Trial reportScience advances2026
Multiomics profiling and experiments in preclinical models revealed RAD51-IN-1 as a synergistic potentiator of anlotinib sensitivity.
Trial report in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04807166 (A Prospective, Single-arm, Multicenter, Exploratory Phase II Study to Evaluate the Efficacy and Safety of Anlotinib Combined With Carboplatin/Paclitaxel as First-line Treatment in Patients With Advanced Ovarian Cancer), which is not on this map. Not yet cited in PubMed.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Prospective, Single-arm, Multicenter, Exploratory Phase II Study to Evaluate the Efficacy and Safety of Anlotinib Combined With Carboplatin/Paclitaxel as First-line Treatment in Patients With Advanced Ovarian Cancer
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10 authors.
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Abstract
Anlotinib has demonstrated preliminary efficacy as a first-line maintenance therapy for ovarian cancer. However, clinical responses vary widely. To investigate resistance mechanisms and explore rational combinations, pretreatment tumors from 18 patients in clinical trial NCT04807166 underwent whole-exome and RNA sequencing and stratified into sensitive and resistant groups based on progression-free survival. VEGFR-related mutations were enriched in sensitive tumors, whereas resistant tumors showed increased activity of DNA repair pathways and Notch signaling. In vitro screening identified strong synergy between anlotinib and the RAD51 inhibitor RAD51-IN-1, which outperformed the Notch inhibitor FLI-06 in resistant patient-derived organoids. Mechanistic studies revealed that RAD51 inhibition was associated with impaired HRR and increased sensitivity to anlotinib. In vivo, combined treatment with anlotinib and RAD51-IN-1 significantly reduced tumor burden without notable toxicity. These findings suggest that RAD51-mediated HRR may contribute to anlotinib resistance and support RAD51 inhibition as a promising approach to overcome therapeutic resistance in ovarian cancer.
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