Clinical Trial

Disease: Relapsed or Refractory Acute Myeloid Leukaemia, AML, (NCT04614636)

Disease info:

Leukaemia is cancer of the white blood cells which are responsible for fighting infection. In leukaemia, the bone marrow produces abnormal levels of white blood cells. Acute myeloid leukaemia (AML) starts in the bone marrow but often quickly spreads into the bloodstream. AML sometimes spreads to other parts of the body such as the lymph nodes, liver, central nervous system and testicles. 

Commonly, AML develops from cells other than lymphocytes that would normally develop into white blood cells. The World Health Organization (WHO) divides AML into several subtypes based off genetic association. AML is also known as acute myelocytic leukaemia, acute myelogenous leukaemia, acute granulocytic leukaemia, and acute non-lymphocytic leukaemia.

Multiple myeloma is a cancer that develops in the bone marrow, the spongy tissue found in the centre of most bones. Multiple myeloma is characterised by abnormalities in plasma cells, a type of white blood cell. In myeloma, these abnormal cells multiply uncontrollably, increasing from about one percent of cells in the bone marrow to the majority of bone marrow cells. The abnormal cells form tumours within the bone, causing bone pain and an increased risk of fractures.

Relapsed refers to when a patient had active treatment that their disease responded to, went off treatment and then the disease came back. Refractory is a disease that is progressing despite active treatment.





The American Cancer Society estimates approximately 20,380 cases of AML will be diagnosed in the U.S. in 2023. Multiple myeloma occurs in approximately 4 per 100,000 people per year.
Official title:
A Phase I, Open-Label, Multicenter Study of FT538 as Monotherapy in Relapsed/Refractory Acute Myelogenous Leukemia and in Combination With Monoclonal Antibodies in Relapsed/Refractory Multiple Myeloma

Study Director: John Byon, MD, Fate Therapeutics, Inc


United States, Colorado

Colorado Blood Cancer Institute, Denver, Colorado, United States, 80218


United States, Minnesota

University of Minnesota Masonic Cancer Center, Minneapolis, Minnesota, United States, 55455


United States, Missouri

Washington University, Saint Louis, Missouri, United States, 63110


United States, New York

Memorial Sloan Kettering Cancer Center, New York, New York, United States, 10065


United States, Tennessee

Sarah Cannon Research Institute at Tennessee Oncology, Nashville, Tennessee, United States, 37203


United States, Texas

St. David's South Austin Medical Center, Austin, Texas, United States, 78704

MD Anderson Cancer Center, Houston, Texas, United States, 77030

Texas Transplant Institute, San Antonio, Texas, United States, 78229

Study start:
Nov. 4, 2020
105 participants
Gene editing method:
Type of edit:
Gene knock-out
Cluster of differentiation 38 (CD38)
Delivery method:
- Ex-vivo
hnCD16 to universally engage monoclonal Antibodies (mAbs) IL15-RF to enable natural killer (NK) cell persistence without the need for exogenous cytokine support CD38 knock-out for resistance to mAb-mediation
IND Enabling Pre-clinical
Phase I Safety
Phase II Safety and Dosing
Phase III Safety and Efficacy

Status: Active not recruiting


The first-in-human, multi-center, dose-escalation Phase 1 clinical trial of FT538 is designed to determine the maximum tolerated dose (MTD) of three once-weekly doses of FT538 in up to 105 adult patients across four dose cohorts (100M cells per dose; 300M cells per dose; 900M cells per dose; and 1.5B cells per dose). The study will assess two treatment regimens: Regimen A as a monotherapy in patients with relapsed / refractory AML; and Regimen B in combination with daratumumab, an FDA-approved anti-CD38 monoclonal antibody, in patients with relapsed / refractory multiple myeloma who have failed at least two lines of therapy.

FT538 is an off-the-shelf adoptive NK cell immunotherapy product candidate designed for enhanced cellular persistence and ADCC while avoiding anti-CD38 mAb-induced fratricide. It is derived from induced pluripotent stem cells (iPSC) that are engineered to lack CD38 expression. Fate Therapeutics has previously shown that this approach prevents daratumumab-induced fratricide among iPSC-derived NK cells, resulting in enhanced long-term daratumumab-mediated antibody-dependent cellular cytotoxicity (ADCC). FT538 is engineered to express an IL-15 receptor alpha fusion protein (IL-15RF; IL-15 tethered to IL-15 receptor α) to enhance persistence and a high-affinity non-cleavable CD16 (hnCD16, FcRγIII) to increase ADCC.

Last updated: Apr. 20, 2024
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