Nitro51 Pharmaceuticals' CP-8 addresses a critical unmet need in oncology: overcoming resistance to DNA damage response (DDR) therapies, especially in HR-proficient cancers that evade PARP inhibitors (PARPi). Unlike existing treatments, CP-8 selectively inhibits RAD51—a key DNA repair protein—via a reversible covalent mechanism, re-sensitizing tumors to PARPi and chemotherapy while sparing healthy tissue.
No FDA-approved RAD51 inhibitors exist
Effective in HR-proficient tumors that evade PARP inhibitors
Active in BRCA wild-type and mutant cancers
CP-8 directly targets RAD51—a master regulator of DNA repair that is overexpressed in many cancers and correlates with drug resistance and decreased patient survival. Unlike existing DDR inhibitors, CP-8 uses a reversible covalent mechanism via synthetic nitroalkene chemistry, specifically targeting Cys-319 on RAD51.
Our preclinical data demonstrates CP-8's efficacy across multiple resistant cancer types, including triple-negative breast cancer (TNBC), high-grade serous ovarian cancer (HGSOC), pancreatic, and metastatic castration-resistant prostate cancer (mCRPC). CP-8 shows equal effectiveness in both BRCA wild-type and mutant cancers.
High synergy with PARP inhibitors (HSA scores >20)
Maintains potency in PARP-resistant cell lines
Effective in human tumor organoids
De-risked based on analog compound clinical data
CP-8 shows strong preclinical efficacy in aggressive, treatment-resistant cancers like triple-negative breast and pancreatic cancer, including BRCA-wild-type tumors. As the first-in-class RAD51 inhibitor, CP-8 expands the DDR landscape and enables novel combination strategies, offering a targeted, low-toxicity approach for patients lacking durable treatment options. We believe CP-8 represents a high-impact, scalable opportunity in precision oncology.
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