Hematology · 2 h ago
Relcobatinib shows selective BCR::ABL1 activity in preclinical CML models
A study in *Leukemia* reports preclinical testing of relcobatinib (ELVN-001), an investigational ATP-competitive BCR::ABL1 inhibitor. The compound showed activity against several resistant mutations in laboratory assays and inhibited tumor growth in a mouse xenograft model; combination with asciminib produced further regression.
- Selective BCR::ABL1 inhibition reported in laboratory assays
- Activity observed against T315I and other resistance mutations
- Combination with asciminib improved tumor regression in mice
- No human efficacy or safety results reported
Relcobatinib (ELVN-001) is an investigational active-site tyrosine kinase inhibitor being developed for chronic myeloid leukemia (CML). Researchers evaluated its selectivity and activity in biochemical and cell-based assays, including models expressing native BCR::ABL1 and clinically relevant resistance mutations. They also tested the drug in a human CML xenograft model in mice, with eight animals randomized to each treatment group.
The authors report that relcobatinib was more selective than other active-site inhibitors and retained in-vitro activity against multiple BCR::ABL1 mutants, including T315I. In the mouse model, monotherapy produced marked antitumor activity; adding asciminib led to further, durable tumor regression. The article provides no human efficacy or safety results.
These findings support continued evaluation of relcobatinib, but do not establish clinical benefit or improved tolerability in patients. Results are preclinical, and the authors’ claims about potential advantages require confirmation in clinical studies. The article notes that relcobatinib is being evaluated in CML trials (NCT05304377 and NCT06787144).
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Leukemia: Relcobatinib, a highly selective ATP-competitive ABL1 tyrosine kinase inhibitor for the treatment of chronic myeloid leukemia ↗This is an automated AI-condensed summary that has not yet been reviewed by an editor. Always consult the full item at the original source.