In Vitro Antitumor Effects of Bapst, a Repositioned Regimen for the Metabolic Therapy of Cancer

Purpose . Key metabolism pathways altered in cancer are glycolysis, glutaminolysis, fatty acid synthesis, cholesterol synthesis, and beta-oxidation. Cancer cells reprogram their metabolism to resist cancer treatment. The BAPST regimen (Benserazide, Apomorphine, Pantoprazole, Simvastatin, Trimetazidine) is a repurposed drug combination that inhibits the key enzymes involved in these five pathways (HK2, GLS1, FASN, HMGCR, and 3-KAT). This study evaluates its vitro antitumor effects. Methods: We evaluated 20 human and three murine/rat cancer cell lines. The cells were treated with BAPST (Benserazide: 65 μM, Apomorphine: 8.49 μM, Pantoprazole: 84.3 μM, Simvastatin: 0.162 μM, Trimetazidine: 2.7 μM) or individual drugs for 24–120 hours. Cell viability and clonogenicity were assessed with crystal violet staining. Results: BAPST reduced viability across all cell lines. Major effects were observed in gastric (100%), pancreatic (>90%), and breast (65–90%) cells. Clonogenicity was entirely inhibited in five of six tested cell lines. Individually, benserazide and apomorphine, showed the highest effect, while pantoprazole a minor one. Simvastatin and trimetazidine had minimal/no inhibition or even increased viability and clonogenicity. Conclusion: BAPST demonstrates potent in vitro antitumor effects across diverse cancer cell lines, warranting further studies to confirm that its effect arises from metabolism enzyme inhibition and impeding metabolic reprogramming, as well as in vivo antitumor efficacy.