Bisphenol A (BPA) is a well-known endocrine-disrupting chemical. Various factors, including extensive environmental contamination, ubiquitous human exposure, and low-dose effects, have contributed to its being banned by several countries. However, the ability of BPA to induce genotoxicity has been hotly debated since both in vitro and in vivo data have shown conflicting results. Based on the general notion that all mutagens are genotoxic, but not all genotoxic chemicals are mutagenic, if BPA is mutagenic, it would most definitely be genotoxic in nature. However, the data on BPA as a potential mutagen are also conflicting and scarce. Here we review studies reporting the genotoxicity and mutagenicity of BPA and discuss why more substantial data is needed to clarify the role of BPA as a genotoxicant or mutagen.

Drug repurposing offers an efficient strategy to identify novel anticancer agents from marketed compounds. We screened a library of ~1400 approved drugs using a PPARE–PPAR-α luciferase reporter assay to uncover modulators of lipid metabolism that induce cancer cell death without direct binding to PPARα. This primary screen identified 224 compounds inhibiting reporter activity by >50%, of which 26 demonstrated ≥50% cytotoxicity in KAIMRC1 breast cancer and HCT116 colorectal cancer cells at 10 µM after 48 h incubation. AI-based DrTarget analysis classified these hits, with Group 1 comprising four previously unrecognized anticancer agents: antibiotics cefditoren pivoxil, tebipenem pivoxil, broxyquinoline, and cosmetic ingredient 1-hexadecanol. Dose–response studies across KAIMRC1, HCT116, and SW480 cells revealed IC₅₀ values as low as ~10 µM, comparable to daunorubicin, a well-known anti-cancer drug. Apoptosis profiling confirmed activation of intrinsic/extrinsic pathways via cytochrome c, SMAC/Diablo, TRAIL-R1/DR4, and phospho-p53 modulation. Based on these findings, we propose the repurposing of Broxyquinoline, 1-Hexadecanol, Cefditoren Pivoxil, and Tebipenem Pivoxil as potential anti-cancer drugs.