COTI-2 reactivates mutant p53 and inhibits growth of triple-negative breast cancer cells

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Breast Cancer Treatment

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COTI-2, a novel thiosemicarbazone derivative, exhibits antitumor activity in HNSCC through p53-dependent and -independent mechanisms

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Restoration of conformation of mutant p53

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Novel anti-cancer drug COTI-2 synergizes with therapeutic agents and does not induce resistance or exhibit cross-resistance in human cancer cell lines

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APR-246 reactivates mutant p53 by targeting cysteines 124 and 277

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Abstract CT033: Safety and early efficacy signals for COTI-2, an orally available small molecule targeting p53, in a phase I trial of recurrent gynecologic cancer

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COTI-2, a potent orally available small molecule targeting mutant p53, with promising efficacy as monotherapy and combination treatment in preclinical tumor models.

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Inhibiting the system xC−/glutathione axis selectively targets cancers with mutant-p53 accumulation

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COTI-2, a new anticancer drug currently under clinical investigation, targets mutant p53 and negatively modulates the PI3K/AKT/mTOR pathway

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Mutant p53: a novel target for the treatment of patients with triple-negative breast cancer?

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COTI-2, a novel small molecule that is active against multiple human cancer cell lines in vitro and in vivo

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APR-246 overcomes resistance to cisplatin and doxorubicin in ovarian cancer cells

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Multiplatform Analysis of 12 Cancer Types Reveals Molecular Classification within and across Tissues of Origin

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Mutational landscape and significance across 12 major cancer types

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APR-246/PRIMA-1MET inhibits thioredoxin reductase 1 and converts the enzyme to a dedicated NADPH oxidase

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The landscape of cancer genes and mutational processes in breast cancer

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Comprehensive molecular portraits of human breast tumours

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Re-oxygenation causes hypoxic tumor regression through restoration of p53 wild-type conformation and post-translational modifications

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Drug Combination Studies and Their Synergy Quantification Using the Chou-Talalay Method

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PRIMA-1 Reactivates Mutant p53 by Covalent Binding to the Core Domain

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