Biomea Fusion Presents at the 2022 ASH Annual Meeting Preclinical Data on BMF-500 Supporting its Potential as the Most Potent and Selective FLT3 Inhibitor to Date
BMF-500, an investigational third generation covalent FLT3 inhibitor, demonstrated preclinically:
- Picomolar affinity to activating FLT3 mutations including FLT3-ITD and various tyrosine kinase domain (TKD) mutations
- Multi-fold higher potency and increased cytotoxicity than commercially available non-covalent FLT3 inhibitor gilteritinib
- Complete tumor regression in mouse models of FLT3-ITD acute myeloid leukemia (AML) and maintenance of effect without continued exposure
Biomea Fusion remains on track to file an IND for BMF-500 in the first half of 2023
Excerpt from the Press Release:
REDWOOD CITY, Calif., Dec. 12, 2022 (GLOBE NEWSWIRE) — Biomea Fusion, Inc. (Nasdaq: BMEA), a clinical-stage biopharmaceutical company dedicated to discovering and developing novel covalent small molecules to treat and improve the lives of patients with genetically defined cancers and metabolic diseases, presented preclinical data today for BMF-500, an investigational covalent FLT3 inhibitor, at the 64th American Society of Hematology (ASH) Annual Meeting. The preclinical poster can be viewed at Biomea’s website at https://biomeafusion.com/publications.
BMF-500, a novel, orally bioavailable, highly potent and selective covalent small molecule inhibitor of FLT3, was discovered and developed in-house at Biomea using the company’s proprietary FUSION™ System and designed to have a therapeutic profile to allow for combinations with standard of care and/or novel targeted agents like BMF-219, Biomea’s investigational covalent menin inhibitor. The company is on track to submit an investigational new drug (IND) application for BMF-500 in the first half of 2023 and, subject to successful IND clearance, plans to initiate clinical trials evaluating BMF-500 as a single agent and in novel combinations shortly thereafter.
“The majority of late-stage and approved FLT3 inhibitors fall short of providing sufficient and sustained inhibition of FLT3 signaling required for maximal benefit.
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