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Tumor-specific DNA repair defects are ubiquitous in cancerous tissue, which offers a potential for clinical gain to build on these perturbations. Intravenous high-dose vitamin C (IVC) triggers the formation of hydrogen peroxide (H O ), which contributes to Fenton chemistry producing hydroxyl radicals (-OH), causing selective damage to DNA. Herein, we evaluated the therapeutic response to IVC and PARP inhibitors (PARPi) in combination in 8 patients with a deficiency of homologous recombination repair system (dHRR) in a 3-year period. Eight