Fate Therapeutics focuses on developing innovative cell therapies for patients with cancer and autoimmune disorders, leveraging its proprietary induced pluripotent stem cell (iPSC) platform. This technology allows the company to generate a diverse range of immune cells that can be engineered to target specific diseases. By utilizing iPSCs, Fate Therapeutics can create off-the-shelf cell products that are designed to enhance the immune response against tumors and other pathological conditions, providing a potentially transformative approach to treatment.

The company’s pipeline includes several product candidates, such as FT522, FT819, and FT825, which are designed to harness the power of engineered immune cells. These candidates are in various stages of development, aiming to address unmet medical needs in oncology and autoimmune diseases. Fate Therapeutics emphasizes the scalability and reproducibility of its manufacturing processes, which are critical for the successful commercialization of its cell therapies, ensuring that they can be produced efficiently and consistently for patient use.

United States

Fate Therapeutics (Nasdaq: FATE) is a clinical-stage biopharmaceutical company dedicated to the development of next-generation cellular immunotherapies for cancer and immune disorders.

Cancer

Immune System Diseases

Fate Therapeutics

Multiple myeloma

We are developing FT576, an investigational, universal, off-the-shelf &nbsp;NK cell cancer immunotherapy derived from a clonal master iPSC line. &nbsp;FT576 incorporates four functional modifications: a proprietary CAR that &nbsp;targets BCMA; a novel high-affinity 158V, non-cleavable CD16 (hnCD16) &nbsp;Fc receptor, which has been modified to augment ADCC; an IL-15 receptor &nbsp;fusion (IL-15RF) that promotes enhanced NK cell activity; and the &nbsp;elimination of CD38 expression to mitigate the potential for NK cell &nbsp;fratricide. Together, these features are intended to enable &nbsp;multi-antigen targeting of myeloma cells, augment ADCC, enhance cell &nbsp;persistence and prevent anti-CD38 monoclonal antibody-induced &nbsp;fratricide.
<a href="https://ir.fatetherapeutics.com/news-releases/news-release-details/fate-therapeutics-reports-positive-interim-data-its-phase-1">Source</a>

FT576 (iNK hnCD16) + daratumumab

B-cell lymphoma

Chronic lymphocytic leukemia

Solid tumor/s

We are developing FT819, an off-the-shelf CAR T-cell cancer &nbsp;immunotherapy derived from a clonal engineered master iPSC line with a &nbsp;novel 1XX CAR targeting CD19 inserted into the T-cell receptor alpha &nbsp;constant (TRAC) locus and edited for elimination of T-cell receptor &nbsp;(TCR) expression. At the 2019 ASH Annual Meeting, we presented new in &nbsp;vivo preclinical data demonstrating that FT819 exhibits durable tumor &nbsp;control and extended survival. In a stringent xenograft model of &nbsp;disseminated lymphoblastic leukemia, FT819 demonstrated enhanced tumor &nbsp;clearance and control of leukemia as compared to primary CAR19 T cells. &nbsp;At Day 35 following administration, a bone marrow assessment showed that &nbsp;FT819 persisted and continued to demonstrate tumor clearance, whereas &nbsp;primary CAR T cells, while persisting, were not able to control tumor &nbsp;growth.

FT819 (CAR-19, TCR-KO)

FT522 (iNK) iPSC-derived NK Cell is the Company’s first product candidate to incorporate its proprietary alloimmune defense receptor (ADR) technology, which has been shown in preclinical studies to increase NK cell potency, enhance functional persistence, and confer resistance to host immune cell alloreactivity.

FT522 (CAR NK Cell Program)

Systemic lupus erythematosus

FT819 (CAR-19, TCR-KO) 

FT825 / ONO-8250 incorporates seven novel synthetic controls of cell function including a CXCR2 receptor to promote cell trafficking, a chimeric TGFβ receptor to redirect immunosuppressive signals in the tumor microenvironment, and a high-affinity, non-cleavable CD16a receptor to enable antibody-dependent cellular cytotoxicity. Preclinical data of FT825 / ONO-8250 presented at the 2023 Society for Immunotherapy of Cancer Annual Meeting demonstrated that the profile of the novel HER2-targeted antigen binding domain is unique and differentiated from that of trastuzumab, exhibiting similar potency with greater specificity for cancer cells expressing HER2.

FT825/ONO-8250

FT538 is the fourth off-the-shelf, iPSC-derived NK cell product &nbsp;candidate from the Company’s proprietary iPSC product platform cleared &nbsp;for clinical investigation by the FDA. The Company has initiated &nbsp;clinical manufacture of FT538 at its GMP facility in San Diego, CA.
FT538 is derived from a clonal master iPSC line engineered with three &nbsp;functional components to enhance innate immunity: a novel hnCD16 Fc &nbsp;receptor that enhances ADCC; an IL-15RF that augments NK cell activity; &nbsp;and the deletion of the CD38 gene (CD38KO), which promotes persistence &nbsp;under oxidative stress and prevents NK cell fratricide in combination &nbsp;with CD38-targeted monoclonal antibody therapy.
<a href="https://ir.fatetherapeutics.com/news-releases/news-release-details/fate-therapeutics-reports-third-quarter-2020-financial-results">Source</a>

FT538 (hnCD16 + IL-15RF + CD38KO)

FT516 is an investigational, universal, off-the-shelf natural killer &nbsp;(NK) cell cancer immunotherapy derived from a clonal master induced &nbsp;pluripotent stem cell (iPSC) line engineered to express a novel &nbsp;high-affinity 158V, non-cleavable CD16 (hnCD16) Fc receptor, which has &nbsp;been modified to prevent its down-regulation and to enhance its binding &nbsp;to tumor-targeting antibodies. CD16 mediates antibody-dependent cellular &nbsp;cytotoxicity (ADCC), a potent anti-tumor mechanism by which NK cells &nbsp;recognize, bind and kill antibody-coated cancer cells. ADCC is dependent &nbsp;on NK cells maintaining stable and effective expression of CD16, which &nbsp;has been shown to undergo considerable down-regulation in cancer &nbsp;patients. In addition, CD16 occurs in two variants, 158V or 158F, that &nbsp;elicit high or low binding affinity, respectively, to the Fc domain of &nbsp;IgG1 antibodies. Scientists from the Company have shown in a &nbsp;peer-reviewed publication (Blood. 2020;135(6):399-410) that &nbsp;hnCD16 iPSC-derived NK cells, compared to peripheral blood NK cells, &nbsp;elicit a more durable anti-tumor response and extend survival in &nbsp;combination with anti-CD20 monoclonal antibodies in an in vivo xenograft mouse model of human lymphoma.
<a href="https://ir.fatetherapeutics.com/news-releases/news-release-details/fate-therapeutics-reports-positive-interim-data-its-phase-1">Source</a>

FT516 (NK cells - engineered CD16 FcR) + rituximab

Acute graft-versus host disease

We are developing ProTmune as an investigational programmed cellular immunotherapy for use as a next-generation allogeneic HSCT cell graft. ProTmune is produced by modulating donor-sourced mPB ex vivo with two small molecules to enhance the biological properties and therapeutic function of the graft’s cells. The programmed mPB graft is administered to a patient as a one-time intravenous therapy. Based on preclinical data, we believe ProTmune has the potential to suppress the GvHD response and maintain the anti-tumor, or graft-versus-leukemia (GvL), activity of donor T cells. There are currently no FDA-approved therapies for the prevention of GvHD in patients undergoing allogeneic HSCT, giving rise to a significant unmet medical need.
<a href="https://fatetherapeutics.com/pipeline/immuno-regulation-candidates/protmune/">Source</a>

ProTmune (CD34+)

Diffuse large B cell lymphoma

FT516 (NK cells - engineered CD16 FcR)

B-cell malignancies

FT596 is an investigational, universal, off-the-shelf natural killer &nbsp;(NK) cell cancer immunotherapy derived from a clonal master induced &nbsp;pluripotent stem cell (iPSC) line engineered with three anti-tumor &nbsp;functional modalities: a proprietary chimeric antigen receptor (CAR) &nbsp;optimized for NK cell biology that targets B-cell antigen CD19; a novel &nbsp;high-affinity 158V, non-cleavable CD16 (hnCD16) Fc receptor, which has &nbsp;been modified to prevent its down-regulation and to enhance its binding &nbsp;to tumor-targeting antibodies; and an IL-15 receptor fusion (IL-15RF) &nbsp;that augments NK cell activity. In preclinical studies of FT596, the &nbsp;Company has demonstrated that dual activation of the CAR19 and hnCD16 &nbsp;targeting receptors enhances cytotoxic activity, indicating that &nbsp;multi-antigen engagement may elicit a deeper and more durable response.
<a href="https://ir.fatetherapeutics.com/news-releases/news-release-details/fate-therapeutics-presents-patient-case-study-demonstrating">Source</a>

FT596 (CAR19, hnCD16, IL-15RF) + rituximab

FT596 (CAR19, hnCD16, IL-15RF) + R-CHOP

One potential strategy to overcome resistance is through the administration of allogeneic NK cells, which have the inherent capability to recognize and directly kill cells with MHC class I down-regulation. The mechanism of killing is through the release of perforins and granzymes, which can lyse tumor cells exposing large amounts of tumor antigens, and the secretion of a number of cytokines and chemokines, both of which can activate and facilitate an adaptive immune response. In addition to direct cytotoxicity, NK cells can also secrete proinflammatory cytokines, which can induce tumor-resident T cells to re-engage and elicit an anti-tumor response, and chemotactic cytokines, which can recruit T cells to the tumor site.
We are developing FT500, an investigational, universal, off-the-shelf NK cell cancer immunotherapy derived from a clonal master iPSC line. To our knowledge, FT500 is the first-ever iPSC-derived cell therapy cleared for clinical investigation in the United States.

Fate Therapeutics

Company Details