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DRUG:

FT536

i
Other names: FT536, iPSC-derived CAR MICA/B cancer immunotherapy , multiplexed engineered CAR-MICA/B NK cells
Associations
Trials
Company:
Fate Therap
Drug class:
MICA inhibitor, MICB inhibitor, NKG2D stimulant
Associations
Trials
1year
FT536 Monotherapy and in Combination With Monoclonal Antibodies in Advanced Solid Tumors (clinicaltrials.gov)
P1, N=5, Terminated, Fate Therapeutics | Trial completion date: Apr 2027 --> Aug 2023 | Active, not recruiting --> Terminated | Trial primary completion date: Jun 2024 --> Aug 2023; This study was terminated by the Sponsor.
Trial completion date • Trial termination • Trial primary completion date • Combination therapy • Metastases
|
EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • MET (MET proto-oncogene, receptor tyrosine kinase) • NRAS (Neuroblastoma RAS viral oncogene homolog)
|
PD-L1 expression • EGFR mutation • HER-2 expression • MET amplification • MET exon 14 mutation • KRAS wild-type • BRAF wild-type • NRAS wild-type
|
Keytruda (pembrolizumab) • Opdivo (nivolumab) • Herceptin (trastuzumab) • Erbitux (cetuximab) • Tecentriq (atezolizumab) • Bavencio (avelumab) • cyclophosphamide • Rybrevant (amivantamab-vmjw) • fludarabine IV • FT536
over1year
FT536 Monotherapy and in Combination With Monoclonal Antibodies in Advanced Solid Tumors (clinicaltrials.gov)
P1, N=5, Active, not recruiting, Fate Therapeutics | Recruiting --> Active, not recruiting | N=322 --> 5
Enrollment closed • Enrollment change • Combination therapy • Metastases
|
EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • MET (MET proto-oncogene, receptor tyrosine kinase) • NRAS (Neuroblastoma RAS viral oncogene homolog)
|
PD-L1 expression • EGFR mutation • HER-2 expression • MET amplification • MET exon 14 mutation • KRAS wild-type • BRAF wild-type • NRAS wild-type
|
Keytruda (pembrolizumab) • Opdivo (nivolumab) • Herceptin (trastuzumab) • Erbitux (cetuximab) • Tecentriq (atezolizumab) • Bavencio (avelumab) • cyclophosphamide • Rybrevant (amivantamab-vmjw) • fludarabine IV • FT536
over2years
New P1 trial • Combination therapy
|
EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • MET (MET proto-oncogene, receptor tyrosine kinase) • NRAS (Neuroblastoma RAS viral oncogene homolog)
|
PD-L1 expression • EGFR mutation • HER-2 expression • MET amplification • MET exon 14 mutation • KRAS wild-type • RAS wild-type • NRAS wild-type
|
Keytruda (pembrolizumab) • Opdivo (nivolumab) • Herceptin (trastuzumab) • Erbitux (cetuximab) • Tecentriq (atezolizumab) • Bavencio (avelumab) • cyclophosphamide • Rybrevant (amivantamab-vmjw) • fludarabine IV • FT536
over3years
[VIRTUAL] FT536: Preclinical development of a novel off-the-shelf CAR-MICA/B NK cell immunotherapy combined with radiation and antibody treatments as a first-of-kind pan-cancer targeting strategy (AACR 2021)
Furthermore, ADCC, induced in combination with cetuximab or trastuzumab, enhanced the potency of FT536 against various solid tumor lines (p <0.05). Ongoing work is focused on the development of in vivo models that combine FT536 with in situ tumor irradiation and mAbs in order to promote durable responses and the elimination of resistant and heterogenous cancer cells. These data demonstrate successful targeting of MICA/B positive tumors by FT536 can be augmented by mAb and radiation therapies as first-of-kind combinatorial strategies to broadly target escape-prone tumors.
Preclinical • IO biomarker • Pan tumor
|
EGFR (Epidermal growth factor receptor) • NKG2D (killer cell lectin like receptor K1)
|
Herceptin (trastuzumab) • Erbitux (cetuximab) • FT536