Slides
Page 1
- 1 - Corporate Presentation February 2026 © 2026 Fate Therapeutics. All rights reserved. TRANSFORMING THE LIVES OF PATIENTS WITH AUTOIMMUNE DISEASES AND CANCER Making Cell Therapies Accessible to All TM
Page 2
- 2 - Forward-Looking Statements This presentation contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, including statements regarding the safety and therapeutic potential of the Company’s product candidates, the advancement of and plans and timelines related to the Company’s ongoing and planned clinical studies and the clinical investigation of its product candidates, the timing for the Company’s receipt and announcement of data from its clinical trials and preclinical studies, the Company’s clinical development and regulatory strategy, the Company’s progress and plans relating to, and the anticipated timing and outcome of, interactions with the FDA and other regulatory authorities, including its expectationsrelating to alignment with regulatory authorities on potential registrationalpathways for FT819, the Company's expectations regarding progress and timelines, and potential payments under its collaboration, and the objectives, plans and goals of its collaboration with Ono Pharmaceutical, Ltd. These and any other forward-looking statements in this presentation are based on management's current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. These risks and uncertainties include, but are not limited to, the risk that results observed in studies of its product candidates, including interim results and results from earlier studies, may not be predictive of final results or results observed in ongoing or future studies involving these product candidates, the risk of a delay in the initiation of, or in the enrollment or evaluation of subjects in, any clinical studies, and the risk that the Company may cease or delay manufacture, or preclinical or clinical development, of any of its product candidates for a variety of reasons (including regulatory requirements, difficulties in manufacturing or supplying the Company's product candidates, prioritization of other of its product candidates for advancement, and any adverse events or other negative results that may be observed during preclinical or clinical development). These statements are also subject to other risks and uncertainties as further detailed in the Company's most recently filed periodic report, and subsequent periodic reports filed by the Company, under the Securities Exchange Act of 1934, as amended, any of which could cause actual results to differ materially from those contained in or implied by the forward-looking statements in this presentation. The Company is providing the information in this presentation as of the date hereof and does not undertake any obligation to update any forward-looking statements contained in this presentation unless required by applicable law.
Page 3
- 3 - Q1 2026 Business Updates & Near-Term Objectives Competitively positioned to accelerate clinical stage development Autoimmune Development (FT819) Next Gen Development w/ Sword & ShieldTM (FT836 & FT839) Cash & Equivalents Milestones Achieved Near Term Next Steps ✓ 15 lupus patients enrolled with 7 initial sites, with 16 total clinical sites now activated1 Complete Phase 1 SLE cohort enrollment by mid-2026 Continue no conditioning dose escalation and multi-dosing ✓ Engaged with FDA under RMAT designation to align on pivotal trial and protocol strategy Gain FDA alignment on registrational protocol and initiate pivotal trial in 2026 ✓ Continued patient treatment expansion beyond SLE with 4 SSc and one IIM patient treated1 Conduct dose expansion in IIM, SSc, and ANCA vasculitis. Expand into RA & additional indications2 ✓ Optimized FT825 patient enrollment strategy Complete dose escalation with a focus on HER2+ patients ✓ Treated 3 patients in FT836 (MICA/B) pan-solid tumor Phase 1 trial1 Complete dose escalation cohorts by mid 2026 ✓ Initiated FT836 in multiple myeloma IIT Enroll first multiple myeloma patient 1H 2026 ✓ Commenced FT839 IND enabling activities Initiate Phase 1 pan-autoimmune trial in 2026 ✓ $205 million in cash, cash equivalents, & investments ✓ 30% reduction in operating expenses in 2025 compared to 2024 Projected operating runway through year-end 2027 1. Data as of February 25th 2. ANCA = Anti-neutrophil cytoplasmic auto -antibody associated vasculitis; IIM = Idiopathic inflammatory myositis; RA = Rheumato id Arthritis; SLE = Systemic Lupus Erythematosus; SSc = Systemic Sclerosis FDA = Food and Drug Administration RMAT = Regenerative medicine advanced therapy Oncology Development (FT825)
Page 4
- 4 - Outpatient Treatment Enabled CAR T-cell Therapy Platform First CAR T-cell therapy in autoimmune without the requirement for hospital stay ✓ Successful dosing of FT819 in an outpatient setting as same-day discharge without extended hospitalization and observation ✓ Elimination of inpatient care and the reduction/elimination of conditioning chemotherapy combined with on-demand availability facilitates broad patient access ✓ Providing off-the-shelf CAR T-cell therapy in community hospital-based treatment settings reduces the burden on healthcare infrastructure, and unlocks a viable, scalable and practical therapeutic paradigm Autologous CAR T-cell Therapy Fate Therapeutics’ CAR T-cell Therapy Removal or tapering of existing medicines Collect white blood cells in the hospital Isolate patient’s T cells and edit through CD19 CAR insertion Manufacture CAR T cells for single/ limited doses Infusion of CAR T cells; Hospitalization ≥2 weeks Intensive conditioning therapy Total therapy time ≥6 weeks Total therapy time ~1 week Minimal conditioning or no conditioning therapy Infusion of readily available CAR T cells Hospitalization ≤3 days Clinic • No leukapheresis means patients can stay on current therapy prior to treatment • Manufactured at large scale to produce uniform and reproducible CAR T-cell drug product • Available on-demand with broad patient accessibility • Safety profile allows for shorter hospitalization Inpatient Care (Hospital Setting) Existing CAR T-cell therapies in autoimmune Limited patient beds & treatment capacity restricts Rx scale Major life disruption, with many weeks of hospital visits Long lag time between diagnosis and Rx availability High healthcare & patient costs Autologous CAR T-cell Therapy Fate Therapeutics’ CAR T-cell Therapy Removal or tapering of existing medicines Collect white blood cells in the hospital Isolate patient’s T cells and edit through CD19 CAR insertion Manufacture CAR T cells for single/ limited doses Infusion of CAR T cells; Hospitalization ≥2 weeks Intensive conditioning therapy Total therapy time ≥6 weeks Total therapy time ~1 week Minimal conditioning or no conditioning therapy Infusion of readily available CAR T cells Hospitalization ≤3 days Clinic • No leukapheresis means patients can stay on current therapy prior to treatment • Manufactured at large scale to produce uniform and reproducible CAR T-cell drug product • Available on-demand with broad patient accessibility • Safety profile allows for shorter hospitalization Minimal conditioning or no conditioning therapy Infusion of readily available CAR T cells Outpatient same-day hospital discharge Removal or tapering of existing medicines Collect white blood cells in the hospital Isolate patient’s T cells and insert CAR motif Manufacture CAR T cells for single/ limited doses Infusion of CAR T cells; hospitalization ≥ 2 weeks Intensive pre- conditioning therapy Off-the-Shelf CAR T-cell Therapy Autologous CAR T-cell Therapy Outpatient Care (Community Setting) Fate Therapeutics CAR T-cell therapies in autoimmune Treatment & recovery occurs in familiar environment On-demand Rx availability supports timely treatment Lower healthcare & patient costs Increases patient accessibility & enables Rx scale
Page 5
- 5 - Making Cell Therapy Accessible to All iPSC Derived Off-the-Shelf Cellular Immunotherapies Utilizing Master Cell Banks to Consistently Manufacture Genetically Engineered Cellular Therapies
Page 6
- 6 - Unique Platform For Delivery Of Off-the-Shelf Cellular Therapies Mass produced, multiplexed-engineered cell products for on-demand patient treatment Single step multiplex gene editing Induced pluripotent stem cell (iPSC) Clonal sorting and selection Single product candidate clone De-selected clones Clonal Master Cell Bank (MCB) iPSC expansion and MCB creation Manufactured starting from MCB Vial Stored Drug Inventory Treat thousands of patients on-demand Gene editing is a one-time event completed at iPSC stage Master cell bank contains clonally identical population Master cell bank is starting material for CAR T-cell manufacture Consistent manufacture results in uniform and homogenous drug product Off-the-shelf drug product supports on- demand delivery for broad patient reach iPSC → any cell in the body
Page 7
- 7 - State of the Art GMP facility (San Diego, CA, USA) • 40,000+ ft2 cGMP manufacturing facility co-located with Fate Therapeutics’ corporate headquarters • Capacity to generate approximately 50,000 doses per year at $3,000 cost of goods per dose • 1 master cell bank with working cell bank intermediates, may produce more than 10 million doses • End-to-end capabilities and controls • Licensed by the State of California, Department of Health Services, Food and Drug Branch • Commissioned and qualified with first drug product manufacturing runs completed • On-site integration with quality, assay development, and process development • Supports USA and international clinical development as well as initial commercial launch Mass Production Of Cell Therapy Drug Products Advanced manufacturing capabilities to provide clinical and early commercial supply
Page 8
- 8 - Accessible CAR T Cell • Potential for profound efficacy in difficult-to-treat diseases • Healthy starting material • One-time uniform iPSC precision engineering event • Off-the-shelf streamlined logistics • Multiple dose paradigm • Homogenous drug product • Reduced hospitalization • Cost-Effective ($) Allogeneic CAR T Cell • Potential for profound efficacy in difficult-to-treat diseases • Healthy starting material • Random, variable, per-batch T-cell engineering • Complex logistics • Multiple dose paradigm • Heterogeneous drug product • Extended hospitalization • Expensive ($$$) • Profound efficacy in difficult-to- treat diseases • Impaired starting material • Random, variable, per-patient T-cell engineering • Complex logistics • Single dose paradigm • Heterogeneous drug product • Extended hospitalization • Prohibitively Expensive ($$$$) Autologous CAR T Cell Highly Differentiated & Scalable Cell Therapy Paradigm Fate’s platform uniquely delivers off-the-shelf cell therapies on-demand to patients in need
Page 9
- 9 - Immune Modulation Therapeutic Landscape Fate’s multiplexed engineered CAR T cells deliver the potency of a living drug with uniformity of traditional biologics Heterogeneous and transient gene expression attenuates complete elimination of disease cell target(s) A living drug with consistent gene expression that is designed to react to disease burden for complete target cell(s) elimination Inability to adapt to disease burden with conventional drug decay kinetics over time No lympho-depleting conditioning, repeat dose and outpatient treatment compatible Low-to-no lympho-depleting conditioning, repeat dose and outpatient treatment compatible No lympho-depleting conditioning, repeat dose and outpatient treatment compatible Dependence on patients’ own immune system engagement for function Pre-selected T cell performance with no dependence on patient immune system Dependence on patients’ own immune system engagement for function Tissue penetration dependent on the efficiency & target of in vivo engineering step Selectable tissue penetration profile including 2º and 3º tissues Limited penetration into 2º and 3º tissues LV: Lentiviral vector; AAV: Adenovirus associated vector; NC: Nanocarriers; LNP: Lipid nanoparticles; mAb: Monoclonal antibodies; TCE: T cell engager Viral Synthetic LV AAV NC LNP In Vivo T Cell Reprogramming mAb T cell engager Protein Engagers Multiplexed Engineered T cells Limited disease reach through reduced genetic engineering capacity Broad disease reach through multiplex- engineering and multi-antigen targeting Limited disease reach through reduced ability for complex protein engineering ‘Off target’ reprogramming & genetic integration potential with variable safety outcomes across patient cohorts On-demand availability and patient access with scaled manufacturing capacity and preferable safety profile Uniform drug product ready on-demand with scaled manufacturing capacity
Page 10
- 10 - Off-the-Shelf Cellular Immunotherapy Product Pipeline Multiplexed-engineered, iPSC-derived product candidates Program CAR/Antigen Target Indication Pre Clinical Phase 1/2 Registrational Partner Autoimmunity FT819 CD19 Systemic Lupus Erythematosus (SLE) (RMAT) Systemic Sclerosis (SSc) ANCA associated Vasculitis (AAV) Idiopathic Inflammatory Myopathies (IIM) FT839 CD19/CD381,2 Pan-Indication (Autoimmune) w/o LCC FT522 CD191 Pan-Indication (Autoimmune) w/o LCC Oncology FT825 HER21 Solid Tumor (s) Undisclosed Undisclosed Solid Tumor (s) FT836 MICA/B1 Pan-Indication (Solid Tumor w/o LCC) FT836 MICA/B1 Multiple Myeloma (Heme Onc) FT839 CD19/CD381,2 Pan-Indication (Heme Onc) w/o LCC FT819-102 NK Cell Asset 1. Product contains hnCD16 that allows combination with licensed monoclonal antibodies, i.e. anti-CD20 to extend antigen targeting capability 2. Product contains CD3 fusion receptor that allows combination with licensed T cell engagers, i.e. anti-BCMA and anti-GPRC5D to extend antigen targeting capability RMAT: FDA Regenerative Medicine Advanced Therapy (RMAT) received in SLE LCC: Lympho-conditioning chemotherapy World rights to FT819, FT836, FT839 and FT522 T Cell Asset IND enabling studies FT825-101 Ongoing R&D activity FT819-102 FT819-102 FT819-102 FT522-102 FT836-101 IND enabling studies FT836 IIT NCT06308978 Enrolling NCT06241456 Enrolling NCT07216105 Enrolling
Page 11
- 11 - Addressing Diseases with Significant Unmet Clinical Need Reaching patients in their communities with an off-the-shelf treatment without lympho-conditioning chemotherapy Inflammatory disease with risk to multiple organs and systems Characterized by fibrosis and vascular damage impacting various organs Inflammation & necrosis of blood vessels leading to endothelial & organ damage Group of disorders that cause chronic inflammation progressive and muscle weakness Autoimmune Disease Oncology Efficacy for many patients is limited by multiple tumor resistance mechanisms Pan Tumor (Solid & Heme) ~1.3M Prevalence HER2+ EGFR+ ~2M Annual mortality Systemic Lupus Erythematosus (SLE) Idiopathic Inflammatory Myositis (IIM) Anti-neutrophil cytoplasmic auto-antibody associated vasculitis (AAV) Systemic Sclerosis (SSc) 1. Izmirly et al. Arthritis Reum 2021 2. Smoyer-Tomic et al. BMC Musc Dissorders 2012 USD ~$105B USD ~$230B Market Size (2024) US & EU Patients 5. SEER, Dyba 2021 6. Market Reports World (Jul2025), BioSpace (Feb 2025) 3. Bergamasco et al. Epi of Systemic Sclerosis 2019 4. Khoo et al. Nature 2023. Rare Disease Advisor, Nat’l Scleroderma Foundation
Page 12
- 12 - Making Cell Therapy Accessible to All FT819 Program CD19 Targeting CAR T-Cell Product Candidate
Page 13
- 13 - Derived from a defined clonal MCB incorporating unique functional elements to balance safety and efficacy: True Off-the-Shelf CAR T-Cell Drug Product • 1XX CAR19: Novel CAR with CD28 costimulatory and modified CD3z signaling domains for optimal safety and activity • TRAC-targeted CAR: CAR inserted in the T-cell receptor alpha constant (TRAC) locus to reproduce endogenous TCR expression for regulated and optimal function • TCR Null: Complete bi-allelic disruption of TRAC ablates TCR expression and eliminates the possibility of GvHD • On-Demand Delivery: Routinely manufactured at large scale from an engineered MCB that uniquely ensures a uniform, off-the-shelf drug product for broad patient access FT819: Off-the-Shelf anti-CD19 CAR T-Cell Product Candidate Safe and effective targeting of CD19+ B cells with broad patient accessibility CD19 CAR T-cell designed to eliminate pathological auto- reactive B-cells with balanced efficacy and safety to establish immune reset and clinical remission2 1. van der Stegen, S.J.C., et al. Nat. Biomed. Eng 6, 1284–1297 (2022). 2. V. Sandhu, et al. Annals of the Rheumatic Diseases, Volume 84, Supplement 1, 2025, Pages 29 -30. CD19 CAR State-of-the-art CAR motif and expression control1 TCR null Complete TCR disruption to prevent GvHD in allogeneic settings
Page 14
- 14 - FT819-102: Phase 1 Study of FT819 in B-cell Mediated Autoimmune Diseases1,2 Uniquely administered with fludarabine-free conditioning or maintenance therapy in the absence of Cy/Flu Highly-Differentiated Therapeutic Approach Available on-demand with: • No patient apheresis reduces patient burden and the need for withdrawal from current therapy • Less-intensive or no conditioning chemotherapy regimens • No discontinuation of maintenance therapy (Regimen B) • Outpatient treatment enabled with patients treated as same-day hospital discharge • Ability to re-dose in inadequate response or relapse • Protocol authorized autoimmune diseases include: Systemic lupus erythematosus (SLE), ANCA-associated vasculitis (AAV), Idiopathic inflammatory myopathy (IIM), Systemic sclerosis (SSc) 1. V. Sandhu, et al. Annals of the Rheumatic Diseases, Volume 84, Supplement 1, 2025, Pages 29 -30 2. https://clinicaltrials.gov/study/NCT06308978 (ClinicalTrials.gov) Clinical Trial NCT063089782 Stop all immuno suppressive medication Continue MMF/MPA or AZA or MTX Patient Enrollment & Clinical Site Status
Page 15
- 15 - FT819-102 Update: Ongoing Phase 1 Study of FT819 in B-cell Mediated Autoimmune Diseases1,2 Patient baseline characteristics treated with FT819 Baseline Parameter Overall (N=13)4 Regimen A, n=11; Regimen B, n=2 SSc, n 1 SLE, n – Clinical Characteristics 12 Age, y, mean (range) 30.8 (19-57) Female, n (%) 11 (92) SLE duration, y, median (range) 8.7 (1-34) Prior therapies, n, median (range) 7 (3-10) Follow-up, month, median (range) 4 (0-19.5) SLEDAI-2K, median (range) 14 (8-20) Lupus nephritis, n (%) 7 (58) UPCr, mean ± SD3 2.6 ± 1.8 PGA, mean ± SD 2.3 ± 0.4 FACIT-Fatigue score, mean ± SD 23 ± 13 SSc = Systemic Scleroris; SLE = Systemic Lupus Erythematosus; SLEDAI-2K = Systemic Lupus Erythematosus Disease Activity Index 2000; UPCr = urine protein-to-creatinine ration; PGA = Physician's Global Assessment; FACIT = Functional Assessment of Chronic Illness Therapy FT819-102 Patient Cohort Representative of Real-World Patient Characteristics 1. Jelcic, et al. Blood. Vol 146, Sup 1, 2025 2. https://clinicaltrials.gov/study/NCT06308978 (ClinicalTrials.gov) Essential Patient Features ➢ Thirteen patients enrolled & treated1 • Ten SLE with fludarabine-free, less-intensive conditioning chemotherapy (Regimen A) • Two SLE without conditioning chemotherapy (on background therapy) (Regimen B) • One SSc with fludarabine-free, less-intensive conditioning chemotherapy (Regimen A) ➢ All SLE patients exhibit high disease burden at baseline • Median disease duration of 8.7 years • Up to 10 prior treatment failures • Median baseline SLEDAI-2K of 14 3. Applicable to lupus nephritis patients only 4. Nov 25, 2025 data cut off date
Page 16
- 16 - Continued absence of high-grade CRS, No ICANS, and No DLTs observed in FT819 treated patients with at least 1 month follow up 3 Safety data in line with FT819-101 in B cell malignancies (NCT04629729) FT819-102 Update: Ongoing Phase 1 Study of FT819 in B-cell Mediated Autoimmune Diseases1,2 Differentiated and preferential safety profile 1. Jelcic, et al. Blood. Vol 146, Sup 1, 2025 2. https://clinicaltrials.gov/study/NCT06308978 (ClinicalTrials.gov) 3. Data cutoff 22nd Oct 2025 Safety Parameter Incidence, n (%) Among Patients with ≥1 Month Follow-up (N=10) CRS, Grade 1-2 3 (30) CRS, Grade ≥3 0 ICANS/neurotoxicity 0 GvHD 0 DLT 0 Grade ≥3 AEs (any) 3 (30) Infection, Grade ≥3* 2 (20) Cytopenia, Grade ≥3† 2 (20) Hypogammaglobulinemia 0 *Infection includes influenza and urinary tract infection. † Cytopenia includes any PTs of anaemia, leukopenia, neutropenia, neutrophil count decreased, lymphopenia, pancytopenia, and thrombocytopenia. AE = adverse event; CRS = cytokine release syndrome; DLT = dose-limiting toxicity; GvHD = graft-versus-host-disease; ICANS = immune effector cell-associated neurotoxicity syndrome;
Page 17
- 17 - FT819 Treatment Demonstrates Early and Sustained Improvement in SLE disease Regimen A: One-time FT819 treatment with less intensive conditioning chemotherapy1,2,3 ✓ Decrease in disease burden with less intensive conditioning chemotherapy is uniquely demonstrated ✓ Completed dose escalation and now enrolling in DL1 & DL2 expansion ✓ No DLT, CRS, GvHD or ICANS across 2 dose levels ✓ Reduced hospitalization, increased patient accessibility during early dose escalation and expansion3 ✓ On-demand CAR T-cell delivery is enabled by scalable manufacturing from a master cell bank Durable (≥18 month) SLE disease remission and complete renal response in LN patients with single dose of FT819 with less intensive conditioning1,3 1. Jelcic, et al. Blood. Vol 146, Sup 1, 2025 2. https://clinicaltrials.gov/study/NCT06308978 (ClinicalTrials.gov) 3. Data cutoff 22nd Oct 2025; Error graphed as SEM where appropriate 0 5 10 15 20 Study Timeline (Months) SLEDAI-2K Score BL 1 3 6 9 12 15 Dose Level 1 (n=5) 182 Dose Level 2 (n=3) Regimen A Individual Patient SLEDAI-2K Scores 0 1 2 3 4 5 6 Study Timeline (Months) UPCr (mg/mg) BL 1 3 6 9 12 15 Dose Level 1 (n=4) 182 Dose Level 2 (n=1) Regimen A Individual Patient UPCr Values 0 1 2 3 Study Timeline (Months) Mean PGA Score BL 1 2 3 6 9 12 15 18 Mean PGA Scores Regimen A (n=8) 0 20 40 60 Study Timeline (Months) Mean FACIT-Fatigue Score (0-52) BL 2 3 6 9 12 15 18 Mean FACIT-Fatigue Scores Regimen A (n=8) 0 5 10 15 20 Study Timeline (Months) Mean SLEDAI-2K Score BL 1 2 3 6 9 12 15 18 Regimen A Mean SLEDAI-2K Scores Dose Level 1 (n=5) Dose Level 2 (n=3) -100 -80 -60 -40 -20 0 Study Timeline (Months) Mean Change from BL in SLEDAI-2K Score (%) 1 3 6 9 12 15 18BL Regimen A Dose Level 1 (n=5) Mean % Change From BL in SLEDAI-2K Scores Dose Level 2 (n=3) Severe fatigue Healthy No fatigue
Page 18
- 18 - ✓ Deep and enduring elimination of peripheral blood B cell subsets and plasmablasts populations ✓ Clinical demonstration of B cell compartment remodeling followed by the re-emergence of naïve B cell states from bone marrow1 ✓ Complete B cell elimination in nasopharyngeal lymphoid tissues within 2 weeks following DL2 treatment with FT819 (N=2) Effective depletion of pathogenic B cell populations & replacement with naïve subsets to normal levels 1-3 FT819 Elicits Rapid and Deep Depletion of B Cells and Immune Remodeling Elimination of B cells in peripheral blood and tissue results in the repopulation of naïve B cell subsets Nasopharyngeal adenoid B cell collection technique Lymphoid tissue residing B cell elimination post FT819 treatment Before After 0.0 0.5 1.0 1.5 2.0 Adenoid B cells (CD45+ CD19+ CD20+) CD3 CD19 T cells B cells B cells T cells Before After SLE Patient 1. Jelcic, et al. Blood. Vol 146, Sup 1, 2025 2. https://clinicaltrials.gov/study/NCT06308978 (ClinicalTrials.gov) 3. Data cutoff 22nd Oct 2025 4. Morbach H et al. Reference values for B cell subpopulations from infancy to adulthood. Clin Exp Immunol. 2010 Nov;162(2):271 -9. Adenoid lymph nodes 0 50 100 150 200 200 300 400 500 Regimen A - Dose Level 1 (n=5) Study Timeline (Months) Absolute cell counts (cells/uL) BL 3 6 12 181 0 50 100 150 200 200 300 400 500 Regimen A - Dose Level 2 (n=3) Study Timeline (Months) Absolute cell counts (cells/uL) BL 1 3 6 12 18 0 20 40 60 80 100 Naive B Cells - Regimen A (n=6) Study Timeline (Months) Naive B Cells (CD27-IgD+ % of CD20+) Dose Level 2 (n=3) Dose Level 1 (n=3) BL 1 2 3 6 12 15 18 0 1 2 3 DL2 DL1 Relative Time to B Cell Nadir Normalized Time to Lowest Point (Time/Mean DL1) n=4 n=3 Regimen A – Dose Level 1 (n=5) Regimen A – Dose Level 2 (n=3) Relative Time to B Cell Nadir Naïve B cells Regimen A (n=6) Normal range4 Normal range4
Page 19
- 19 - 0 1 2 3PGA Score 1M 3M 6M 9M 12M 15M 0 5 10 15 20 SLEDAI-2K Score 1M 3M 6M 9M 12M 15M DL1: 360M cells 0 1 2 3PGA Score 1M 3M 6M 9M 12M 15M 6004 ✓ Two patients treated with a one-time dose of FT819 (DL1; 360M) as an add on therapy show disease activity improvement absent of any conditioning chemotherapy ✓ B cell elimination and clonal repertoire remodeling in the absence of lympho-conditioning ✓ No DLT, CRS, GvHD or ICANS as of data cutoff. Arthritis Hematuria Proteinuria Pyuria Rash Increased DNA binding Alopecia Pleurisy Low complement Leukopenia Mucosal ulcers BL 1M 3M 6M 9M 0 5 10 15 20 SLEDAI-2K Score BL 1M 0 5 10 15 20 B1-DL1 B2-DL1SLEDAI-2K(N=2) PGA (N=2) Sustained Response in SLE Achieved Without Lympho-Conditioning Regimen B: FT819 (DL1) as add-on to maintenance therapy exhibit improvement in disease activity 1. Fazeli P, et al. Arthritis Rheumatol. 2025; 77 (suppl 9). 2. Tuncel J, at al. Arthritis Rheumatol. 2025; 77 (suppl 9). 3. https://clinicaltrials.gov/study/NCT06308978 (ClinicalTrials.gov) 4. Data cutoff 25th Sep 2025 SLEDAI-2K composition scores per patient at baseline (pre-FT819) and at specified study time points1-4 BL = baseline; D = Day; DL= dose level; M = month; SLEDAI-2K = Systemic Lupus Erythematosus Disease Activity Index 2000. PGA = Physician global assessment. Data cutoff date 25th September 2025 BL BL
Page 20
- 20 - Preliminary Efficacy in SSc Patient Following FT819 Treatment First SSc patient with 3-month follow-up shows meaningful disease improvement using less-intensive conditioning chemotherapy Patient Case Study2 • 31Y/F with interstitial lung disease (ILD) and dermatomyositis (DM) • 6Y since original diagnosis • Refractory to 7 prior therapies ✓ Received one time dose of FT819 with less-intense fludarabine- free conditioning ✓ No CRS, GvHD, or ICANS observed ✓ mRSS = 22 at baseline, dropping to 15 at 3 months evaluation time point ✓ Patient also experienced meaningful improvements in overall disease severity vs baseline (CGA 6 → 2; PtGA 5 → 0) ✓ Meaningful real-world benefits noted in physical function and daily activities at 3M evaluation time point (SHAQ score 0) Systemic Sclerosis (SSc) Disease • Patients with severe systemic sclerosis (SSc) can face high morbidity, early mortality, and limited treatment options1 • No current FDA licensed therapy, except Tocilizumab and Nintedanib in SSc associated ILD1 • Immunosuppressant refractory patients represent a well-defined, high-risk subgroup suitable for transformative therapy • Novel therapies that provide deep clinical responses could support accelerated pathways • Case-level efficacy signals can justify rapid transition from proof-of-concept to registrational strategy 1.C. Denton et al. The 2024 British Society for Rheumatology guideline for management of systemic sclerosis, Rheumatology, Volume 63, Issue 11, November 2024, Pages 2956–2975 2. Data cut-off 9th Feb 2026 Diagnosis: Systemic Sclerosis (SSc) with interstitial lung disease (ILD) & dermatomyositis (DM) 31-year-old female ~6 yrs since diagnosis mRSS= Modified Rodnan Skin Score; CGA = Clinical Global Assessment; PtGA = Patient Global Assessment; SHAQ = Scleroderma Health Assessment Questionnaire
Page 21
- 21 - Clinical & Regulatory Advancement Differentiated Off-the-Shelf CAR T cell Regulatory & Operational Development ➢ True off-the-shelf CAR T cell, consistently manufactured from a precisely engineered master cell bank, that addresses the key challenges faced by autologous, allogenic and in vivo re-programming approaches. ➢ Recent reported data1 from 12 SLE patients treated with FT819 showed progressive and durable reductions in disease activity, including mean SLEDAI- 2K score reductions of up to 78% by six months from the dose level 2 (DL2) cohort, complete renal responses in lupus nephritis, and sustained B-cell depletion with immune remodeling. ➢ > 60 patients treated across FT819-101 (B cell malignancies) & FT819-102 (autoimmune) programs; Favorable safety with no ICANs, GvHD or CRS > Grade 2, underscoring a differentiated safety profile supporting same day outpatient administration. ➢ Ongoing Ph1 trial in ANCA vasculitis, myositis, SLE, and SSc (ages 12-70 years); allowing redosing after relapse or inadequate response. ➢ 15 SLE patients treated across 7 initial sites, 4 SSc and 1 IIM patients treated as part of cohort expansion2. ➢ 16 total clinical sites now activated (academic and community sites)2. ➢ Engaged with FDA under RMAT designation to align on SLE LN pivotal trial and protocol strategy to commence in 2H 2026. FT819 Product Candidate Executive Summary & Next Steps Strategic highlights and value drivers Current FT819 Disease Indications Systemic Sclerosis (SSc) ANCA vasculitis Myositis (DM/PM/IMNM) Systemic Lupus Erythematosus (SLE) 1. Jelcic, et al. Blood. Vol 146, Sup 1, 2025 (ASH December 2025 Presentation) 2. As of data cut-off 25th February
Page 22
- 22 - Making Cell Therapy Accessible to All NEXT GENERATION OFF-THE-SHELF CAR T CELLS
Page 23
- 23 - Seven-Point Edited HER2-Directed CAR T-Cell Therapy Designed for Enhanced Solid Tumor Efficacy FT825/ONO-8250: Off-the-shelf anti-HER2 CAR T-cell product candidate • TCR Null: Complete bi-allelic disruption of TRAC ablates TCR expression and eliminates the possibility of GvHD • Novel HER2-Directed CAR: Potent and preferential targeting of tumor cells expressing HER2 with H2CasMab-2 CAR expression and optimized for enhanced activity • hnCD16: Enables ADCC in combination with therapeutic monoclonal antibodies to complement CAR to overcome tumor heterogeneity through multi-antigen targeting • TGFβ-SRR: TGFβ signal redirection receptor provides resistance to TGFβ-mediated suppression commonly found in TME of solid tumors • CXCR2: Enhancement of migration into solid tumors • IL7RF: Enhances CAR T cell, potency, persistence and self-renewal • CD38 KO: Potential to enhance metabolic cell fitness Overcoming the Challenges in Solid Tumors HER2-targeted CAR T-cell designed to overcome tumor heterogeneity, improve cell trafficking, and resist tumor microenvironment mediated immune suppression 1. Hosking MP et al. Cell Stem Cell. 2025 May 30:S1934-5909(25)00187-0. 2. https://ir.fatetherapeutics.com/news-releases/news-release-details/fate-therapeutics-highlights-cancer-selective-her2-targeting
Page 24
- 24 - Herceptin® H2CasMab-2 On Target On Tumor On Target Off Tumor2 Novel Cancer-Specific CAR Binder Limits Off Tumor Toxicity FT825/ONO-8250 designed for preferential and multi-antigen targeting • Novel binder (H2CasMab-2) preferentially targets HER2 expressed on tumor cells with limited on-target off-tumor toxicity • FT825/ONO-8250 shows flexible multi-antigen targeting via enhanced antibody-directed cellular cytotoxicity (ADCC) 0 10 20 30 40 0 100 200 300 400 500 Days Post Tumor Transplant Tumor Volume (mm3) mAb administration **** P<0.0001 vs vehicle 0 10 20 30 40 0 100 200 300 400 500 Days Post Tumor Transplant Tumor Volume (mm3) ADC administration **** P<0.0001 vs vehicle 0 10 20 30 40 0 100 200 300 400 500 Days Post Tumor Transplant Effector administration **** P<0.0001 vs vehicle 0 10 20 30 40 0 100 200 300 400 500 Days Post Tumor Transplant Effector administration **** P<0.0001 vs vehicle Herceptin® Enhertu® FT825/ ONO-8250 FT825/ ONO-8250 + mAb Herceptin® HER2+ Normal Tissue HER2+++ Tumor Tissue In contrast to Herceptin® H2CasMab-2 shows limited On Target-Off Tumor toxicity 1. Hosking MP et al. Cell Stem Cell. 2025 May 30:S1934-5909(25)00187-0. 2. Moja Let al. Cochrane Database Syst Rev. 2012 Apr 18;2012(4)
Page 25
- 25 - FT825/ONO-8250-101: A Phase 1 Study of FT825 in Advanced Solid Tumor Phase 1 Study: FT825/Ono0825 with/without monoclonal antibody combination (NCT06241456) Regimen A: FT825 Monotherapy • Dose levels 1 and 2 have been evaluated. Enrollment is ongoing at Dose Level 3 • No dose-limiting toxicities to date • Preliminary observations at the lower doses indicate clinical activity, including stable disease (per RECIST v1.1) • HER2+ Breast, Gastric, GEJ, HER2Mut NSCLC • HER2+ salivary, endometrial, other cancers Early Clinical Observations • Colorectal (KRAS WT or BRAF V600E) • NSCLC (EGFRMut) • HNSCC Regimen B: FT825 Combination with Cetuximab 1. https://clinicaltrials.gov/study/NCT06241456 (ClinicalTrials.gov). Clinical Trial NCT062414561
Page 26
- 26 - Problem Statement ➢ Most tumors lack distinct lineage markers, making it difficult to distinguish tumor from healthy tissue. ➢ Single mechanism therapies often drive immune escape, enabling resistant/refractory tumor variants. ➢ Tumor microenvironments suppress immune function and impede cell access, creating zones of immune exclusion. Proposed Solution(s) ✓ Target disease or altered self markers to enable cell specific killing across diverse tumor types/pathological settings. ✓ Deploy multiplex targeting to apply simultaneous immune pressure via distinct mechanisms of action. ✓ Navigate immune suppressive niches and convert inhibitory cues into immune activating signals. Problem Statement ➢ Autoimmune, inflammatory diseases & hematological malignancies arise from dysregulated T, B and myeloid cell function across secondary and tertiary immune sites. ➢ Current therapies offer broad immune suppression or narrowly target specific cells, frequently falling short of effective immune control. Proposed Solution(s) ✓ Multiplex targeting of lineage and/or activation markers enables selective elimination of pathogenic cells whilst minimizing broad immune suppression and its associated risks. ✓ Deploy multiplex targeting to apply simultaneous immune pressure via distinct mechanisms of action. ✓ Navigate immune suppressive niches and convert inhibitory cues into immune activating signals. Overcoming Multiple Challenges Across Diverse Tumors Indications Broad Elimination of Pathological Immune Cell Subsets & Compartments Engineering a Portfolio of Attributes to Unlock Multi-Disease Therapy Potential Integrating modular attribute cell systems to operate & synergize with the patients’ immune system Engineered Attribute System(s): ✓ Single and/or multi-CAR systems targeting MICA/B, B7-H3 & others ✓ High affinity non cleavable CD16 (hnCD16) ✓ TGFβ signal redirect receptor (TGFβ SRR) ✓ Synthetic CXCR2 & endogenous trafficking receptors ✓ Allo-Defense Receptor (ADR) & CD58 KO Synapse Engineering ✓ T Cell Enhancers Engineered Attribute System(s): ✓ Single and/or multi-CAR systems targeting CD19, BCMA & CD38 ✓ High affinity non cleavable CD16 (hnCD16) & CD3 Fusion Receptor ✓ TGFβ signal redirect receptor (TGFβ SRR) ✓ Synthetic CXCR2 & endogenous trafficking receptors ✓ Allo-Defense Receptor (ADR) & CD58 KO Synapse Engineering ✓ T Cell Enhancers
Page 27
- 27 - Sword & ShieldTM Technology Shields from Rejection & Drives Persistence Best-in-class allo-immune evasion system to enhance persistence & eliminate the need for lympho-conditioning 1. Li W et al. Front Immunol. 2022 Dec 2;13:1052717. 2. Hu, X., et al. Nat Biotechnol 42, 413–423 (2024). Strategy Combination with Intense CCT HLA-I & HLA-II Knockout HLA-I & HLA-II Knockout + HLA-E1 HLA-I & HLA-II Knockout + CD472,3 Sword & ShieldTM ADR4 + CD58 Knockout5 Avoid host CD8 T cells + + + + +++ Avoid host CD4 T cells + + + + +++ Avoid host NK cells + - +/- +/- +++ Avoid host Treg suppression + - - - +++ Induce proliferation + - - - +++ Lymphodepletion + - - - +++ Avoid toxicity associated immunosuppression x ✓ ✓ ✓ ✓ 3. Hu X, et al. Nat Commun. 2023 Apr 10;14(1). 4. Mo F et al, Nat Biotechnol. 2021 Jan; 39(1):56-63. 5. Hamer Q et al. Cell Stem Cell. 2024 Sept 5;31(9):1376-1386.e8.
Page 28
- 28 - • MICA/B CAR: An innovative CAR targeting strategy that uniquely distinguishes tumors from healthy tissue • hnCD16: Enables ADCC when combined with therapeutic monoclonal antibodies to complement CAR specificity to provide additional antigen / target cell coverage • Sword & ShieldTM (ADR/CD58 null): An Allo-Defense Receptor that targets activated allo-reactive T-cells; CD58 null to impede allo-reactive T cell recognition & binding • T Cell Enhancer(s): Optimized regulation of cell persistence & potency • Enhanced biodistribution & microenvironment performance: Engineered chemokine receptor surface profile to augment tissue trafficking; enhanced performance in inhibitory microenvironments via TGFβ signal redirection receptor (SRR) • TCR Null: Complete bi-allelic disruption of TRAC ablates TCR expression and eliminates the possibility of GvHD • CD38 Null: Potential to enhance metabolic cell fitness and allow combination with CD38 targeting mAbs Multi-antigen targeting via MICA/B CAR and hnCD16, with ADR technology designed to reduce/eliminate need for conditioning chemotherapy True Off-the-Shelf Next Generation Multi-Antigen Targeting CAR T Cell Drug Product Product Candidate Engineered Attribute Systems FT836: Off-the-Shelf Anti-MICA/B CAR T Cell Product Candidate Next-gen ADR-armed CAR T cell targets stress ligands MICA/B to eliminate a broad spectrum of tumors
Page 29
- 29 - Targeting MICA/B Overcomes Tumor Evasion & Unlocks Pan-Tumor Potential Stress-ligand recognition of diseased cell states permits indication-agnostic therapy MICA/B shedding is a common immune evasion mechanism utilized by cancer3,4 1. Ferrari de Andrade, L. Science. 2018 Mar 30;359(6383):1537-1542. 2. Goulding J et al. Cell Med. 2023 Jul 14;4(7):457-477. 3. Lakes, N. et al Cell Med. 2023 Jul 14;4(7):398-400 Novel recognition of MICA/B α3 domain unlocks pan-tumor recognition1,2 Variable α1/2 domain Conserved α3 domain MICA/B NKG2D 3MICA/B mAb 3MICA/B CAR NKG2D MICA/B is widely expressed cross multiple cancer indications5 4. Goulding J et al. J Cancer Biol. 2023;4(2):49-53. 5. Dhar P et al. Curr Opin Immunol. 2018 Apr;51:55-61
Page 30
- 30 - Phase 1 FT836-101 Study in Pan Solid Tumor Open to Enrollment1 Evaluation of FT836 with/without monoclonal antibody combination with optional tumor priming therapy 1. https://clinicaltrials.gov/study/NCT07216105 (ClinicalTrials.gov). CA A C A A A A A 6 A 6 6 C 6 C 6 C 6 6 6 5 5 (C 5 6 C C C C FT836 Clinical Study Schema FT836: A Highly-Differentiated Therapeutic Approach Clinical Trial NCT072161051 ➢ Novel cancer antigen targeting system that uniquely distinguishes tumor from healthy tissue. ➢ Combining with HER2 and EGFR targeting mAbs augments activity & allows heterogenous tumor targeting to minimize tumor escape. ➢ Contains multiplex engineered cellular systems to enhance persistence and cancer killing capability; traffic to and operate within suppressive tumor environments; whilst simultaneously avoiding T cell exhaustion. ➢ Requires no patient apheresis and no lympho- conditioning chemotherapy. ➢ Delivered with a shortened hospitalization requirement and can be re-dosed in patients who have shown clinical benefit ➢ Protocol authorized solid tumors include; • Breast (BC); Colorectal (CRC); Ovarian (OVC); Head & Neck (HNSCC); Endometrial (EC); Gastric (GEJ) & Lung (NSCLC). Tumor Priming 56 FT836 retreatment is available in patients who have shown clinical benefit Safety & activity assessment up to 2 years
Page 31
- 31 - Patient Case Study1: Heavily pretreated 45/M with stage IV refractory metastatic colorectal carcinoma (CRC) with prior cetuximab treatment failure, was dosed with 1 cycle of FT836 in combination with cetuximab without receiving any lympho pre-conditioning chemotherapy ✓ No CRS, ICANS or DLTs observed ✓ Confirmed MICA/B and EGFR expression in tumor bearing lymph node pre-FT836 treatment ✓ FT836 drug product detected in blood post FT836 treatment ✓ Demonstrated decrease in CEA and LDH correlated with total mass reduction in all target lesions by ~20% by week 7 FT836: Next Generation Pan Tumor CAR T-cell Therapy Early evidence of potential anti-tumor activity Early Evidence of FT836 Anti-Tumor Activity BL D29 0 200 400 600 CEA (ng/mL) BL D29 0 200 400 600 800 LDH (U/L) BL D46 10 15 20 25 Tumor Lesions (mm) Lymph nodes Pulmonary nodules Patient Clinical Measurements Live FT836 Cells Detected in Peripheral Blood H&E EGFR MICA/B CD8 Patient Tumor Antigen Expression at Screen 1. Interim data cut-off 23rd January CEA = Carcinoembryonic antigen; LDH = Lactate dehydrogenase 0 10⁴ 10⁵ 10⁶ FT836 Post Treatment 0 10⁴ 10⁵ 10⁶ 0 10³ -10³ 10⁴ 10⁵ FT836 Pre Treatment Peripheral Blood FT836
Page 32
- 32 - Clinical Advancement Novel CAR targeting system Next Gen CAR T-Cell FT836 Product Candidate Executive Summary & Next Steps Strategic highlights and value drivers ➢ MICA/B is a broadly expressed stress antigen relevant to multiple tumor types and other diseases ➢ Targeting MICA/B α3 domain uniquely overcomes tumor evasion mechanisms of escape ➢ Multiple functional edits to enhance potency, persistence, trafficking and multi-antigen targeting ➢ Sword and ShieldTM technology to provide allo-protection ➢ 3 patients enrolled in FT836-101 Ph1 pan-solid-tumor trial ➢ Multiple myeloma IIT initiated, with FPI anticipated in Q1 2026 Pan Solid Tumor Ageing/ Fibrosis Multiple Myeloma (Heme Onc) Infectious Disease Possible FT836 Disease Indications
Page 33
- 33 - Product Candidate Engineered Attribute SystemsTrue Off-the-Shelf Next Generation Multi-Antigen Targeting CAR T Cell Drug Product Multi-antigen targeting via CD19 CAR, CD38 CAR, hnCD16 and CD3FR, with ADR technology designed to reduce/eliminate need for conditioning chemotherapy FT839: Off-the-Shelf Anti-CD19 & Anti-CD38 CAR T Cell Product Candidate Next-gen ADR-armed CAR T cell targets select immune cell subsets to unlock multi-disease therapy potential • 1XX CD19 CAR: Novel CAR with CD28 costimulatory and modified CD3ζ signaling domains for optimal safety and activity • CD38 CAR: A unique targeting strategy to eliminate activated and/or senescent immune cell subsets • Sword & ShieldTM (ADR/CD58 null): An Allo-Defense Receptor that targets activated allo-reactive T-cells; CD58 null to impede allo-reactive T cell recognition & binding • hnCD16: Enables ADCC when combined with therapeutic monoclonal antibodies to complement CAR specificity to provide additional antigen / target cell coverage • CD3 Fusion Receptor: Provides additional antigen / target cell subset targeting in combination with T cell engagers • T Cell Enhancer(s): Optimized regulation of cell persistence & potency • Enhanced biodistribution & microenvironment performance: Engineered chemokine receptor surface profile to augment tissue trafficking; enhanced performance in inhibitory microenvironments via TGFβ signal redirection receptor (SRR) • TCR Null: Complete bi-allelic disruption of TRAC ablates TCR expression and eliminates the possibility of GvHD • CD38 Null: Potential to enhance metabolic cell fitness and allow combination with CD38 targeting mAbs
Page 34
- 34 - Clinical Advancement Novel multi- antigen targeting system Next Gen CAR T-Cell ➢ CD19 + CD38 comprehensively targets B-cell, plasma cell lineage and activated immune cells, including aberrant T cell, NK cell and myeloid cells ➢ Ability to synergize with mAbs and T cell engagers utilizing built in hnCD16 and CD3 fusion receptor ➢ Multiple functional edits that enhance potency, persistence, trafficking, and multi-antigen targeting ➢ Sword and ShieldTM technology to provide allo-protection ➢ Anticipated IND filing 2H 2026 ➢ Future pan autoimmune and hematologic malignancy evaluation leading to broad indication expansion FT839 Product Candidate Executive Summary & Next Steps Strategic highlights and value drivers Possible FT839 Disease Indications Nervous System Autoimmune Diseases (AID) Complex Multi Organ/Tissue AID Hematological AID Connective Tissue AID Skin AID Pan Heme Onc
Page 35
- 35 - Making Cell Therapy Accessible to All NEXT GENERATION OFF-THE-SHELF CAR NK CELLS
Page 36
- 36 - Multi-Antigen Targeting CAR NK Cell Armed with ADR to Avoid the Need for Conditioning Chemotherapy FT522: Off-the-shelf anti-CD19 CAR NK cell product candidate • 1XX CAR19: Novel CAR with CD28 costimulatory and modified CD3z signaling domains for optimal safety and activity • ADR: 4-1BB CAR targeting allo-reactive T-cells • IL15R Fusion: Cell potentiation without cytokine support • CD38 Null: Potential to enhance metabolic cell fitness and allow combination with CD38 targeting mAbs • hnCD16: Enables ADCC when combined with therapeutic monoclonal antibodies to complement CAR to overcome tumor heterogeneity through multi-antigen targeting Multi antigen targeting via CD19 CAR and hnCD16, with ADR technology designed to reduce/eliminate need for conditioning chemotherapy True Off-the-Shelf Next Gen CAR NK cell Drug Product ADR armed NK Cells Uniquely Able to Proliferate and Persist
Page 37
- 37 - FT522 Phase 1 Basket Study in Autoimmunity IND cleared: Clinical development strategic planning ongoing Basket Trial Design AAV = Antineutrophilic cytoplasmic antibody-associated vasculitis IIM = Idiopathic inflammatory myositis SLE = Systemic lupus erythematosus SSc = Systemic sclerosis Regimen A (RA): treatment of participants with FT522 as add -on to Rituximab induction regimen Regimen B (RB): treatment of participants, who are currently on background maintenance therapy and have been at a stable dose for at least 3 months, with FT522 and Rituximab • Depending on participant population, background maintenance therapies include MMF, AZA, LEF, MTX, and avacopan All cohorts and regimens cleared to open in parallel and escalate independently No Conditioning; Multiple Indications; Induction and Maintenance Regimens
Page 38
- 38 - February 2026 © 2026 Fate Therapeutics. All rights reserved. www.fatetherapeutics.com TRANSFORMING THE LIVES OF PATIENTS WITH AUTOIMMUNE DISEASES AND CANCER Making Cell Therapies Accessible to All TM