Announcement • May 11
Fate Therapeutics Showcases Ft819, Ft839, and Ft836 Clinical and Preclinical Activity in Autoimmune Diseases and Cancer
Fate Therapeutics, Inc. presented data featuring its off-the-shelf CAR T-cell programs FT819, FT839, and FT836 at the American Society of Gene and Cell Therapy (ASGCT) Annual Meeting to be held in Boston, MA, May 11–15, 2026. FT819 is the Company’s off-the-shelf, CD19-targeted, iPSC-derived CAR T-cell program, which is currently being investigated in a Phase 1 study for patients with moderate-to-severe systemic lupus erythematosus (SLE) including lupus nephritis and extrarenal lupus (NCT06308978). Data presented shows that in Regimen B of the Phase 1 study with a data cutoff of April 9, 2026, a single dose of FT819 without conditioning chemotherapy and in the presence of background therapy demonstrated meaningful clinical responses at dose level 1 in patients with active SLE, with 3 of 3 patients achieving systemic lupus erythematosus responder index (SRI-4) and 2 of 3 patients achieving lupus low disease activity state (LLDAS). The positive clinical outcomes were supported mechanistically by the observation that B cells in the periphery as well as in secondary lymphoid tissue (nasopharyngeal swabs) were significantly depleted. Notably, depletion (79% on average) of major B cell clones (as defined by B cell receptor sequencing) were observed, with the depletion lasting up to 12 months following treatment. Collectively, preliminary data demonstrate that treatment with FT819 without conditioning chemotherapy and in the presence of background therapy can drive comprehensive changes in B cell repertoire that are associated with clinical benefit, alongside a favorable safety profile. Patient treatment at the higher dose of 900 million cells (dose level 2) has been initiated. FT839 is a next generation, off-the-shelf dual CAR T-cell therapy targeting CD19 and CD38 to deplete multiple pathogenic immune cell populations that drive hematological and complex autoimmune diseases, including rheumatoid arthritis (RA), type I diabetes, and multiple sclerosis. Preclinical data to be presented show broad, selective depletion of pathogenic immune cell subtypes in RA and SLE disease samples, including over 99% of B cells, plasmablasts, and plasma cells and more than 90% of activated CD4+ and CD8+ T cells, while sparing non-activated T cells, which comprise most of the endogenous T-cell population. The presentation will also demonstrate that targeting capabilities of FT839 are further enhanced through synergistic pairing with standard-of-care (SOC) therapeutic monoclonal antibodies (mAb; e.g. rituximab) or clinically approved T-cell engagers (e.g. epcoritamab), to activate either the engineered Fc receptor, hnCD16, or the novel CD3 Fusion receptor, respectively, improving cytolytic activity by ~3.5-6x on CAR antigen negative targets. With Sword and ShieldTM technology, FT839 persistence is enhanced ~60x compared to CAR T cells lacking Sword and ShieldTM engineering in HLA-mismatched allogeneic settings, while the generation and expansion of product-specific immune cell responses are severely blunted (~1/900), thereby reducing the need for intensive conditioning chemotherapy. Importantly, non-product specific T cells were spared. FT839 is produced through a scalable and reproducible process that enables on-demand availability of a homogenous CAR T-cell therapy, overcoming key accessibility and safety limitations of autologous CAR T-cell therapies, selectively depleting disease-driving B lineage and activated T cells for the treatment of patients with complex autoimmune and hematological diseases. FT836 is a next generation, off-the-shelf CAR T-cell therapy that targets the novel and inducible pan-tumor antigens MICA/B. FT836 is engineered to enable rational combination with SOC therapeutics such as mAbs, chemotherapy, radiotherapy, and immune modulators across both hematological malignancies and solid tumor settings. Integrated engineered elements, including Sword and Shield™ technology, support broader and more universal application without the requirements for conditioning chemotherapy. Preclinical data to be presented demonstrate potent and durable control of multiple solid and liquid xenograft tumor models of varying origin and antigen expression by FT836 activity as a monotherapy or in combination with mAbs, such as trastuzumab, cetuximab, or daratumumab (up to 100% tumor control), underscoring its broad and universal therapeutic potential in cancer. FT836 also features Sword and Shield™ technology, enabling improved persistence (~20-30x) and selective containment of product-specific immune cell responses (~5x product specific and ~1x nonspecific), thereby enabling clinical strategies that are not reliant on conditioning chemotherapy. FT836 is shown to be rationally combined with established SOC therapeutics, including chemotherapy or radiotherapy, that complement its unique mechanisms of action and engineering profile to specifically upregulate both MICA/B (~2-3x) and the CXCR2 ligand CXCL8 (3-4X) expression, enhancing both the cytolytic activity (~5x) and specific trafficking (~2-3x) of FT836. In addition, FT836 is compatible with multiple myeloma standard of care therapeutics such as Bortezomib and Lenalidomide which further enhances the cytolytic activity of FT836 (1.25x + lenalidomide). Collectively, these data demonstrate the broad utility of FT836 and its ability to rationally combine with SOC therapeutic agents without the need for conditioning chemotherapy, supporting expanded patient access across both hematological and solid tumor indications. FT836 is currently being evaluated clinically in advanced solid tumor patients in combination with the trastuzumab and cetuximab (NCT07216105) and in relapsed and/or refractory multiple myeloma in combination with daratumumab (NCT07221032). FT819 is an off-the-shelf CD19-targeting chimeric antigen receptor (CAR) T-cell product engineered to improve safety and efficacy. Analogous to master cell banks used to mass produce biopharmaceutical drug products such as monoclonal antibodies, a precisely engineered clonal master induced pluripotent stem cell (iPSC) bank serves as the starting cell source to manufacture FT819, overcoming numerous limitations associated with patient- and donor-sourced CAR T-cell therapies. FT819 is well-defined and uniform in composition, produced at a low cost of goods, and can be stored in inventory for off-the-shelf, on-demand availability to enable access for a broad patient population.
