Research identifies a new Polθ polymerase inhibitor that enhances therapeutic effects in HR-deficient cancers, suggesting strong synthetic lethality.
DNA polymerase theta (Polθ) is a key enzyme in the theta-mediated end-joining (TMEJ) and a promising target for synthetic lethality-based cancer therapy, particularly in homologous recombination (HR)-deficient tumors. Herein, we designed and optimized a series of Polθ polymerase inhibitors, exploiting a previously unexplored binding pocket to enhance potency, cellular activity, and pharmacokinetics. Compound 33 exhibited low-nanomolar Polθ inhibition, strong antiproliferative activity in DLD1 BRCA2 KO cells, and high sensitivity to MDA-MB-436 cells. In combination with Olaparib, it significantly enhanced DNA damage accumulation, induced γH2AX levels, and achieved 85% tumor growth inhibition (TGI) in the MDA-MB-436 xenograft model. Pharmacokinetic studies confirmed a favorable dose-dependent profile, and preliminary safety evaluations indicated good tolerability. These findings establish compound 33 as a potent Polθ inhibitor with strong synthetic lethality effects, supporting its further preclinical development as a novel Polθ-targeted therapeutic agent.
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Yu et al. (2025) studied this question.
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