persistence	in	all	treated	patients	at	last	follow-up.	No	Grade	3	or	greater	CRS	was	observed	using	intravenous (“IV”) or intra-ventricular obe-cel administration. Two cases of Grade 3 ICANS were reported following IV infusion, whereby the first	patient	had several	neurological	deficits that	evolved	despite ICANS treatment	and	were compatible with	progressive	PCNSL,	as	confirmed	with	the	month	1	MRI	scan,	and	the	second	patient	had	neurological	deficits	that improved	with	steroids/anakinra.	We	observed	encouraging	response	rates	in	six	patients	evaluable	for	efficacy	following IV	administration	of	obe-cel.	The	ORR	was four	out	of	six	patients (67%),	with	2	CRs	and	2	PRs.	These four	responding patients	are	without	disease	progression	at	the	last	follow	up	date.	Two	patients	died	from	progressive	PCNSL	while	part of	the	study.	We	expect	to	report	longer	follow-up	from	this	trial	and	enrolment	of	additional	patients	is	ongoing. Obe-cel	for	Lupus	and	Other	Autoimmune	Diseases In addition to advancing AUCATZYL/obe-cel for oncology indications, we are advancing obe-cel for the treatment of autoimmune diseases. We have initiated a Phase 1 clinical trial in patients with severe, refractory systemic lupus erythematosus.	We	have	initiated	a	Phase	2	clinical	trial	in	patients	with	severe,	refractory	lupus	nephritis	and	we	have initiated	a	Phase	1	clinical	trial	in	patients	with	progressive	Multiple	Sclerosis. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 16

 Background	of	SLE SLE is an autoimmune disease characterized by the formation of autoantibodies and immune complex–mediated inflammation and organ damage, including the skin, joints, central nervous system, heart, lung, and kidneys. Disease severity	changes	over	time	with	periods	of	no	disease	activity	alternated	by	periods	with	disease	flares/relapses.	In	some cases	SLE	can	be	life	threatening	and	chronic	disease	can	be	life	shortening.	The	disease	onset	is	generally	between	the ages	of	20	and	40,	and	it	affects	predominantly	women.	The	estimated	prevalent	population	of	SLE	patients	in	the	United States, United Kingdom, Germany, France Spain, Italy and Japan is approximately 550,000 patients, of which approximately	60%	(330,000	patients)	experience	moderate	to	severe	disease.	Roughly	15%	will	be	refractory	to	standard therapies;	potentially	addressable	by	CAR	T	therapy. Currently	available treatments	are	not	curative	and	are	associated	with	certain	safety	concerns.	Many	patients require life-long	immunosuppression,	often	with	high-dose	corticosteroids,	cyclophosphamide,	or	mycophenolate	mofetil,	which reduce	inflammation	by	non-specifically	targeting	the	immune	system.	This	results	in	low-level	disease	activity	in	only	25– 44%	of	patients	in	the	long	term,	while	sustained	complete	remission	is	rare.	Approximately	10%	of	patients	with	LN,	a form	of	the	disease	associated	with	kidney	organ	damage,	develop	end-stage	renal	disease	in	5	years.	Side	effects	of	the current	treatment	strategies	include	infections	in	the	short	term	and	risk	for	malignancy	and	cardiovascular	disease	in	the long	term,	contributing	to	the	reduced	life	expectancy	of	patients	with	SLE.	These	outcomes,	together	with	the	inability	to reverse	disease	progression	support	the	need	for	developing	better	strategies	to	treat	SLE. Autoreactive	B	cells	with	autoantibody formation	play	a	key role in the	pathogenesis	of	SLE.	However,	B	cell	depleting agents,	such	as	the	anti-CD20	antibody	rituximab,	did	not	statistically	improve	clinical	outcomes	compared	to	placebo	in randomized	studies	in	SLE	and	LN. Three	different	biologics	have	recently	been	approved	in	SLE: 1. Anifrolumab,	a	type	I	interferon	(“IFN”)	receptor	antagonist,	has	also	been	approved	in	the	United	States	and	EU and	is	indicated	as	an	add-on	for	the	treatment	of	adult	patients	with	moderate	to	severe	SLE	who	are	receiving standard	therapy. 2. Obinutuzumab, a next-generation anti-CD20 B-cell depleting IgG, has been approved by the FDA for patients with	LN	in	combination	with	standard	of	care	therapy. 3. Belimumab, an anti-BAFF/BLyS	monoclonal antibody, has been approved as add-on therapy in adult patients with	active,	autoantibody-positive	SLE	with	a	high	degree	of	disease	activity	despite	standard	therapy. Despite	these	approvals,	some	patients	have	insufficient	response,	lack	of	response,	or	lack	of	sustained	response	and	are at	risk	for	further	organ	damage	despite	standard	therapy.	Hence,	challenges	remain	with	treatment-resistant	disease. Another	strategy	to	induce	deeper	depletion	of	the	B	cell	compartment	originates	from	the	highly	effective	treatment	of patients	with	B	cell	malignancies	using	CD19	CAR	T	cells.	A	clinical	study	by	Mackensen	and	colleagues	published	in	2023 showed	a	deep	depletion	of	CD19+	B	cells	and	plasma	blasts in	SLE-affected	tissues	could	trigger	an	immune	reset	that could	allow	the	cessation	of	immunosuppressive	treatment	in	patients	with	SLE.	In	this	study,	autologous	T	cells	from	8 patients	with	SLE	were	transduced	with	a lentiviral	anti-CD19	CAR	vector,	expanded	and	reinfused	at	a	dose	of	1&times;10x6 CAR	T	cells	per	kg	body	weight into	the	patients	after lymphodepletion	with	fludarabine	and	cyclophosphamide.	CAR	T cells	expanded	in	vivo	and	led	to	deep	depletion	of	B	cells	with	improvement	of	clinical	symptoms	and	normalization	of laboratory parameters including seroconversion of anti-ds DNA antibodies. Remission of SLE according to standard criteria	was	achieved	in	all	patients	after	3	months,	and	drug-free	remission	was	maintained	during	longer	follow-up	after CAR	T	cell	administration. Based	on	the	important	role	of	B	cells	in	the	SLE	disease	pathogenesis	and	the	preliminary	evidence	of	safety	and	activity of	CD19	CAR	T	cell therapy in this	disease,	we	have	hypothesized	that treatment	with	a	single infusion	of	obe-cel	may have	the	potential	to	eliminate	the	malfunctioning	autoreactive	B	cells	and	ameliorate	disease	in	SLE	patients	in	a	similar fashion. We believe obe-cel's potential advantages over other autoimmune therapies that are approved or in development	include	its	differentiated	mechanism	of	action	via	its	fast-off	rate	CD19	binder,	the	existing	clinical	data	and approval	in	r/r	B-ALL	and	our	established	manufacturing	and	commercial	capabilities.	In	particular,	the	favourable	safety profile	in	adult	r/r	B-ALL	observed	in	the	FELIX	study,	with	low	rates	of	high-grade	CRS	and	ICANS	in	the	cancer	setting, have	the	potential	to	drive	acceptability	of	a	cell	therapy	approach	in	the	rheumatology	setting. Additionally, the fast-off rate kinetics observed with obe-cel show increased T-cell engraftment and profound B-cell depletion	in	B-cell	malignancies.	These	properties	have	the	potential	to	drive	a	deeper	cut	into	CD19+	B	cells	and	plasma blasts in	SLE-affected	tissues,	and	could	potentially trigger	an immune	reset in	patients.	Obe-cel is the	only	autologous CD19 CAR T-cell therapy being developed for lupus with an approval in another indication. We expect that data supporting	the	safety	and	manufacture	of	obe-cel	in	r/r	B-ALL	could	potentially	be	useful	to	support	the	development	of obe-cel in autoimmune indications. Finally, our established commercial systems and	manufacturing infrastructure for AUCATZYL/obe-cel	could	be	leveraged	to	support	an	autoimmune	indication. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 17

 Clinical	Development	in	SLE,	LN	and	other	Autoimmune	Diseases Obe-cel	in	SLE	and	lupus	nephritis	(“LN”) The	CARLYSLE	trial	is	a	single-arm,	open-label,	Phase	1	trial	to	determine	the	safety,	tolerability,	and	preliminary	efficacy of	obe-cel	in	patients	with	severe,	refractory	SLE.	The	primary	goal	of	this	trial	is	to	confirm	the	fixed	dose	of	obe-cel	in adult	SLE	patients. Data from the ongoing Phase 1 CARLYSLE study evaluating obe-cel in patients with severe refractory systemic lupus erythematosus	was	presented	at	the	ASH	Annual	Meeting	in	December	2025.	Nine	adult	patients	were	infused	with	obe- cel,	including	six	at	the	50M	dose	and	three	at	the	100M	dose. Obe-cel	was	well	tolerated	in	all	patients.	No	dose	limiting	toxicities	(DLTs)	or	cases	of	ICANS	were	observed	at	the	50M dose.	Grade	one	cytokine	release	syndrome	(CRS)	was	observed	in	three	patients	at	the	50M	dose	and	three	patients	at the	100M	dose.	Hypertension	was	observed in five	patients	at the	50M	dose,	with three	of those	patients	having	pre- existing	history	of	hypertension.	A	case	of	transient	Grade	three	liver	toxicity	was	observed	in	one	patient	of	the	100M cohort. At	the	50M	dose,	three	patients	(50%)	achieved	CRR	(Complete	Renal	Response)	and	five	patients	(83%)	achieved	DORIS (Definition	of	Remission in SLE)	with	a	median	onset	of	5.1	months (range:	4.9–8.9),	without	evidence	of	new	disease activity	at	a	median	of	12	months	of	follow	up	(range:	8.5–16.3).	All	non-renal	manifestations	of	the	disease	resolved	by month four. Urinary protein creatinine (UPC) ratio levels decreased over time, demonstrating significant decline or absence of disease activity. Data show high peak expansion and deep B cell aplasia consistent with known obe-cel characteristics in	oncology indications.	Peak	expansion	was reached	at	a	median	of	10	days (range:	9–13).	The	median time	to	loss	of	CAR	T-cell	persistence	based	on	Kaplan-Meier	analysis	was	3.0	months.	The	B-cell	reconstitution	profiles suggest	that	obe-cel	may	induce	a	reset	of	pathologic	autoimmunity. Emerging	data	in	the	100M	cohort	is	consistent	with	the	50M	adult	cohort,	and	evaluation	is	ongoing. We have recently transitioned this program into a Phase 2 potentially pivotal study known as LUMINA, following successful preliminary results from the	Phase	1	CARLYSLE trial. 50M	has	been selected	as the recommended	Phase	2 dose.	The	objective	of	the	study	is	to	assess	the	safety	and	effectiveness	of	a	single	infusion	of	obe-cel in	patients	with severe, refractory systemic lupus erythematosus (SLE) with active lupus nephritis (LN) in participants age 12-65. The endpoints will be the proportion of participants achieving a complete renal response (signs of kidney inflammation disappearing)	and	DORIS.	The	study	is	a	single-arm,	open-label	trial	involving	approximately	30	participants	.	Autolus	has aligned	with	FDA	on	a	Phase	2	trial	design	in	LN	and	potential	registrational	path	to	approval.	The	LUMINA	Phase	2	trial	is now	enrolling. Furthermore,	additional	evidence	of	CD19	CAR	T	cell	treatment	in	other	autoimmune	diseases	has	been	shown	by	others, including efficacy in patients	with idiopathic inflammatory	myositis, systemic sclerosis,	myasthenia gravis and	multiple sclerosis.	Depending	on	the	outcome	of	the	dose	confirmation	study	in	SLE,	we	intend	to	investigate	obe-cel	in	additional autoimmune disease indications. Other autoimmune indications include patients with MS. The phase 1 study in MS (BOBCAT)	is	currently	ongoing. Obe-cel	in	progressive	multiple	sclerosis	(“MS”) Autolus	is	advancing	obe-cel	into	initial	clinical	development	in	progressive	MS.	The	first	patient	in	the	BOBCAT	trial	was dosed	in	October	2025.	This	Phase	1	trial,	expected	to	include	up	to	18	adult	patients,	will	evaluate	the	safety,	tolerability, and preliminary efficacy of obe-cel in participants	with refractory progressive forms of	multiple sclerosis. The primary endpoint is to assess safety and tolerability of obe-cel. Key secondary endpoints include evaluating the preliminary efficacy	of	obe-cel	using	change	from	baseline	in	standard	efficacy	measures.	We	plan	to	provide	updates	on	the	initial Phase	1	data	in	late	2026. AUTO1/22	Our	Programmed	T	Cell	Therapy	for	the	Treatment	of	ALL,	other	B-cell	malignancies Introduction	to	AUTO1/22 AUTO1/22	is	a	dual-targeting	CAR	T	which	builds	on	the	obe-cel	approach	utilizing	the	same	CD19	CAR,	alongside	a	novel CD22	CAR	designed	to	reduce	antigen	negative	relapse	of	disease.	Antigen	negative	relapse	is	a	common	cause	of	relapse in	patients	with	paediatric	ALL. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 18

 AUTO1/22	Phase	1	Clinical	Trial	in	Paediatric	ALL	(CARPALL	Trial) We	commenced	a	Phase	1	clinical	trial	in	paediatric	patients	with	relapsed	or	refractory	ALL	with	our	dual	expressing	CAR product	candidate,	AUTO1/22	in	late	2020.	In	a	publication	in	Blood	in	October	2023,	we	presented	data	demonstrating	a high	level	of	activity,	with	83%	of	patients	(10	of	12	patients	evaluated)	experiencing	MRD	negative	complete	remissions, and a favourable tolerability profile in a very challenging patient population. Patients on study	were high risk,	with 4 patients	who	had failed	prior	CD19	CAR therapy, 3	patients	with	a	CD19-negative	disease component, 3	patients	with non-CNS	EMD	and	6	patients	who	had	received	prior	blinatumomab. Of 10 responding patients, 5 had emergence of	MRD (2) or frank relapse (3)	with CD19 and CD22 expressing disease associated with loss of CAR T-cell persistence. Importantly, there were no cases of relapse due to antigen-negative escape,	with	a	median	follow-up	of	8.7	months.	Overall	survival	was	75%	at	6	and	12	months.	Six	and	12-month	event free	survival	(EFS)	were	75%	and	60%	respectively. Our	collaborators	at	UCL	are	currently	evaluating	an	alternative	manufacturing	process	and	initiated	an	extension	to	the CARPALL	Phase	1	clinical	trial in	a	cohort	of	paediatric	patients	with	relapsed	or	refractory	ALL	in	2025.	We	expect	that they	will	report	the	first	data	from	this	study	in	late	2026. AUTO8:	Our	Multiple	Myeloma	Program Introduction	to	AUTO8 AUTO8	is	a	next-generation	product	candidate	for	multiple	myeloma	and	Amyloid	Light-chain	(“AL”)	amyloidosis.	AUTO8 comprises	two	independent	CARs	for	the	multiple	myeloma	targets,	BCMA	and	CD19.	We	have	developed	an	optimized BCMA	CAR	which	is	designed	for	improved	killing	of	target	cell	that	express	BCMA	at	low	levels.	This	has	been	combined with fast	off-rate	CD19	CAR from	obe-cel.	We	believe that the	design	of	AUTO8	has the	potential to induce	deep	and durable responses and extend the durability of effect over other approved BCMA CARs and those currently in development. Background	of	Multiple	Myeloma According to data from the Global Burden of Disease Study 2020, there were approximately 156,000 new cases of multiple	myeloma	and	113,000	deaths	in	2019.	The	American	Cancer	Society	estimates	that	in	the	United	States	in	2024, approximately	35,780	new	cases	will	be	diagnosed	and	approximately	12,540	deaths	are	expected	to	occur	from	multiple myeloma.	With	currently	available	treatments	the	five-year	survival	rate	is	approximately	58%. Treatment choices for multiple myeloma vary with the aggressiveness of the disease and related prognostic factors. Newly diagnosed patients in good physical health	with active disease generally receive high-dose chemotherapy	with autologous	stem	cell	transplantation	(“ASCT”).	Eligibility	for	ASCT	is	established	primarily	by	age	and	comorbidities.	When transplantation is not an option, treatment traditionally consists of systemic chemotherapy, with adjunctive use of radiation. The therapeutic landscape of	multiple	myeloma	has changed significantly in the past decade	with the introduction of novel immunomodulatory agents, such as lenalidomide, as	well as	monoclonal antibodies, such as daratumumab, and proteasome inhibitors, including bortezomib and carfilzomib. The past decade has also seen major progress in the understanding of the molecular oncogenesis of plasma cell neoplasms, which has significantly influenced the clinical management of multiple myeloma. Despite these major advances, most cases of multiple myeloma have remained incurable.	A	considerable	number	of	multiple	myeloma	patients	ultimately	experience	a	final	tumour	relapse	without	any additional,	effective	treatment	option.	Patients	with	relapsed	or	refractory	disease	typically	have	a	poor	prognosis. Recently approved therapeutic approaches include products that target BCMA on multiple myeloma cells, including redirected T cell therapies such as T cell engagers and CAR T cell therapies. Despite recent progress, there remains significant unmet clinical need among patients with multiple myeloma. We believe our programmed T cell product candidate,	AUTO8,	with	its	dual-targeting	approach,	has	the	potential	to	lead	to	higher	levels	of	efficacy	and	durability	of effect	compared	to	other	products	and	redirected	T	cell	therapies	that	bind	to	BCMA	alone. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 19

 Background	to	light	chain	(“AL”)	amyloidosis AL	amyloidosis	is	a	rare,	acquired	disorder	characterized	by	the	abnormal	folding	and	deposition	of	light	chains,	which	are fragments	of	antibodies,	as	amyloid	fibrils	in	vital	organs.	These	light	chains	are	produced	by	a	clone	of	abnormal	plasma cells in the bone marrow. The deposited amyloid causes organ dysfunction and damage, primarily to the heart and kidneys,	but	also	affecting	other	organs	and tissues.	Early	diagnosis is crucial to	prevent	end-stage	organ	damage,	and current	available	treatments,	such	as	daratumumab,	aim	to	control	the	light	chain-producing	plasma	cells	to	slow	or	halt disease	progression	and	improve	quality	of	life. BCMA	CAR	T-cell	therapies,	originally	developed	for	multiple	myeloma,	have	shown	promising	initial	safety	and	efficacy	in AL	amyloidosis	patients including rapid reduction	of the	disease	biomarkers	and	organ responses in	clinical trials. The therapeutic	approach	has	the	potential	to	eliminate	the	disease-causing	plasma	cells	by	targeting	the	cause	of	the	disease potentially	offers	longer	term	outcomes	for	these	patients. Clinical	Development	of	AUTO8 In	collaboration	with	UCL,	we	commenced	a	Phase	1	clinical	trial	in	patients	with	relapsed	or	refractory	multiple	myeloma in	March 2022. The phase 1 study is an iterative, staggered design trial with two separate parallel cohorts for direct comparison	of	the	BCMA	CAR	alone	and	AUTO8	(the	BCMA	CAR	in	combination	with	the	CD19	CAR	from	obe-cel).	As	of November	13,	2023	(data	cut-off),	11	patients	have	been	infused	with	either	BCMA	CAR	at	50	million	(n=3)	or	150	million (n=3)	cells,	or	AUTO8	at	50	million	(n=3)	or	150	million	(n=2).	At	a	median	follow-up	of	6	months	we	observed	100%	ORR, with	3	PR,	1	VGPR,	7	CR/sCR	(all	evaluable	MRD	negative).	Two	patients	remained	in	ongoing	sCR	>	12	months.	No	cases of	ICANS	or	CRS	≥	Gr	3	were	observed	across	all	subjects	during	the	period.	While	persistence	data	from	the	dual	targeting cohort	is	immature,	it	demonstrates	expansion	of	three	CAR	populations	and	suggests	a	trend	to	increased	persistence	of D8	BCMA	CAR	expressing	T	cells.	The	study	is	ongoing	and	continues	to	recruit	patients. In	collaboration	with	UCL,	we	commenced	a	Phase	1	clinical	trial in	patients	with	relapsed	or	refractory	AL	amyloidosis. We dosed	the	first	patient	on	the	study	in	October	2025	and	we	expect	to	report	the	first	data	from	this	study	in late 2026. Our	Solid	Tumour	Programs Solid tumours present a particular challenge to CAR T cell therapies, since solid tumours tend to fend	off T cells	with upregulation	of	checkpoint	inhibition	and	a	hostile	microenvironment.	In	addition,	contrary	to	haematological	cancer	cells that	are	readily	accessible	to	programmed	T	cells	in	the	circulating	blood	of	a	patient,	solid	tumours	are	more	difficult	for programmed T cells to track down in sufficient numbers to impact the disease. In addition, the persistence of programmed	T cells tends to	be limited,	which	also leads to	a reduced	effect	on solid tumour cells. In	addition to the programs	we are currently pursuing described below,	we intend to continue to evaluate other possible solid tumour indications. AUTO6:	Our	Neuroblastoma	Program Introduction	to	AUTO6	and	AUTO6NG Under our license agreement with University College of London Business Ltd. (“UCLB”), we have been granted an exclusive, worldwide license to AUTO6 (1RG-CART), a programmed T cell product candidate targeting the glycosphingolipid GD2. Cancer Research	UK (“CRUK”) has completed an exploratory Phase 1 clinical trial of AUTO6 in paediatric	patients	with	neuroblastoma.	We	are	developing	a	next-generation	product	candidate,	which	we	refer to	as AUTO6NG, incorporating additional programming modules designed to improve efficacy, safety and persistence of AUTO6. Background	of	Neuroblastoma Neuroblastoma is a cancer that develops from immature nerve cells found in several areas of the body, and most commonly arises in and	around the adrenal glands,	which	have similar origins to	nerve cells and sit atop the kidneys. However, neuroblastoma can also develop in other areas of the abdomen and in the chest, neck and near the spine, where	groups	of	nerve cells exist.	Neuroblastoma	most commonly	affects children	age five	or younger, though it	may rarely	occur	in	older	children.	According	to	the	American	Cancer	Society,	there	are	approximately	700	to	800	new	cases	of neuroblastoma	each	year	in	the	United	States. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 20

 Preclinical	Studies	of	AUTO6/6NG In preclinical in vitro studies, AUTO6 selectively, effectively and efficiently killed GD2-expressing tumour cells while sparing	cells that	did	not	express	GD2. In	addition, the	RQR8	safety switch	activation	by rituximab	was tested in	vitro, where	the	addition	of	rituximab	was	shown	to	activate	the	safety	switch	and	eliminate	the	programmed	T	cells	from	the culture,	and	residual	cells	did	not	possess	any	intrinsic	anti-GD2	activity.	This	safety	switch	activation	was	also	observed	in vivo in	a	mouse	model,	where	the	murine	analogue	of	rituximab	was	able	to	deplete	the	GD2-targeting	programmed	T cell product candidate from the bone marrow, blood, lymph node and spleen of animals that had previously been engrafted	with	programmed	T	cells. In	2016,	in	collaboration	with	Cancer	Research	UK’s	Centre	for	Drug	Development	we	initiated	a	single-arm	Phase	1	dose escalation	trial	of	AUTO6	in	relapsed	or	refractory	neuroblastoma	at	two	paediatric	cancer	centres in	the	U.K.	The	trial evaluated the safety and efficacy of AUTO6. In 2020 the data from the AUTO6 Phase 1 clinical trial	was published in Science Translational	Medicine. The results from the study showed that AUTO6 can induce rapid regression of bulky disease in a solid tumour setting without inducing on-target, off-tumour toxicity, despite dose dependent CAR T expansion. CAR	T cell expansion	was	observed in all 6 patients treated	at the	higher cell dose cohorts in this Phase	1 study.	Three	of	these	six	patients	demonstrated	evidence	of	transient	CAR	T	cell	activity,	including	CRS,	and	regression	of soft	tissue	and	BM	disease	activity. The	GD2	binder	used	in	AUTO6	has	been	designed	to	minimize	on-target,	off-tumour	neurotoxicity	associated	with	GD2 expression	at	low	levels	in	pain	fibres	and	the	brain.	Despite	the	presence	of	clear	CAR	T	cell	activity,	no	neurotoxicity	was observed. The publication also suggests that, whilst AUTO6 is a valid and safe strategy for targeting neuroblastoma, further	modifications	are	required	to	promote	CAR	T	cell	persistence	and	induce	deeper	and	more	durable	responses	for these	patients. In	November	2019,	we	reported	preclinical	data	of	AUTO6NG.	Building	on	AUTO6,	in	AUTO6NG	we	introduced	additional programming modules in order to help the programmed T cells persist in and withstand the hostile tumour microenvironment. AUTO6NG is a programmed	T cell therapy incorporating the	GD2-targeted	CAR T and	RQR8 safety switch from	AUTO6	but	also incorporating three	additional	programming	modules: (i) an IL7	CCR	designed to increase persistence,	(ii)	a	dominant	negative	TGFbRII	protein	designed	to	block inhibitor	signals	from	TGFb	and	(iii)	a	truncated SHP2	protein	designed	to	block	inhibitor	signals	from	PD1.	These	modules	are	delivered,	or	transduced,	into	the	T	cells	via two	viral	vectors.	Both	single-	and	dual-transduced	CAR	T	cells	were	evaluated	in	vitro	for	antitumour	activity,	cytokine secretion,	T	cell	proliferation,	survival,	and	resistance	to	immunosuppressive	pathways. The addition of these three modules in the AUTO6NG product candidate significantly augmented its function by extending	T cell	persistence	and rendering	modified	T cells resistant to	TGFb-	and	PD1/PDL1-driven immune inhibition when compared to AUTO6 in vitro. Additionally, intravenous delivery of AUTO6NG in mice with established tumour burden	exhibited	potent	antitumour	activity	and	extended	survival,	whereas	AUTO6	showed	no	activity	in	that	model. We	presented	new	preclinical	data	for	AUTO6NG	in	June	2020	at	the	American	Association	for	Cancer	Research	Virtual Annual	Meeting	2020.	GD2	was	evaluated	as	a therapeutic	CAR	T target	antigen in	small	cell lung	cancer (“SCLC”).	We observed	that	AUTO6	alone	has	demonstrated	efficacy	in	an	in	vitro	SCLC	model;	however,	successful	tumour	targeting alone	was	not	sufficient	to	drive	meaningful	in	vivo	efficacy	in	the	same	SCLC	model.	We	presented	new	preclinical	data demonstrating the	ability to target	GD2 in	SCLC	cell line	models in vitro, and the requirement for	enhancing	modules, designed	to	overcome	TME	suppressive	mechanisms,	to	drive	superior	in	vivo	efficacy	in	a	SCLC	mouse	model.	The	data suggests	that	AUTO6NG	can	overcome	the	immune	suppressive	mechanisms	in	the	TME. Clinical	Development	Strategy	of	AUTO6NG GD2	is	expressed	in	numerous	paediatric	and	adult	tumours	including	neuroblastoma,	osteosarcoma,	soft	tissue	sarcoma, melanoma,	astrocytoma	and	SCLC.	A	Phase	1	clinical	trial	of	AUTO6NG	in	r/r	neuroblastoma	was initiated in	December 2023	in	collaboration	with	UCL.	This	study	is	currently	enrolling	patients. Commercialization	and	Manufacturing	Plans	for	our	Clinical-Stage	Programs We are developing our clinical-stage programs for the treatment of patients with late-stage or rare haematological cancers	and	solid	tumours,	most	of	whom	are	treated	in	specialized	treatment	centres	or	hospitals.	With	our	experience in gene therapy, transplantation and oncology,	we aim to provide high levels of service and scientific engagement at these treatment centres, and to pilot and establish systems necessary for product delivery by the time of launch. By focusing	on	these	centres,	we	can	begin	to	build	our	commercialization	capabilities	with	limited	resources.	We	are	also planning to advance obe-cel in autoimmune indications, and plan to leverage our established clinical and commercial manufacturing	infrastructure,	including	our	purpose-built	manufacturing	facility,	the	Nucleus. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 21

 We have retained worldwide commercial rights for our product candidates. We plan to expand our global commercialization capabilities over time such that we are able to commercialize any product candidate in a broader number	of	countries	over	time,	but	with	a	focus	on	achieving	an	early	presence	in	the	US,	U.K.	and	parts	of	Europe,	i.e. countries	where	we	have	obtained	a regulatory	approval.	We	may	pursue	strategic	collaborations	with third	parties in order to maximize the commercial potential of our product candidates. Under the terms of the License and Option Agreement	with	BioNTech,	BioNTech	currently	has	an	option	to	co-promote	or	co-commercialize	AUTO6NG.	We	generally expect	to	launch	any	of	our	products	that	receive	regulatory	approval	in	the	United	States	first,	followed	by	the	U.K.,	EU and	subsequently	in	other	major	markets	to	the	extent	commercially	feasible.	BioNTech's	product	option	for	AUTO1/22 was	not	exercised	and	has	expired,	so	we	have	regained	full	rights	to	commercialize	AUTO1/22. In	addition to the	Nucleus,	which is currently	used	exclusively for commercial	manufacture	of	AUCATZYL,	we	maintain separate	manufacturing	capabilities	for	our	clinical-stage	programs.	For	clinical	trial	supply,	we	have	established	cell	and vector manufacturing capacity at the Cell and Gene Therapy Catapult in Stevenage, U.K., where we maintain a cell manufacturing	suite. Our	early-stage	programs	such	as	AUTO1/22	and	AUTO6NG	are	manufactured	in	collaboration	with	the	UCL	study	teams. However, phase-appropriate process development activities have been initiated within our laboratories in order to leverage	our	existing	manufacturing	capabilities	for	progression	to	a	late-stage	clinical	program. Our	License	and	Option	Agreement	with	BioNTech	SE In	February	2024,	we	entered	into	a	License	and	Option	Agreement	(the	“BioNTech	License	Agreement”)	with	BioNTech pursuant to which we granted to BioNTech an exclusive, worldwide, sublicensable license (the “License”) to certain binders	and	to	exploit	products	that	express	in	vivo	such	binders	(collectively,	the	“Binder	Licensed	Products”). In	addition to the License	we	also	granted	BioNTech several time-limited	options (the “Options”) to	acquire	additional rights to specified clinical-stage product candidates, binders and technologies, described in	more detail below. In the event	that	all	Options	are	fully	exercised,	we	would	be	eligible	to	receive	maximum	aggregate	future	payments	of	up	to $582 million. This maximum amount includes the potential milestone payments for the Binder Licensed Products described below, all option exercise fees and potential milestone payments for licenses to optioned products and technologies,	and	additional	payments that	BioNTech	may	pay to	us for	an increased revenue interest	with respect to obe-cel	as	described	below. License	and	Options In	consideration	for	the	License	and	the	Options,	BioNTech	made	an	initial	payment	to	us	of	$10	million,	which	is	part	of the	$50	million	of	total	upfront	payments	received. We	are	eligible	to	receive	milestone	payments	of	up	to	$32	million	in	the	aggregate	upon	the	achievement	of	specified clinical	development	and	regulatory	milestones	for	each	Binder	Licensed	Product	that	achieves	such	milestones.	We	are also	eligible	to	receive	a	low	single-digit	royalty	on	net	sales	of	Binder	Licensed	Products,	subject	to	customary	reductions, which reductions	are subject to specified limits. The royalty	will be increased if	BioNTech, its affiliates	or sublicensees commercialize a Binder Licensed Product in an indication and country in which we or our affiliates or licensees also commercializes a product containing the same binders. Under the BioNTech License Agreement, BioNTech is solely responsible for,	and	has sole	decision-making	authority	with respect to,	at its	own	expense, the	exploitation	of	Binder Licensed	Products. We	also	agreed	to	grant	BioNTech	the	following	time-limited	Options: • an option to obtain exclusive rights to co-fund development costs of our development-stage programs AUTO1/22	and	AUTO6NG,	in	return	for	agreed	upon	economic	terms,	including	an	option	exercise	fee,	milestone payments and a profit-sharing arrangement for each such product candidate, with additional options to co- promote	or	co-commercialize	such	product	candidate.	The	product	option	for	AUTO1/22	was	not	exercised	and has	expired	as	of	8	February	2025; • an	option	to	obtain	an	exclusive	worldwide	license	to	exploit	products	that	express	certain	additional	binders	in vivo	or,	with	respect	to	certain	binders,	in	an	antibody	drug	conjugate	(“Binder	Option”); • an	option to	obtain	a co-exclusive	worldwide license to	exploit	products that	express in vivo	our	modules for activity	enhancement,	with	a	non-exclusive	right,	in	certain	agreed	instances,	to	exploit	products	that	include	our modules	for	activity	enhancement	but	do	not	express	in	vivo	such	modules	(the	“Activity	Enhancement	Option”); and AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 22

 • an	option	to	obtain	a	non-exclusive	worldwide	license	to	exploit	products	that	contain	our	safety	switches	(the “Safety Switch Option” and, together with the Binder Option and the Activity Enhancement Option, the “Technology	Options”). The	option	exercise	fee	for	each	Technology	Option	is	a	low	seven-digit	amount.	Each	of	the	Activity	Enhancement	Option and	the	Safety	Switch	Option	must	be	exercised	with	respect	to	a	given	biological	target	or	combination	of	targets.	There is	a	cap	on	the	total	option	exercise	fee	if	multiple	options	are	exercised	with	respect	to	a	given	target. There	is	also	a	cap	on	milestone	payments	across	all	agreements	entered	into	as	the	result	of	BioNTech	exercising	one	or more of the Technology	Options and a cap on royalties payable on any given product for	which	multiple	Options are exercised. Obe-cel	Product	Revenue	Interest Under the	BioNTech License	Agreement, BioNTech has also agreed to financially support the expansion of the clinical development	program	and	planned	commercialization	of,	obe-cel.	In	exchange	for	the	grant	of	rights	to	future	revenues from	the	sales	of	obe-cel,	BioNTech	has	made	an	upfront	payment	to	us	of	$40	million,	(&pound;31.8	million),	representing	the remainder	of	the	$50	million	total	upfront	payment).	We	will	pay	BioNTech	a low	single-digit	percentage	of	annual	net sales	of	obe-cel,	including	revenues	from	sales	of	AUCATZYL,	which	may	be	increased	up	to	a	mid-single	digit	percentage in	exchange	for	milestone	payments	of	up	to	$100	million	in	the	aggregate	on	achievement	of	certain	regulatory	events for	specific	new	indications	upon	BioNTech's	election.	In	May	2025,	we	made	our	initial	payments	of	the	revenue	share interest	to	BioNTech,	and	as	of	December	31,	2025	we	have	paid	&pound;1.1	million	($1.5	million)in	revenue	share	interest	to BioNTech. Manufacturing	and	Commercial	Agreement Under the terms of the BioNTech License and Option Agreement, Autolus Limited has agreed to grant BioNTech the option	to	negotiate	a	joint	manufacturing	and	commercial	services	agreement	pursuant	to	which	the	parties	may	access and leverage	each	other’s	manufacturing	and	commercial capabilities, in	addition to	Autolus’ commercial site	network and infrastructure, with respect to certain of each parties’ CAR T products, including BioNTech’s product candidate BNT211 (the	“Manufacturing	and	Commercial	Services	Agreement”	or	“MCSA”).	The	MCSA, if	entered into,	would	also grant	BioNTech	access	to	the	Company’s	commercial	site	network	and	infrastructure.	On	6	August	2025,	the	MCSA	option expired	unexercised. Termination Unless	earlier	terminated,	the	BioNTech	License	Agreement	will	continue	for	so	long	as	royalties	are	payable	in	respect	of Binder Licensed	Products	and the revenue interest is	payable in respect	of	obe-cel	products. Subject to	a cure	period, either	party	may	terminate	the	agreement	in	the	event	of	the	other	party’s	uncured	material	breach	or	the	insolvency	of the	other	party.	BioNTech	may	terminate	the	agreement,	in	whole	or	in	part,	for	any	or	no	reason	upon	a	specified	period of	prior	written	notice. Our	License	Agreement	with	UCL	Business	Ltd. In	September	2014,	we	entered	into	an	exclusive	license	agreement	with	UCLB,	the	technology	transfer	company	of	UCL, for	the	development	and	commercialization	rights	to	certain	T	cell	programming	modules	(the	“UCLB	Agreement”).	The UCLB	Agreement	was	amended	and	restated	in	March	2016	to	also	include	certain	development	and	commercialization rights	to	improvements	and	new	T	cell	programming	modules.	The	UCLB	Agreement	was	further	amended	and	restated	in March	2018	to	include	a	license	to	AUTO1,	for	which	UCL	is	conducting	Phase	1	clinical	trials	in	paediatric	and	adult	ALL patients.	The	UCLB	Agreement	was	further	amended	and	restated	in	October	2020	to	reflect	our	election	to	have	various patent	rights	assigned	to	us,	and	to	include	a	license	to	new	technology	and	further	licenses	to	obe-cel	for	which	UCL	is conducting	Phase	1	clinical	trials	in	PCNSL	patients.	Under	the	UCLB	Agreement,	subject	to	certain	limitations,	exceptions and retained rights of	UCLB,	we received an exclusive license of certain patent rights and know-how	owned by	UCLB covering	T	cell	programming	modules.	The	licensed	rights	cover	obe-cel,	AUTO4/5	and	AUTO6	targeting	modules,	as	well as additional T cell programming modules and technologies, including dual-targeting technology, pattern recognition technology,	safety	switches	(including	RQR8),	tunable	T	cells,	manufacturing	processes	as	well	as	certain	technology	for evading tumour	micro-environments.	We also have option rights and rights of first negotiation to obtain an exclusive license	for	development	and	commercialization	rights	to	certain	new	T	cell	programming	modules. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 23

 In	exchange	for	the	rights	under	the	original license	agreement,	we	granted	UCLB	equity	that	was	ultimately	converted into	1,497,643	of	our	ordinary	shares.	We	also	agreed	to	pay	a	management	fee,	milestone	payments	and	royalties	upon future	net	sales	of	any	products	that	use	the	in-licensed	rights.	The	management	fee	of	&pound;120,000	was	payable	in	equal instalments	on	the	first	four	anniversaries	of	our	entry	into	the	original	license	agreement.	In	exchange	for	the	additional rights	we	received	in	March	2016	when	the	license	agreement	was	amended,	we	issued	UCLB	additional	equity	that	was ultimately converted into 313,971 of our ordinary shares, and we also made a one-time payment of &pound;150,000. In exchange for the additional rights	we received in	March 2018	when the license agreement	was further amended,	we made	an	initial	payment	of	&pound;1.5	million	and	paid	an	additional	&pound;0.35	million	in	connection	with	UCLB's	transfer	of	clinical data	to	us	in	December	2020. Under the license agreement, as amended, we are obligated to pay UCLB	milestone payments upon the initiation of certain clinical activities in an aggregate amount of &pound;0.18	million, the receipt of specified regulatory approvals in an aggregate amount of &pound;37.5 million, the start of commercialization in an aggregate amount of &pound;18 million, and the achievement	of	net	sales	levels	in	an	aggregate	amount	of	&pound;51	million.	On	a	per-product	basis,	these	milestone	payments range from &pound;1 million to &pound;18.5 million, depending on which T cell programming modules are used in the product achieving	the	milestone.	On	November	8,	2024	we	were	notified	by	the	FDA	that	our	obe-cel	BLA	was	approved,	allowing for the marketing of AUCATZYL in the US for the treatment of adult patients (18 years and older) with r/r B-ALL. Consequently, we paid a regulatory milestone payment of &pound;10.0 million to UCLB. On July 17, 2025, the European Commission	granted	marketing	approval	for	AUCATZYL	for	the	treatment	of	adult	patients	(26	years	and	older)	with	r/r	B- ALL	which	triggered	a	&pound;6.0	million	regulatory	milestone	payment	that	we	paid	during	the	three	months	ended	September 30,	2025	in	accordance	with	the	UCLB	Agreement.	Under	the	terms	of	the	license,	we	have	the	right	to	grant	sub-licenses to	third	parties,	subject	to	certain	restrictions.	If	we	receive	any	income	in	connection	with	such	sublicenses,	we	must	pay UCLB	a	percentage	of	the	income	allocable	to	the	value	of	the	sublicensed	intellectual	property	rights	ranging	from	low twenties	to	mid-single	digits,	decreasing	based	on	the	development	expenses	incurred	by	us	and	the	passage	of	time.	In 2025, less than &pound;10,000	was payable to UCLB by us relating to the income allocable to the value of the sublicensed intellectual	property rights.	UCLB	has retained the right to	use the licensed	T cell programming	modules for academic research	purposes	at	UCL	and	with	other	academic	institutions,	subject	to	certain	restrictions. Upon	commercialization	of	any	of	our	products	that	use	the	in-licensed	patent	rights,	we	are	obligated	to	pay	UCLB	a	flat royalty for each licensed product ranging from the low- to mid-single digits, depending on which technologies are deployed in the licensed product, based on worldwide annual net sales of each licensed product, subject to certain reductions,	including	for	the	market	entry	of	competing	products	and	for	loss	of	patent	coverage	of	licensed	products.	We may	deduct	from	the	royalties	payable	to	UCLB	half	of	any	payments	made	to	a	third	party	to	obtain	a license	to	such third	party’s	intellectual	property	that	is	necessary	to	exploit	any	licensed	products. Once	net	sales	of	a licensed	product	have	reached	a	certain	specified	threshold,	we	may	exercise	an	option	to	buy	out UCLB’s rights to the remaining milestone payments, royalty payments, and sublicensing revenue payments for such licensed	product,	on	terms	to	be	negotiated	at	the	time. As	mentioned	above,	we	acquired	ownership	of	the	majority	of	the	licensed	patent	rights	under	the	license	agreement (with the exception of the RQR8 patent rights) by virtue of a Deed of Assignment from	UCLB	which	was executed in October	2020.	Our	payment	and	diligence	obligations	remain	unaffected	by	the	assignment	of	the	licensed	patent	rights to	us. Under the license agreement,	we are solely responsible, at our expense, for developing the products that use the in- licensed	patent	rights	and	obtaining	all	regulatory	approvals	for	such	products	worldwide.	We	are	also	solely	responsible, at	our	expense,	for	commercializing	the	products	worldwide	after	receiving	regulatory	approval.	Further,	we	are	obligated to use commercially reasonable efforts to develop certain products using the patent rights pertaining to the T cell programming modules we have licensed from UCLB. Failure to achieve diligence obligations may result in loss of exclusivity	or	termination	of	the	license	on	a	program-by-program	basis. The	UCLB	Agreement	expires	on	a	product-by-product	and	country-by-country	basis	upon	the	expiration	of the	royalty term	with	respect	to	each	product in	each	country.	We	may	unilaterally	terminate	the	UCLB	Agreement	for	any	reason upon	advance	notice	to	UCLB.	Either	party	may	terminate	the	UCLB	Agreement	for	the	uncured	material	breach	by	the other	party	or	for	the	insolvency	of	the	other	party.	If	UCLB	terminates	the	UCLB	Agreement	following	our	insolvency	or our	material	breach	of	the	agreement,	or	if	we	terminate	the	agreement	unilaterally,	all	rights	and	licenses	granted	to	us will	terminate,	and	all	patent	rights	and	know-how	transferred,	licensed	or	assigned	to	us	pursuant	to	the	agreement	will revert back to	UCLB. In addition,	UCLB has the right to negotiate	with us for the grant of an exclusive license to our improvements	to	the	T	cell	programming	modules	we	have	licensed	on	terms	to	be	agreed	upon	at	the	time. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 24

 Financial	review Financial	position As	of	November	8,	2024,	we	have	one	product	approved	for	commercial	sale	in	the	United	States,	AUCATZYL,	of	which the first commercial sale of AUCATZYL in the United States was made during January 2025. We have funded our operations	to	date	primarily	with	proceeds	from	government	grants,	sales	of	our	equity	securities	including	ADSs,	through public	offerings	and	pursuant	to	our	at-the-market	equity	facility,	through	U.K.	research	and	development	tax	credits	and receipts	from	the	SME	and	RDEC	schemes,	out-licensing	arrangements,	strategic	collaboration	agreements	and	sale	of	our commercial	product. Since	our	inception,	we	have	incurred	significant	operating	losses.	For	the	years	ended	31	December	2025	and	2024,	we incurred	net	losses	of	&pound;222.7	million	and	&pound;161.0	million,	respectively.	As	of	31	December	2025,	we	had	retained	losses	of &pound;842.0	million. As at 31 December 2025, we had cash and cash equivalents and financial assets at fair value through other comprehensive income (i.e. marketable securities) of &pound;77.4 million (2024: &pound;181.4 million) and &pound;146.1 million (2024: &pound;287.7	million), respectively.	We used &pound;178.6	million (2024: &pound;175.4	million) in its operating activities during the year ended	31	December	2025. On	18	July	2025,	we	were	notified	by	the	European	Commission	that	the	we	have	been	granted	marketing	approval	for AUCATZYL (obecabtagene autoleucel) for the treatment of adult patients (26 years and older) with r/r B-ALL which triggered	a	&pound;6.0	million	regulatory	milestone	payment	that	we	paid	during	the	year	ended	31	December	2025	in	pursuant to	the	UCLB	License	Agreement	which	was	capitalised	to	intangible	assets Financial	performance	for	the	year During	the	year	ended	31	December	2025,	we	generated	product	revenue,	net	amounting	to	&pound;56.0	million,	from	the	sale of	AUCATZYL	in	the	United	States.	We	did	not	generate	any	product	revenue	for	the	year	ended	31	December	2024,	as AUCATZYL	was	approved	by	the	FDA	for	commercial	use	on	8	November	2024	and	was	not	launched	in	the	U.S.	market until	2025. License revenue	amounting to	&pound;0.8	million for the	year	ended	31	December	2025 related	primarily to license revenue recognised	pursuant	to	the	License	and	Option	Agreement	with	Moderna.	During	the	year	ended	31	December	2025,	we were	notified	by	Moderna	of the	achievement	of	a	clinical	milestone	of	&pound;0.8	million relating to	one	of	our	proprietary binders	that	was	licensed	in	2022.	License	revenue	of	&pound;8.0	million	for	the	year	ended	31	December	2024	primarily	related to	license	revenue	recognised	pursuant	to	the	License	and	Option	Agreement	with	BioNTech. Cost of sales increased to &pound;77.6	million for the year ended	31	December 2025 from	&pound;11.1	million for the year ended 31 December 2024 relating to increase in salaries and other employment related costs, including share-based compensation	expense, for	employees	engaged in	manufacturing	activities related	to	AUCATZYL,	as	well	as	outsourced professional services. It also consisted of direct production costs relating to commercial product manufactured, and allocated facility costs including maintenance, depreciation, utilities and rent. Cost of sales was recognised from November	8,	2024,	the	date	of	the	FDA	approval	of	AUCATZYL. Research	and	development	expenses	decreased	by	&pound;28.3	million	to	&pound;84.7	million	for	the	year	ended	31	December	2025 from	&pound;113.0	million	for	the	year	ended	31	December	2024	primarily	due	to: • a	decrease	of	&pound;16.2	million	in	salaries	and	other	employment	related	costs	including	share-based	compensation expense, which was mainly driven by the reallocation of employees to commercial manufacturing activities included	in	cost	of	sales	and	inventories; • a	decrease	of	&pound;14.8	million related to information technology infrastructure, support for information	systems, facility	costs	and	depreciation,	including	the	allocation	of	expense	from	research	and	development	to	cost	of	sales and	inventories	related	to	commercial	manufacturing	following	the	FDA	approval	of	AUCATZYL	in	November	2024; and • a	decrease	of	&pound;2.0	million	in	legal	fees	and	professional	consulting	fees	in	relation	to	research	and	development activities;	offset	by: • an	increase	of	&pound;4.6	million	in	clinical	trial	costs,	manufacturing	costs	and	material	transportation	costs	relating	to research	and	development	activities. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 25

 General	and	administrative	expenses	increased	by	&pound;21.5	million	to	&pound;100.8	million	for	the	year	ended	31	December	2025 from	&pound;79.2	million	for	the	year	ended	31	December	2024	primarily	due	to: • an	increase	of	&pound;14.4	million	in	salaries,	other	employment	related	costs	and	termination	benefits	including	share- based	compensation	expenses,	which	was	mainly	driven	by	an increase in the	number	of	employees	engaged in general	and	administrative	activities; • an	increase	of	&pound;5.5	million	in	commercial	costs,	including	legal	and	professional	fees	due	to	increased	activity	in support	of	U.S.	and	international	market	access;	and • an	increase	of	&pound;1.6	million	in	information	technology	infrastructure	and	support	for	information	systems,	facility costs, depreciation and impairment on right of use assets and related property and equipment relating to the conduct	of	corporate	and	commercial	operations	including	increase	in	space	utilized	for	these	activities. Finance	income	decreased	to	&pound;16.7	million	for	the	year	ended	31	December	2025,	as	compared	to	&pound;33.0	million	for	the year ended	31	December 2024. The	decrease	of &pound;16.4	million primarily relates to lower aggregate balances and yield associated	with	the	Group’s	cash,	cash	equivalents	and	available-for-sale	securities	during	the	year	ended	31	December 2025	as	compared	to	the	year	ended	31	December	2024. Finance	expense	increased	to	&pound;31.8	million	for	the	year	ended	31	December	2025	as	compared	to	&pound;11.1	million	for	the year	ended	December	31,	2024.	The	increase	of	&pound;27.4	million	is	primarily	due	to	changes	in	the	assumptions	used	in	the valuation	of	the	Collaboration	Agreement	with	Blackstone	and	the	BioNTech	License	and	Option	Agreement	for	the	year ended	31	December	2025	compared	to	the	year	ended	31	December	2024. Income	tax	resulted	to	an	expense	of	&pound;1.6	million	for	the	year	ended	31	December	2025	from	income	tax	benefit	of	&pound;12.7 million for the	year	ended	31	December	2024	primarily	due	to	an increase in	Autolus Inc.'s taxable income	due	to the recognition of product revenue, net and related intra-group recharges during the year ended 31 December 2025 compared	2024. Net	Cash	Used	In	Operating	Activities During	the	year	ended	31	December	2025,	we	used	net	cash	of	&pound;92.0	million	in	operating	activities	primarily	related	to increases in accounts receivable, inventories net, operating lease liability and prepaid expenses working capital movements,	reflecting	the	timing	of	payments,	partially	offset	by	accounts	payable	and	accrued	expenses	working	capital movements. Net	Cash	Used	In	Investing	Activities During the year ended 31 December 2025, we used &pound;11.6 million of cash in investing activities, primarily relating purchases	of	property	and	equipment	and	intangibles	assets	offset	by	interest	income	received. Net	Cash	Provided	By	Financing	Activities During the year ended 31 December 2025, net cash provided financing activities was &pound;0.8 million related to lease incentives received net of interest offset by lease liabilities, principal payments, and payments of revenue share to Blackstone	and	BioNTech. We expect to incur significant expenses and operating losses for the foreseeable future as we market and continue commercialization	of	AUCATZYL,	advance	our	other	product	candidates	through	preclinical	and	clinical	development,	and seek regulatory	approval	and	pursue	commercialization	of	any	additional	approved	products.	As	a result,	we	will	need significant	additional	capital	to	fund	our	operations	until	such	time	as	we	can	generate	significant	revenue	from	sales	of AUCATZYL	or	other	products	for	which	we	may	obtain	regulatory	approval. As a result, we	will need substantial additional funding to support our continuing operations and pursue our growth strategy.	We have funded our operations to date primarily	with proceeds from product revenue, government grants, sales	of	our	equity	securities,	through	public	offerings	and	pursuant	to	our	at-the-market	equity	facility,	United	Kingdom research and	development tax credits and receipts from the SME	and	RDEC schemes, out-licensing arrangements and strategic	collaboration	and	financing	agreements.	.	We	may	be	unable	to	raise	additional	funds	or	enter	into	such	other agreements	or	arrangements	when	needed	on favourable terms,	or	at all. If	we fail to raise capital	or	enter into such agreements	as,	and	when,	needed,	we	may	have	to	significantly	delay,	scale	back	or	discontinue	the	development	and commercialisation	of	one	or	more	of	our	drug	candidates	or	delay	our	pursuit	of	potential	in-licences	or	acquisitions. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 26

 Going	Concern The	Group's	and	Parent	Company	financial	statements	have	been	prepared	on	the	going	concern	basis	after	assessing	the Group’s cash flow forecasts and principal risks. The Group has incurred recurring losses and negative cashflows from operations since inception, including net losses of &pound;222,656,000 for the year ended 31 December 2025. The Group anticipates incurring additional losses until such time, that it can generate significant positive cashflows from sales of AUCATZYL	and	other	product	candidates	in	development.	Additional	financing	will	be	needed	by	the	Company	to	fund	its operations	and	to	develop	its	product	candidates. As	of 31	December	2025, the	Group	had retained losses	of &pound;841,997,000, equity attributable to equity	holders	of the parent of &pound;135,166,000, cash and cash equivalents of &pound;77,393,000 and financial assets at fair value through other comprehensive income (“marketable securities”) of &pound;146,100,000. The Group's board of directors (“Directors”) have reviewed	and	approved	an	operating	budget	for	the	three-year	period	to	31	December	2028	(the	"base	case	budget”),	in accordance	with the	Group's normal budgeting and forecasting	processes.	Whilst the	Directors have such longer-term forecasting	models to	establish the	strategic funding	needs, they	have	also	used	this	base	case	budget to	consider the cash	needs	of	the	Group	and	Parent	Company,	for	the	period	to	31	October	2027	(the	going	concern	assessment	period) being	a	period	more	than	12	months	from	the	date	of	approval	of	the	financial	statements. Although the Group retains the ability to extend its cash runway through mitigating actions, including reducing or deferring product development activities and other discretionary expenditure, such measures are not currently contemplated by the	Directors. This reflects the facts that following the successful launch of AUCATZYL in the	United States	and	the	United	Kingdom,	the	Group	is	focused	on	executing	its	growth	strategy,	including	further	development	and commercialisation	of	its	pipeline	and	expansion	of	AUCATZYL	sales.	This	is	therefore	the	realistic	expected	direction	of	the Group	and	Parent	Company,	and	appropriate	forecasting	considerations	in	the	going	concern	review	context. The	Directors’	projections	therefore	assume	continued	investment	in	product	development	and	commercial	activities	in line	with	the	Group’s	strategic	objectives. As	an	early	commercial-stage	biopharmaceutical	company,	the	Group	is	still	in	progress	towards	reaching	profitability	and expects	that,	based	on	the	base	case	budget,	and if	no	further	external financing is	assumed, its	current	and	projected cash,	cash	equivalents	and	marketable	securities	will	be	sufficient	to	fund	its	operations	into	October	2027	under	the	base case scenario, and up to 30 June 2027	under a stress test scenario. As a result, the	Group	will be required to secure additional funding within the going concern assessment period. The ability to obtain such funding is not within the Group’s	control	and	remains	subject	to	market	conditions	and	other	external	factors. The	base	case	budget	includes	assumptions	regarding: • Increases	in	product	revenues	and	gross	margin, • Cost	reductions	and	efficiencies,	including	the	restructuring	actions	announced	in	April	2026,	and • Expected timing of cash inflows from	U.K. R&D tax credits, including the	U.K. R&D tax credit claimed by the Group in its corporate tax return for the accounting period to 31 December 2023 that is subject to ongoing discussions	with	the	United	Kingdom	tax	authority. These assumptions are subject to uncertainty due to numerous factors, including the Group’s limited sales history following its recent product launches in the United States of America and United Kingdom, its ability to obtain and implement cost reductions, expected timings of cash inflows from	U.K. R&D tax credits and other factors outside the Group’s	control.	While	management	believes	these	assumptions	are	reasonable,	actual	results	may	differ,	and	the	Group may	utilise	its	cash	resources	sooner	than	currently	expected.	When	applying	severe	but	plausible	downside	sensitivities, including	reduction	in	forecast	sales	growth	rates,	maintaining	costs	to	current	levels	and	the	timing	and	quantum	of	U.K. R&D tax credit receipts,	without taking any other	mitigating actions such as a delay in planned	R&D	activities or cost reduction	measures,	the	Group	would	extinguish	existing	liquidity	by	30	June	2027. As	a	result,	in	both	the	base	case	and	downside	scenarios,	the	Group	will	be	required	to	secure	additional	funding	within the	going concern	assessment	period to	maintain sufficient liquidity.	Accordingly, this	need to raise	additional funding represents a	material uncertainty that	may cast significant doubt on the	Group’s and the Parent Company’s ability to continue	as	a	going	concern,	and	therefore,	that	it	may	be	unable	to	realise	its	assets	and	discharge	its liabilities	in	the normal	course	of	business. AUTOLUS	THERAPEUTICS	PLC Strategic	Report For	the	year	ended	31	December	2025 27

 Notwithstanding the	existence	of this	material	uncertainty, the	Board	believes that the	adoption	of the	going concern basis	of	accounting	is	appropriate	for	the	following	reasons: • The	Directors	continue	to	pursue	a	number	of	options	to	secure	longer-term	funding	for	the	Group	and	Parent Company,	including	equity	financings,	debt	financings,	partnerships,	or	other	sources; • The	Group	has	demonstrated	a	track	record	of	raising	capital through	prior	equity issuances	and	collaboration agreements undertaken prior to the commercialisation of AUCATZYL. Following the successful launch of the product	in	the	United	St…

EX-99.2 · ex992noticeofagm2026.htm

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 1 THIS DOCUMENT IS IMPORTANT AND REQUIRES YOUR IMMEDIATE ATTENTION. If you are in any doubt as to the action to be taken, please seek your own independent financial advice from your stockbroker, solicitor, accountant or other appropriately authorised independent financial adviser. If you have recently sold or transferred all of your ordinary shares in Autolus Therapeutics plc, you should forward this document and any accompanying documents to your bank, stockbroker or other agent through whom the sale or transfer was effected for transmission to the purchaser or transferee. If you have sold or transferred only part of your holdings, you should retain these documents. The registered office of Autolus Therapeutics plc is The MediaWorks, 191 Wood Lane, London W12 7FP, United Kingdom. Autolus Therapeutics plc is incorporated and registered in England and Wales under the Companies Act 2006, with company number 11185179. Autolus Therapeutics plc’s website is www.autolus.com and telephone number is +44 20 3829 6230. Autolus Therapeutics plc Notice of Annual General Meeting 2026 To be held at: Opera Boardroom, Sofitel, Terminal 5, London Heathrow Airport, London, TW6 2GD On: Monday 29 June 2026, commencing at 11:00 a.m. (British Summer Time).

 2 How to vote Autolus Therapeutics plc (“Autolus” or the “Company”) has ordinary shares, which are capable of being held in certificated form or dematerialised and held in CREST, and may also be represented by American Depositary Shares (“ADSs”), with each ADS representing one ordinary share. Your votes matter. You are strongly encouraged to vote your ordinary shares by appointing the chair of the annual general meeting (“AGM”) as your proxy. Registered holders of ordinary shares may also attend the AGM in person. For more information: - Holders of ordinary shares should refer to the notes starting on page 9; and - Holders of ADSs should refer to the notes starting on page 11. How to attend The Company’s AGM will be held at the Opera Boardroom, Sofitel, Terminal 5, London Heathrow Airport, London, TW6 2GD on 29 June 2026. The AGM will commence at 11:00 a.m. (British Summer Time). If you receive your notifications by email, you will be asked to show a copy, either on an electronic device or as a printout. Please bring your admission card, if you have one and be prepared to provide evidence of your shareholding and/or identity. If you are attending on behalf of a registered holder of the ordinary shares you must bring photographic proof of identity and evidence of your appointment to represent that shareholder, including their admission card if possible. This includes people appointed as proxies, corporate representatives and those with power of attorney. If you are bringing a guest, please let us know in advance. How to order paper copies You can order a paper copy of this notice or any other company report at www.autolus.com. Copies will also be available at the AGM.

 Chair’s Letter 3 Dear Shareholder, 2026 Annual General Meeting of Autolus Therapeutics plc On behalf of the Company’s board of directors (each, a “Director” and together, the “Board”) and senior management, I look forward to welcoming you to the Company’s 2026 Annual General Meeting at the Opera Boardroom, Sofitel, Terminal 5, London Heathrow Airport, London TW6 2GD on 29 June 2026. The AGM will start at 11:00 a.m. British Summer Time. At the AGM, we will be discussing our performance during the fiscal year ending on 31 December 2025, and our strategy. Full details of the fiscal year in review are set out in the 2025 Autolus Annual Report and Accounts (the “2025 Annual Report and Accounts”), which can be found at www.autolus.com. Business of the AGM The business we will discuss at the AGM is made up of resolutions that we regularly bring to shareholders. For a more fulsome update on the Company’s business, and full details of the fiscal period in review, you should consult the Company’s 2025 Annual Report and Accounts, including the associated reports of the Directors and auditors, and also the Company’s 2025 Annual Report on Form 10-K, which can be found at www.autolus.com. Recommendation The formal notice of AGM is set out on pages 4 – 5 of this notice and an explanation of each of the resolutions to be considered at the AGM may be found starting from page 6. The Directors consider that all of the resolutions that are being proposed to the AGM are in the best interests of the Company and its shareholders as a whole and are most likely to promote the success of the Company for the benefit of its shareholders as a whole. Accordingly, the Directors unanimously recommend that you vote in favour of the resolutions as each of the Directors with personal holdings of ordinary shares in the Company intends to do in respect of their own beneficial holdings of ordinary shares. Your votes do matter. Information about how to vote at the AGM is given on pages 9 and 11 respectively of this notice. If you cannot attend the AGM, please vote your ordinary shares by appointing a proxy. Thank you for your ongoing support of Autolus. Michael Bonney Non-Executive Chair 5 June 2026

 Notice of 2026 Annual General Meeting 4 Notice is hereby given that the 2026 Annual General Meeting of Autolus Therapeutics plc will be held at the Opera Boardroom, Sofitel, Terminal 5, London Heathrow Airport, London TW6 2GD on 29 June 2026 at 11:00 a.m. (British Summer Time), for the transaction of the following business. This notice is being sent to you because, as of Wednesday, 3 June 2025 (being the latest practicable date before publication of this notice), you are registered as a holder of ordinary shares in the register of members of the Company. However, this notice will also be made available to holders of ADSs and contains information relevant to holders of ADSs. Resolutions 1-6 will be proposed as ordinary resolutions, meaning that, for each of resolutions 1-6 to be passed, more than half of the votes cast must be in favour of the resolution. The Board considers that all resolutions to be considered at the AGM are in the best interests of the Company and its shareholders and are most likely to promote the success of the Company for the benefit of its shareholders as a whole and recommends that you vote in favour of such resolutions. You can order a paper copy of this notice or any other company report at www.autolus.com. Ordinary resolutions Resolution 1 Report and accounts To receive and adopt the Company’s accounts for the financial year ended 31 December 2025 and the associated reports of the Directors and auditors (the “2025 Annual Report and Accounts”). See the notes on page 6. Resolution 2 Directors’ remuneration report To approve the Directors’ remuneration report (excluding the Directors’ remuneration policy set out on pages 41-54 of the Directors’ remuneration report), which is set out on pages 38- 67 of the 2025 Annual Report and Accounts. See the notes on page 6. Resolution 3 Appointment of auditors and determination of auditors’ remuneration To appoint Ernst & Young LLP (US) as auditors of the Company to hold office from the conclusion of the 2026 AGM until the conclusion of the 2027 AGM and to authorise the Directors to determine the auditors’ remuneration. See the notes on page 6. Resolution 4 Director re-election To re-elect Mr. M Bonney as a Director. See the notes and biography on page 7. Resolution 5 Director re-election To re-elect Dr. E Leiderman as a Director. See the notes and biography on page 8. Resolution 6 Director re-election To re-elect Mr. R.W. Azelby as a Director. See the notes and biography on page 8.

 Notice of 2026 Annual General Meeting (cont’d) 5 Alex Driggs Company Secretary 5 June 2026 The registered office of Autolus Therapeutics plc is The MediaWorks, 191 Wood Lane, London W12 7FP, United Kingdom. Autolus Therapeutics plc is incorporated and registered in England and Wales under the Companies Act, with company number 11185179. Autolus Therapeutics plc’s website is www.autolus.com and telephone number is +44 20 3829 6230.

 Notes to Resolutions 6 Notes to resolution 1 Report and accounts The Companies Act requires the directors of a public company to lay before the company in general meetings copies of the directors’ reports, the independent auditor’s report and the audited financial statements of the company in respect of each financial year. For the financial year ended 31 December 2025, these are all contained in the 2025 Annual Report and Accounts. In accordance with best practice, the Company proposes an ordinary resolution to receive and adopt the 2025 Annual Report and Accounts, a copy of which may be found at: www.autolus.com/investor-relations/news-and-events/agm. Notes to resolution 2 Directors’ remuneration report Resolution 2 seeks shareholder approval for the Annual Statement by the Chair of the Compensation Committee and Annual Report on Remuneration which can found on pages 38-67 of the 2025 Annual Report and Accounts, but excluding the Directors’ remuneration policy on pages 41-54. The Directors’ report on remuneration sets out details of each Director’s remuneration during the financial year ended 31 December 2025. In accordance with the relevant regulations, the resolution is an advisory vote and does not affect the remuneration already paid to any Director. Notes to resolution 3 Appointment of auditors and determination of auditors’ remuneration Resolution 3 seeks shareholder approval for the appointment of Ernst & Young LLP (US) as the Company’s auditors until the conclusion of the next AGM at which the Company’s accounts are laid before shareholders. This resolution also seeks authority to give the Directors power to set the remuneration of the Company’s auditors. The Directors recommend Ernst & Young LLP’s (US) appointment and seek authority to determine their remuneration. The Board will delegate to the audit committee the authority to determine the auditors’ remuneration. The audit committee will continue to consider the reappointment of the external auditor each year before making a recommendation to the Board. The audit committee reviews the fee structure, resourcing and terms of engagement for the external auditor annually. Notes to resolutions 4, 5, and 6 Re-election of Directors The Directors are divided into three classes designated as “Class I”, “Class II” and “Class III”. Only the Directors in Class II are required by the Company’s articles of association to retire and offer themselves for re-election at the 2026 AGM of the Company. At the following two annual general meetings, the Directors in Class III and Class I, respectively, shall retire from office and be eligible for re-appointment. In accordance with this requirement, Messrs. Bonney and Azelby and Dr. Leiderman retire and offer themselves for re-election as Directors. Mr. John Berriman, the other member of

 Notes to Resolutions (cont’d) 7 Class II, also retires, but has opted not to offer himself for re-election as Director at the 2026 AGM and, accordingly, his term of office will conclude following the 2026 AGM. The nomination committee identifies, evaluates and recommends to the Board candidates for appointment or reappointment as Directors and for appointment as company secretary. The nomination committee keeps the diversity, mix of skills, experience and knowledge of the board under regular review and seeks to ensure an orderly succession of Directors. The outside directorships and broader commitments of the non-executive Directors (including time commitments) are also monitored by the nomination committee. The nomination committee’s reasons for the election or re-election of Directors are set out with the biography of each Director, as are descriptions of the directors’ skills and experience. In respect of each of the non-executive Directors—Mr. M Bonney, Dr. E Leiderman and Mr. R Azelby—the Board has fully considered whether each Director is free from any relationship that could materially interfere with the exercise of his or her independent judgment. The Board has determined that each of the non-executive Directors is considered to be independent. Mr. M Bonney, Dr. E Leiderman and Mr. R Azelby are recommended by the board for re- election. Notes to resolution 4 Michael Bonney Non-Executive Director Mr. Bonney has served as the chair of our board of directors since April 2024. He also serves as chair of the board for Santa Ana Bio, Inc. since September 2025 and of Immunic, Inc. since May 2026. He served as a director of Alnylam Pharmaceuticals, Inc. between December 2014 and December 2025; he previously served as chair of Alnylam from December 2015 to August 2021 and as its executive chair from August 2021 to January 2023. Mr. Bonney previously served as the Chair of the board of directors of Kaleido Biosciences, Inc., a biotechnology company, from June 2017 until August 2021. Between August 2018 and October 2020, he served as Kaleido’s Executive Chair and served as Kaleido’s Chief Executive Officer from June 2017 until August 2018. Mr. Bonney was a Partner at Third Rock Ventures, a healthcare venture firm, from January to July 2016. Mr. Bonney previously served as the Chief Executive Officer and a member of the board of directors of Cubist Pharmaceuticals, Inc., a biopharmaceutical company (now a wholly owned subsidiary of Merck & Co., Inc.), from June 2003 until his retirement in December 2014. From January 2002 to June 2003, he served as Cubist’s President and Chief Operating Officer. Mr. Bonney previously served as the Chair of the board of directors of Magenta Therapeutics, Inc. and as a director of Bristol-Myers Squibb Company, Celgene Corporation (which was acquired by Bristol-Myers Squibb), Syros Pharmacetuicals, Inc. and Sarepta Therapeutics, Inc. Mr. Bonney holds a B.A. in economics from Bates College. We believe that Mr. Bonney is qualified to serve on our board of directors because of his experience serving in leadership positions at a wide variety of biotechnology companies. Notes to resolution 5 Elisabeth Leiderman, M.D. Non-Executive Director Lis Leiderman has served on our board of directors since December 2023. She currently serves as Chief Financial Officer for Prilenia Therapeutics B.V., since April 2026. Previously, Dr. Leiderman served as Chief Financial & Corporate Development Officer for Dewpoint Therapeutics, a clinical-stage biotechnology company applying condensate biology to the

 Notes to Resolutions (cont’d) 8 discovery and development of novel therapeutics, from June 2024 to September 2025. Before joining Dewpoint, she served as Chief Financial Officer and Chief Business Officer at Atsena Therapeutics, a clinical-stage ophthalmology gene therapy company, between November 2022 and November 2023. Before joining Atsena, from September 2020 to October 2022, Dr. Leiderman was Chief Financial Officer and Head of Corporate Development at Decibel Therapeutics, a gene therapy company focused on hearing and balance disorders. From January 2020 to August 2020, Dr. Leiderman served as Chief Business Officer for Complexa, Inc. Prior to Complexa, Dr. Leiderman was Senior Vice President, Head of Corporate. Development at Fortress Biotech from November 2016 to November 2019. Earlier in her career from 2007 to 2016, Dr. Leiderman developed her transaction and capital markets expertise in the healthcare investment banking groups at Nomura, Credit Suisse, Jefferies and UBS. Dr. Leiderman began her career in medical affairs at AstraZeneca, where she analyzed product and industry trends related to the central nervous system. Dr. Leiderman earned an M.D. from the Sackler School of Medicine at Tel Aviv University, an M.B.A. from The Wharton School at the University of Pennsylvania and a B.A. from The University of Pennsylvania. We believe that Dr. Leiderman is qualified to serve on our board of directors because of her extensive experience as a pharmaceutical company executive, her financial and operational expertise, and her leadership skills. Notes to resolution 6 Robert Azelby Non-Executive Director Robert Azelby has served as a director since January 2024. Mr. Azelby served as President and Chief Executive Officer of Eliem Therapeutics, Inc., a biopharmaceutical company, from October 2020 to February 2023. Prior to Eliem, he served as the Chief Executive Officer of Alder BioPharmaceuticals, Inc. from June 2018 until its acquisition by H. Lundbeck A/S in October 2019. Mr. Azelby previously served as Executive Vice President, Chief Commercial Officer of Juno Therapeutics, Inc. from 2015 through its acquisition by Celgene in March 2018. Earlier, during a 15-year tenure at Amgen, Mr. Azelby served in commercial roles including Vice President and General Manager of Amgen Oncology, Vice President of Oncology Sales, Vice President of the Commercial Effectiveness Unit and General Manager of Amgen Netherlands. He currently serves as a non-executive director of ADC Therapeutics SA since June 2023, Cardinal Health since March 2024 and Terns Pharmaceuticals since February 2025. Mr. Azelby previously served on the Board of Directors of Chinook Therapeutics Inc. between April and August 2023, Clovis Oncology Inc. from October 2018 until July 20 23, Eliem Therapeutics Inc. from October 2020 until February 2023, Alder BioPharmaceuticals Inc. from June 2018 until November 2019, and Immunomedics, Inc. from February 2020 to October 2020. He holds a BA in Economics and Religious Studies from the University of Virginia and an MBA from Harvard Business School. We believe that Mr. Azelby is qualified to serve on our board of directors because of his broad experience in our industry, his commercial and management background, and his track record of effective leadership.

 Voting information for holders of ordinary shares and ADSs 9 Holders of ordinary shares When is my voting entitlement fixed? To vote at the AGM you must be a registered holder of ordinary shares at 6:00 p.m. (British Summer Time) on Thursday 25 June 2026 (or, if the AGM is adjourned, at 6:00 p.m. (British Summer Time) on the day two working days prior to the adjourned meeting). Your voting entitlement will depend on the number of ordinary shares that you hold at that time. The holders of ordinary shares are entitled to one vote per share on all matters that are subject to shareholder vote. How can I vote at the AGM? If you are a registered holder of ordinary shares, you can appoint the chair of the AGM or any other person to attend, speak and vote on your behalf. This person is called your proxy. Your proxy does not have to be a shareholder, but must attend the AGM to represent you. We recommend that shareholders appoint the chair of the AGM as their proxy. You can instruct your proxy how to vote. Where no specific instruction is given by you, your proxy may vote at their discretion or refrain from voting, as they see fit. You can appoint more than one proxy provided it is in relation to different shares within your holding. You can appoint a proxy and submit voting instructions: - by logging on to www.investorcentre.co.uk/eproxy and following the instructions; - by completing and returning the paper form of proxy (if one has been sent to you). Please read the instructions carefully to ensure you have completed and signed the form correctly. Any alterations must be initialled; or - via CREST (see further notes on starting on page 14). If you own shares jointly with one or more other persons, then where more than one of the joint holders completes a proxy appointment, only the appointment submitted by the most senior holder will be accepted. For this purpose, seniority is determined by the order in which the names of the joint holders appear in the Company’s register of members in respect of the joint holding (the first-named being the most senior). By when do I have to submit my vote? Proxy appointments and voting instructions, including any amendments, must be received by Computershare Investor Services, the Company’s registrar (the “Registrar”), by 11:00 a.m. (British Summer Time) on Thursday 25 June 2026 (or, if the AGM is adjourned, 48 hours (excluding non-working days) prior to the time of the adjourned meeting). If you miss this deadline and wish to submit a new vote or amend an existing vote, you can only do so by attending the AGM in person and voting.

 Voting information for holders of ordinary shares and ADSs (cont’d) 10 I already voted but have changed my mind – can I change my vote? You can submit a new voting instruction at any time before the time and date above. If you wish to amend a paper form of proxy, you must do so in writing and sign your new form of proxy. The voting instruction received last will be the one that is followed. I hold shares on behalf of several others – can I vote part of the holding separately? You can appoint more than one proxy using a paper form provided it is in relation to different shares. Corporate shareholders may either appoint one or more proxies using the paper form or via CREST, or alternatively appoint one or more corporate representatives in relation to different shares. Multiple proxies and corporate representatives may all attend and speak at the AGM and may vote the shares that their respective appointments represent in different ways. I am a CREST member – can I use the CREST system to vote? CREST members who wish to appoint a proxy or proxies through the CREST electronic proxy appointment service may do so by using the procedures described in the CREST Manual (available via www.euroclear.com/CREST). CREST ID number: 3RA50 CREST Personal Members or other CREST Sponsored Members, and those CREST members who have appointed a voting service provider(s), should refer to their CREST sponsor or voting service provider(s), who will be able to take the appropriate action on their behalf. I have a power of attorney from a shareholder – how can I vote? You can vote using the paper form of proxy only. You must ensure that the valid power of attorney and the form of proxy have been deposited with the Registrar, Computershare Investor Services at The Pavilions, Bridgwater Road, Bristol BS99 6ZY, United Kingdom, by 11:00 a.m. (British Summer Time) on Thursday 25 June 2026 (or, if the AGM is adjourned, 48 hours (excluding non-working days) prior to the time of the adjourned meeting).

 Voting information for holders of ordinary shares and ADSs (cont’d) 11 Holders of ADSs When is my voting entitlement fixed? To vote at the AGM you must be a holder of ADSs at 5:00 p.m. (New York Time) on Wednesday 27 May 2026 (the “ADS Record Date”). Your voting entitlement will depend on the number of ADSs you hold at that time. The holders of ADSs are entitled to one vote per ADS on all matters that are subject to shareholder vote. How can I attend the AGM in person? ADS holders cannot attend or vote at the AGM. How can I vote the Ordinary Shares represented by my ADSs at the AGM? If you are a registered holder of ADSs as of the ADS Record Date you will be able to instruct the depositary, Citibank, N.A. (the “Depositary”), to vote the Ordinary Shares represented by your ADSs on your behalf by completing and returning an ADS voting instruction card to the Depositary no later than the time and date specified in the ADS voting instruction card. The Depositary will send to registered holders of ADSs as of the ADS Record Date an ADS voting instruction card and an explanatory Depositary Notice. Please read the instructions carefully to ensure you have completed and signed the ADS voting instruction card correctly. Any alterations must be initialled. If you are an ADS holder holding via a bank, broker or nominee, you would need to contact such said party to submit your vote through your bank, broker or nominee and complete the paperwork required by said party by their required deadlines. By when do I have to submit my vote? Paper voting instructions, including any amendments, must be received by the Depositary by 10:00 a.m. (New York Time) on Wednesday 24 June 2026 in the manner and at the address specified in the ADS voting instruction card. If your instructions are not received by the Depositary by the appointed times, then under the terms of the Deposit Agreement between the Company and the Depositary your ADSs may, under certain circumstances, be voted by a person designated by the Company. I already voted but have changed my mind – can I change my vote? You can submit a new ADS voting instruction card at any time during the ADS voting period. If you wish to amend the ADS voting instruction card you must do so in writing and sign your new ADS voting instruction card. The ADS voting instruction card received last by the Depositary prior to the expiration of the ADS voting period will be the one that is followed. I hold my ADSs in street name – can I still vote? You should contact your bank, broker or nominee for information on how to vote your ADSs.

 12 A copy of this notice and other information required by the Companies Act can be found at www.autolus.com/investor-relations/news-and-events/agm. Information rights Under the Companies Act, there are a number of rights that may now be available to indirect investors of the Company, including the right to be nominated by the registered holder to receive general shareholder communications direct from the Company. The rights of indirect investors who have been nominated to receive communications from the Company in accordance with section 146 of the Companies Act (“nominated persons”) do not include the right to appoint a proxy. However, nominated persons may have a right under an agreement with the registered shareholder who holds the shares on their behalf to be appointed (or to have someone else appointed) as a proxy. Alternatively, if nominated persons do not have such a right or do not wish to exercise it, they may have a right under such an agreement to give instructions to the person holding the shares as to the exercise of voting rights. If you have been so nominated to receive general shareholder communications direct from the Company, it is important to remember that your main contact in terms of your investment remains with the registered shareholder or custodian or broker, or whoever administers the investment on your behalf. You should also deal with them in relation to any rights that you may have under agreements with them to be appointed as a proxy and to attend, participate in, and vote at the AGM, as described above. Any changes or queries relating to your personal details and holding (including any administration thereof) must continue to be directed to your existing contact at your investment manager or custodian. The Company cannot guarantee dealing with matters that are directed to us in error. The only exception to this is where the Company is exercising one of its powers under the Companies Act and writes to you directly for a response. Statements related to the audit Members satisfying the thresholds in section 527 of the Companies Act can require the Company to publish a statement on its website setting out any matter relating to: - the audit of the Company’s accounts (including the auditor’s report and the conduct of the audit) that are to be laid before the AGM; and - any circumstances connected with an auditor of the Company ceasing to hold office since the last AGM, that the members propose to raise at the AGM. The Company cannot require the members requesting the publication to pay its expenses in connection with the publication. The company must forward a copy of the statement to the auditors when it publishes the statement on the website. The business which may be dealt with at the AGM includes any such statement that the company has been required to publish on its website. Shareholder requisition rights Members satisfying the thresholds in section 338 of the Companies Act can require the Company to give to members of the Company entitled to receive notice of the AGM, notice of a resolution which may properly be moved, and which those members intend to move, at the AGM, provided in each case that the requirements of that section are met and provided that

 Annex (cont’d) 13 the request is received by the company not later than six weeks before the AGM or if later the time at which notice is given of the AGM. Total voting rights and share capital As at 3 June 2026 (the latest practicable date before the publication of this notice), the issued share capital of the Company was 266,150,040 ordinary shares. Contact information Autolus Therapeutics plc Registered Office: The MediaWorks 191 Wood Lane W12 7FP London United Kingdom Tel: +44 20 3829 6230 Registrar Computershare Investor Services plc The Pavilions Bridgwater Road Bristol BS99 6ZZ United Kingdom Shareholder helpline - for information relating to your ordinary shares, please contact the Registrar on +44 370 703 6238. Calls outside the United Kingdom will be charged at the applicable international rate. The Registrar is open between 9:00 a.m. – 5:30 p.m. (British Summer Time), Monday to Friday excluding public holidays. ADS Depositary Citibank ADS Holder Services P.O. Box 43077 Providence, Rhode Island 02940-3077, USA Tel: 1-877-CITI-ADR (toll free) Tel: 1-781-575-4555 (outside US) Fax 1-201-324-3284 E-mail at: Citibank@shareholders-online.com

 Annex (cont’d) 14 Notes: The following notes further explain your general rights as a shareholder and your right to attend and vote at the AGM or to appoint someone else to vote on your behalf. Shareholders are strongly encouraged to vote your shares by appointing the chair of the AGM as your proxy. 1. You can vote either: 1.1. by logging on to www.investorcentre.co.uk/eproxy and following the instructions; 1.2. you may request a hard copy form of proxy directly from the Registrar, Computershare Investor Services, on Tel: +44 370 703 6238. Calls cost 12 pence per minute plus your phone company’s access charge. Calls outside the United Kingdom will be charged at the applicable international rate. Lines are open between 9:00 a.m. – 5:30 p.m. (British Summer Time), Monday to Friday excluding public holidays in England and Wales; or 1.3. in the case of CREST members, by utilising the CREST electronic proxy appointment service in accordance with the procedures set out in notes 5-7 below. 2. The completed form of proxy, voting instruction via www.investorcentre.co.uk/eproxy or any CREST Proxy Instruction (as described in notes 5-7 below), as the case may be, must be received by Computershare Investor Services by 11:00 a.m. (British Summer Time) on Thursday 25 June 2026 (or, if the AGM is adjourned, 48 hours (excluding non-working days) prior to the time of the adjourned meeting). 3. If you return more than one proxy appointment, either by paper or electronic communication, the appointment received last by the Registrar before the latest time for the receipt of proxies will take precedence. You are advised to read the terms and conditions of use carefully. Electronic communication facilities are open to all shareholders and those who use them will not be disadvantaged. 4. The return of a completed form of proxy, electronic filing or any CREST Proxy Instruction (as described in notes 5-7 below) will not prevent a shareholder from attending the AGM and voting in person if he/she wishes to do so. 5. CREST members who wish to appoint a proxy or proxies through the CREST electronic proxy appointment service may do so for the AGM (and any adjournment of the AGM) by using the procedures described in the CREST Manual (available from www.euroclear.com/site/public/EUI). CREST Personal Members or other CREST sponsored members, and those CREST members who have appointed a service provider(s), should refer to their CREST sponsor or voting service provider(s), who will be able to take the appropriate action on their behalf. 6. In order for a proxy appointment or instruction made by means of CREST to be valid, the appropriate CREST message (a “CREST Proxy Instruction”) must be properly authenticated in accordance with Euroclear UK & International Limited’s specifications and must contain the information required for such instructions, as described in the CREST Manual. The message must be transmitted so as to be received by Computershare Investor Services (ID number 3RA50) by 11:00 a.m. (British Summer Time) on Thursday 25 June 2026 (or, if the AGM is adjourned, 48 hours (excluding non-working days) prior to the time of the adjourned meeting). For this purpose, the time of receipt will be taken to mean the time (as determined by the timestamp applied to the message by the CREST application host) from which the issuer’s agent is able to retrieve the message by enquiry to CREST in the manner prescribed by CREST. After this time, any change of instructions to proxies appointed through CREST should be communicated to the appointee through other means. 7. CREST members and, where applicable, their CREST sponsors or voting service providers should note that Euroclear UK & International Limited does not make available special procedures in CREST for any particular message. Normal system timings and limitations will, therefore, apply in relation to the input of CREST Proxy Instructions. It is the responsibility of the CREST member concerned to take (or, if the CREST member is a CREST personal member, or sponsored member, or has appointed a voting service provider(s), to procure that his CREST sponsor or voting service provider(s) take(s)) such action as shall be necessary to ensure that a message is transmitted by means of the CREST system by any particular time. In this connection, CREST members and, where applicable, their CREST sponsors or voting system providers are referred, in particular, to those sections of the CREST Manual concerning practical limitations of the CREST system and timings. The Company may treat as invalid a CREST Proxy Instruction in the circumstances set out in Regulation 35(5)(a) of the Uncertificated Securities Regulations 2001.

 Annex (cont’d) 15 8. Any shareholder attending the AGM has the right to ask questions. The Company must cause to be answered any such question relating to the business being dealt with at the AGM but no such answer need be given if: (a) to do so would interfere unduly with the preparation for the AGM or involve the disclosure of confidential information; (b) the answer has already been given on a website in the form of an answer to a question; or (c) it is undesirable in the interests of the Company or the good order of the AGM that the question be answered. 9. The Company shall make available for inspection any of the following documents during normal business hours at the Company’s registered office prior to and at the AGM: 9.1. copies of the executive director’s service contract; and 9.2. copies of the letters of appointment of the non-executive directors. 10. You may not use any electronic address (within the meaning of section 333(4) of the Companies Act) provided in either this notice or any related documents (including the form of proxy) to communicate with the Company for any purposes other than those expressly stated. A copy of this notice, and other information required by the Companies Act, can be found on the Company’s website at www.autolus.com.

EX-99.3 · ex993formofproxy.htm

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 MR A SAMPLE < DESIGNATION> SAMPLE STREET SAMPLE TOWN SAMPLE CITY SAMPLE COUNTY AA11 1AA MR A SAMPLE < Designation> Additional Holder 1 Additional Holder 2 Additional Holder 3 Additional Holder 4 Form of Proxy - Annual General Meeting to be held on 29 June 2026 Kindly Note: This form is issued only to the addressee(s) and is specific to the unique designated account printed hereon. This personalised form is not transferable between different: (i) account holders; or (ii) uniquely designated accounts. The Company and Computershare Investor Services PLC accept no liability for any instruction that does not comply with these conditions. Explanatory Notes: 1. Every holder has the right to appoint some other person(s) of their choice, who need not be a shareholder, as his proxy to exercise all or any of his rights, to attend, speak and vote on their behalf at the meeting. If you wish to appoint a person other than the Chairman, please insert the name of your chosen proxy holder in the space provided (see reverse). If the proxy is being appointed in relation to less than your full voting entitlement, please enter in the box next to the proxy holder's name (see reverse) the number of shares in relation to which they are authorised to act as your proxy. If returned without an indication as to how the proxy shall vote on any particular matter, the proxy will exercise his discretion as to whether, and if so how, he votes (or if this proxy form has been issued in respect of a designated account for a shareholder, the proxy will exercise his discretion as to whether, and if so how, he votes). 2. To appoint more than one proxy, an additional proxy form(s) may be obtained by contacting the Registrar's helpline on 0370 703 6238 or you may photocopy this form. Please indicate in the box next to the proxy holder's name (see reverse) the number of shares in relation to which they are authorised to act as your proxy. Please also indicate by marking the box provided if the proxy instruction is one of multiple instructions being given. All forms must be signed and should be returned together in the same envelope. 3. The 'Vote Withheld' option overleaf is provided to enable you to abstain on any particular resolution. However, it should be noted that a 'Vote Withheld' is not a vote in law and will not be counted in the calculation of the proportion of the votes 'For' and 'Against' a resolution. 4. Pursuant to Regulation 41 of the Uncertificated Securities Regulations 2001, entitlement to attend and vote at the meeting and the number of votes which may be cast thereat will be determined by reference to the Register of Members of the Company at close of business on the day which is two days before the day of the meeting. Changes to entries on the Register of Members after that time shall be disregarded in determining the rights of any person to attend and vote at the meeting. 5. To appoint one or more proxies or to give an instruction to a proxy (whether previously appointed or otherwise) via the CREST system, CREST messages must be received by the issuer's agent (ID number 3RA50) not later than 48 hours before the time appointed for holding the meeting. For this purpose, the time of receipt will be taken to be the time (as determined by the timestamp generated by the CREST system) from which the issuer's agent is able to retrieve the message. The Company may treat as invalid a proxy appointment sent by CREST in the circumstances set out in Regulation 35(5)(a) of the Uncertificated Securities Regulations 2001. 6. The above is how your address appears on the Register of Members. If this information is incorrect please ring the Registrar's helpline on 0370 703 6238 to request a change of address form or go to www.investorcentre.co.uk to use the online Investor Centre service. 7. Any alterations made to this form should be initialled. 8. The completion and return of this form will not preclude a member from attending the meeting and voting in person. To be effective, all proxy appointments must be lodged with the Company’s Registrars at: Computershare Investor Services PLC, The Pavilions, Bridgwater Road, Bristol BS99 6ZY by 25 June 2026 at 11.00 am. View the Annual Report online: www.autolus.com/investor-relations Cast your Proxy online...It's fast, easy and secure! You will be asked to enter the Control Number, Shareholder Reference Number (SRN) and PIN shown opposite and agree to certain terms and conditions. All Correspondence to: Computershare Investor Services PLC The Pavilions, Bridgwater Road, Bristol, BS99 6ZY Register at www.investorcentre.co.uk - elect for electronic communications & manage your shareholding online! www.investorcentre.co.uk/eproxy 1245PIN: C0000000000SRN: Control Number: 921549 199762_256523_MAIL/000001/000001/SG601/i13 * 0 0 0 0 0 1 0 1 0 1 0 0 5 0 * 0 0 0 0 0 1

 Form of Proxy Please complete this box only if you wish to appoint a third party proxy other than the Chairman. Please leave this box blank if you want to select the Chairman. Do not insert your own name(s). I/We hereby appoint the Chairman of the Meeting OR the person indicated in the box above as my/our proxy to attend, speak and vote in respect of my/our full voting entitlement* on my/our behalf at the Annual General Meeting of Autolus Theraputics plc to be held at Opera Boardroom, Sofitel, Terminal 5, London Heathrow Airport, London, TW6 2GD on 29 June 2026 at 11.00 am, and at any adjourned meeting. * For the appointment of more than one proxy, please refer to Explanatory Note 2 (see front). Please mark here to indicate that this proxy appointment is one of multiple appointments being made. I/We instruct my/our proxy as indicated on this form. Unless otherwise instructed the proxy may vote as he or she sees fit or abstain in relation to any business of the meeting. Signature Date In the case of a corporation, this proxy must be given under its common seal or be signed on its behalf by an attorney or officer duly authorised, stating their capacity (e.g. director, secretary).  C0000000000 Ordinary Resolutions For Against Vote Withheld 1. To receive and adopt the Company’s accounts for the financial year ended 31 December 2025 and the associated reports of the Directors and auditors (the “2025 Annual Report and Accounts”). 2. To approve the Directors’ remuneration report (excluding the Directors’ remuneration policy set out on pages 41 to 54 of the Directors’ remuneration report), which is set out on pages 38 to 67 of the 2025 Annual Report and Accounts. 3. To appoint Ernst & Young LLP (US) as auditors of the Company to hold office from the conclusion of the 2026 AGM until the conclusion of the 2027 AGM and to authorise the Directors to determine the auditors’ remuneration. 4. To re-elect Mr. M Bonney as a Director. 5. To re-elect Dr. E Leiderman as a Director. 6. To re-elect Mr. R.W. Azelby as a Director. Intention To Attend Please indicate if you intend to attend the AGM 427H 80 OTA * Please use a black pen. Mark with an X inside the box as shown in this example.