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ORIC® Pharmaceuticals Announces Preclinical Rinzimetostat (ORIC-944) Presentations at the 2026 American Association for Cancer Research (AACR) Annual Meeting
SOUTH SAN FRANCISCO, Calif. and SAN DIEGO, March 17, 2026 (GLOBE NEWSWIRE) -- ORIC Pharmaceuticals, Inc. (Nasdaq: ORIC), a clinical stage oncology company
About this update from Oric Pharmaceuticals, Inc.
[{"type":"text","content":"SOUTH SAN FRANCISCO, Calif. and SAN DIEGO, March 17, 2026 (GLOBE NEWSWIRE) -- ORIC Pharmaceuticals, Inc. (Nasdaq: ORIC), a clinical stage oncology company focused on developing treatments that address mechanisms of therapeutic resistance, today announced that multiple abstracts highlighting the potential of rinzimetostat (ORIC-944), a potent and selective allosteric inhibitor of PRC2 to treat prostate cancer, have been accepted for poster presentations at the 2026 American Association for Cancer Research (AACR) Annual Meeting taking place April 17-22, 2026 in San Diego, CA. All regular abstracts are available for viewing via AACR’s online itinerary planner located here. Poster presentations details: Date & Time:Wednesday, April 22, 2026, 9:00 a.m. - 12:00 p.m. PTSession Category:Experimental and Molecular TherapeuticsSession Title:Novel Strategies to Reverse Drug ResistanceLocation:Poster Section 14 Title:Rinzimetostat, an allosteric EED inhibitor with best-in-class properties for the treatment of prostate cancer, is effective in PRC2 methyltransferase-resistant settings in preclinical studiesAbstract Number:7120Poster Number:Board Number 9 Abstract HighlightsRinzimetostat is a potent and highly selective next-generation allosteric PRC2 inhibitor targeting the EED subunit that has demonstrated potential best-in-class efficacy and safety in a dose exploration trial in combination with androgen receptor (AR) inhibitors. To further evaluate the possible benefits of inhibiting PRC2 activity through EED targeting, preclinical studies investigated rinzimetostat versus EZH2- or EZH1/2-targeting agents in the context of proposed acquired resistance mechanisms. Biochemical assays demonstrated that rinzimetostat maintained potent inhibition of PRC2 complexes containing either EZH1 or EZH2 as the enzymatic subunit, while EZH2 or EZH1/2 dual inhibitors showed reduced activity in EZH1-containing complexes. Consistent with the biochemical data, rinzimetostat retained antitumor activity in prostate cancer cells overexpressing EZH1, while EZH2 inhibitors mevrometostat and tazemetostat lost potency in this context. Rinzimetostat also maintained inhibition of H3K27me3 in prostate cancer cells expressing the clinically reported EZH2-inhibitor acquired resistance mutation EZH2 Y666N, while EZH2 inhibitors did not reduce H3K27me3. In addition, in pr...