CIS-DIAMMINE-[1,1-CYCLOBUTANE-DICARBOXYLATO]PLATIN

Carboplatin is a second-generation platinum anti-tumor drug. Its anti-cancer activity is similar to that of cisplatin, but its nephrotoxicity, ototoxicity, neurotoxicity, especially gastrointestinal reactions, are significantly lower than those of cisplatin, and its anti-tumor spectrum is not as good as that of cisplatin. wide. Its mechanism of action is mainly to cause cross-linking between and within DNA strands, interfere with DNA molecules, and inhibit cellular DNA synthesis. It mainly acts on the N-7 and O-6 atoms of guanine in DNA, producing cytotoxic effects. Because the cyclobutane ring in the carboplatin molecule serves as a ligand more stable than the chloride ion group in cisplatin, it was initially thought that carboplatin might not be as ototoxic, nephrotoxic, and neurotoxic as cisplatin, but the systemic biological Scientific evaluation and a large number of clinical trials have proven that although the nephrotoxicity, bone marrow suppression, ototoxicity and neurotoxicity of carboplatin are not as serious as cisplatin, the damage to the body still cannot be ignored. There is cross-resistance between the anti-tumor effect of carboplatin and cisplatin in vivo, so tumor cells that are insensitive to cisplatin are also resistant to carboplatin. From studies on in vitro tumor lines and transplanted breast cancer Chemicalbook mice, it was found that carboplatin not only inhibits tumor growth, but also has a certain radiosensitization effect. Many cisplatin analogs have been produced and studied in the past 10 years, and carboplatin was the first to be approved for clinical use. It is a platinum (Ⅱ) coordination complex that is structurally and chemically different from cisplatin in that it uses bicarboxycyclobutane to replace the chloride ligand in early drugs. Like cisplatin, carboplatin reacts with DNA to produce inter- and intra-strand cross-links. The result of DNA damage is that the replication and transcription properties of DNA are impaired, which is likely to be responsible for the cell-killing effect of this drug. Replacing the carboxyl ligand of carboplatin with water molecules hydrates more slowly than the chlorine ligand of cisplatin. As a result of these reactions, each drug generates active cross-links, and differences in their pharmacokinetics illustrate their relative potential. When used as a single drug, the dose of carboplatin is 4 times greater than that of cisplatin. DNA cross-linking occurs more slowly in cells after application of carboplatin than after application of cisplatin. Carboplatin is cell cycle non-specific. The above information was edited and compiled by Xiao Nan of ChemicalBook.

Carboplatin is a second-generation platinum anti-tumor drug. Its anti-cancer activity is similar to that of cisplatin, but its nephrotoxicity, ototoxicity, neurotoxicity, especially gastrointestinal reactions, are significantly lower than those of cisplatin, and its anti-tumor spectrum is not as good as that of cisplatin. wide. Its Chemicalbook mechanism of action is mainly to cause cross-linking between and within DNA strands, interfere with DNA molecules, and inhibit cellular DNA synthesis. It mainly acts on the N-7 and O-6 atoms of guanine in DNA, producing a cytotoxic effect.