ArticleOncology letters2026
KRAS (G12D)-selective inhibitor MRTX1133 suppresses proliferation and differentially modulates chemosensitivity in ovarian mucinous carcinoma.
Article in Oncology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Ovarian mucinous carcinoma (OMC) is a rare subtype of ovarian cancer characterized by frequent KRAS mutations and a poor response to platinum- and taxane-based chemotherapy, underscoring the need for novel therapeutic strategies. MRTX1133, a recently developed non-covalent and selective KRAS (G12D) inhibitor, has demonstrated potent antitumor activity in pancreatic and colorectal cancers; however, its efficacy in OMC remains unexplored. In the present study, the antitumor effects of MRTX1133 in the KRAS (G12D)-mutant OMC cell line MCAS and its interactions with conventional chemotherapeutic agents were evaluated. Cell viability was assessed using WST-1 assays, ERK phosphorylation was evaluated by western blotting and gene expression levels were analyzed by reverse transcription-quantitative PCR. Results indicated that MRTX1133 suppressed MCAS cell proliferation in a concentration-dependent manner, whereas proliferation of KRAS wild-type and KRAS (G12S)-mutant cells was not significantly inhibited. Treatment markedly inhibited ERK phosphorylation, suggesting suppression of the MAPK pathway. MRTX1133 reduced the mRNA expression of Ki-67 and numerous cyclins (D1, A2 and B1), suggesting attenuation of proliferative signaling. When combined with cytotoxic agents, including paclitaxel, SN38, gemcitabine and cisplatin, MRTX1133 reduced the sensitivity to cell cycle-dependent chemotherapeutic agents, namely paclitaxel, SN38 and gemcitabine, while not affecting the activity of the non-cell cycle-dependent agent cisplatin. The present study therefore provided preclinical evidence for the potential utility of KRAS (G12D)-targeted therapy in OMC and highlights the importance of sequential rather than concurrent scheduling of MRTX1133 with cell cycle-dependent chemotherapy to optimize therapeutic efficacy.
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