(rel)-Oxaliplatin, a DNA synthesis inhibitor, induces DNA crosslinking damage, inhibits DNA replication and transcription, and stimulates apoptosis. This compound has applications in cancer research [1] [2] [3].

(rel)-Oxaliplatin demonstrates potent anticancer activity through various mechanisms across multiple cell lines. When applied to HCC, HCCLM3, and Hep3B cells for 24-72 hours at concentrations of 2-128 μM, it inhibits cell proliferation and triggers apoptosis. In CEM cells exposed for 15-240 minutes at 10 μM, it induces both primary and secondary DNA damage, specifically interstrand DNA cross-links (ISC) and DNA-protein cross-links (DPC). Additionally, (rel)-Oxaliplatin shows significant cytotoxicity against a diverse panel of cancer cell lines, including bladder carcinoma (RT4, TCCSUP), ovarian carcinoma (A2780), colon carcinoma (HT-29), glioblastoma (U-373MG, U-87MG), and melanoma (SK-MEL-2, HT-144), with IC50 values ranging from 0.17 to 30.9 μM after 24 hours of exposure. Detailed analyses on cell viability, protein expression, and cell cycle progression reveal its mechanisms of action, such as dose- and time-dependent reductions in cell viability, modulation of apoptotic protein expression (decreasing Bcl-2 and Bcl-xL, increasing Bax), and an increase in the percentage of apoptotic cells, thus demonstrating its broad and effective anti-tumor activities.

(rel)-Oxaliplatin, administered intraperitoneally at dosages of 5-10 mg/kg over a period of 32 days, effectively inhibits tumor growth in nude mice. This was observed in a study using HCCLM3 tumor xenografts, where the treatment resulted in a significant reduction in tumor volume.