Anapc11 inhibitors for the treatment of triple negative breast cancer

By targeting ANAPC11 with siRNA and siRNA precursors, the ferroptosis defense mechanism of TNBC cells is disrupted, enhancing their sensitivity to ferroptosis inducers. When combined with chemotherapy drugs, this addresses the drug resistance problem in TNBC treatment and achieves significant anti-tumor effects.

CN122214347APending Publication Date: 2026-06-16THE FIRST HOSPITAL OF CHINA MEDICIAL UNIV
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Patent Information

Application Number
CN202610662355.X
Authority / Receiving Office
CN · China
Patent Type
Applications(China)
Current Assignee / Owner
Filing Date
2026-05-13
Publication Date
2026-06-16

AI Technical Summary

Technical Problem

Current treatments for triple-negative breast cancer lack effective targeted drugs, and tumor cells often escape chemotherapy through ferroptosis defense mechanisms, resulting in poor treatment outcomes.

Method used

It provides siRNA and siRNA precursors targeting ANAPC11, which, when loaded into exosomes, reduce ANAPC11 expression, break the ferroptosis defense mechanism, enhance tumor sensitivity to ferroptosis inducers, and enhance therapeutic effects when used in combination with chemotherapy drugs or immunotherapy drugs.

Benefits of technology

It significantly inhibits ANAPC11 expression, increases the sensitivity of tumor cells to ferroptosis inducers, significantly inhibits tumor cell proliferation and tumorigenesis, provides new therapeutic targets and personalized treatment plans, and improves the treatment effect of TNBC.

✦ Generated by Eureka AI based on patent content.

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Abstract

The application discloses an ANAPC11 inhibitor for treating triple-negative breast cancer. Specifically, the siRNA of the application can effectively knock out ANAPC11, treat triple-negative breast cancer, and also increase the sensitivity of tumors to ferroptosis. The siRNA targeting ANAPC11 of the application is combined with a ferroptosis inducer or a chemotherapy drug, so that the killing effect on tumor cells can be effectively improved, especially for tumors with ferroptosis drug resistance.
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