MOMA Therapeutics Advances in Precision Medicine with New PARP1 Inhibitor and Clinical Updates
MOMA Therapeutics, a clinical-stage biopharmaceutical company, has in-licensed a next-generation selective PARP1 inhibitor, now known as MOMA-989, with plans for its development as a single agent and in combination with MOMA-313. The company also provided an update on the clinical progress of MOMA-313, a highly potent and selective polymerase theta (Polθ) inhibitor, and outlined the clinical path for MOMA-341, a highly potent and selective Werner helicase inhibitor with a novel chemical scaffold.
MOMA-989 is an oral, highly potent, brain-penetrant development candidate with a potentially best-in-class compound profile. Selective targeting of PARP1 has shown significant potential for patients with tumors displaying homologous recombination deficiency (HRD). MOMA plans to file an IND with the U.S. FDA by the end of 2025 and anticipates early single agent efficacy data in the second half of 2026.
MOMA-313 is currently in a Phase 1a dose escalation study, evaluating its potential as monotherapy and in combination with olaparib, an approved, non-selective PARP inhibitor. An initial readout of olaparib combination efficacy data is anticipated in mid-2026, with development of the proprietary combination with MOMA-989 to initiate in late 2026.
MOMA-341 is on track for an IND filing during the first quarter of 2025. It is a highly differentiated oral, potent and selective, covalent Werner helicase inhibitor with a novel chemical scaffold. The company plans to assess its potential as a treatment for patients with cancers demonstrating microsatellite instability (MSI-H), with an initial readout of early single agent efficacy data anticipated in mid-2026.
MOMA Therapeutics is dedicated to targeting highly dynamic proteins that underlie human disease via an oral, small molecule approach, utilizing its proprietary KNOMATIC™ platform. The company has existing discovery partnerships with Roche and Bayer, as well as a wholly owned pipeline.