Carboplatin (Synonyms: CBDCA, CDDCA, cis-Diammine(1,1-cyclobutanedicarboxylato)platinum(II), NSC 201345, NSC 241240)

Carboplatin (NSC 241240) is a non-specific DNA cross-linking agent that inhibits DNA synthesis and transcription. Its main target is DNA rather than specific proteins^[1]. Carboplatin is commonly used in cancer treatment research and is an effective anticancer drug, especially for ovarian cancer, breast cancer, etc. ^[2]. Platinum drugs are not recommended to be dissolved in DMSO because they are easily inactivated^[3].

In vitro, ten ovarian cancer cells were treated with Carboplatin (0-100μM) for 24h, and all showed strong or moderate cell inhibitory activity. Among them, OV2978 and TOV2881EP cells showed strong sensitivity to Carboplatin, with IC₅₀ <1 μM^[4]. Carboplatin (0-100μM) treated Brca1 and Brca2 cells for 72h, which significantly reduced cell survival rates, with IC₅₀ of 3.4μM and 1.9μM, respectively^[5].

In vivo, carboplatin (25 mg/kg) was intraperitoneally injected into mice inoculated with OVCAR5 tumor cells and significantly inhibited tumor growth^[6]. Carboplatin (15 mg/kg) was intraperitoneally injected into NOD-SCID xenograft mice and combined with panobinostat significantly inhibited tumor growth, showing a synergistic anticancer effect^[7].

References:
[1] Doshi G, Sonpavde G, Sternberg C N. Clinical and pharmacokinetic evaluation of satraplatin[J]. Expert opinion on drug metabolism & toxicology, 2012, 8(1): 103-111.
[2] Thomadaki H, Scorilas A. Molecular profile of breast versus ovarian cancer cells in response to treatment with the anticancer drugs cisplatin, carboplatin, doxorubicin, etoposide and taxol[J]. 2008.
[3] Hall M D, Telma K A, Chang K E, et al. Say no to DMSO: dimethylsulfoxide inactivates cisplatin, carboplatin, and other platinum complexes[J]. Cancer research, 2014, 74(14): 3913-3922.
[4] Sauriol S A, Simeone K, Portelance L, et al. Modeling the diversity of epithelial ovarian cancer through ten novel well characterized cell lines covering multiple subtypes of the disease[J]. Cancers, 2020, 12(8): 2222.
[5] Clark C C, Weitzel J N, O'Connor T R. Enhancement of synthetic lethality via combinations of ABT-888, a PARP inhibitor, and carboplatin in vitro and in vivo using BRCA1 and BRCA2 isogenic models[J]. Molecular cancer therapeutics, 2012, 11(9): 1948-1958.
[6] Patel M, Wang Y, Bartom E T, et al. The ratio of toxic-to-Nontoxic mirnas predicts platinum sensitivity in ovarian cancer[J]. Cancer research, 2021, 81(15): 3985-4000.
[7] Wang L, Syn N L X, Subhash V V, et al. Pan-HDAC inhibition by panobinostat mediates chemosensitization to carboplatin in non-small cell lung cancer via attenuation of EGFR signaling[J]. Cancer letters, 2018, 417: 152-160.