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.
卡铂（Carboplatin；NSC 241240）是一种非特异性DNA交联剂，抑制DNA合成和转录，其主要靶点是DNA，而不是特定的蛋白质[1]。Carboplatin通常用于癌症治疗研究，是一种有效的抗癌药物，特别是用于卵巢癌、乳腺癌等[2]。铂类药物不建议用DMSO溶解，易失活[3]。
在体外，Carboplatin（0-100μM）处理十种卵巢癌细胞24h，均表现出较强或中等的细胞抑制活性，其中OV2978和TOV2881EP细胞对Carboplatin表现出很强的敏感性，IC50<1 μM[4]。Carboplatin（0-100μM）处理Brca1和Brca2细胞72h，显著降低了细胞存活率，IC50分别为3.4μM、1.9μM[5]。
在体内，Carboplatin（25mg/kg）通过腹腔注射治疗接种OVCAR5肿瘤细胞的小鼠，显著抑制了肿瘤生长[6]。Carboplatin（15mg/kg）通过腹腔注射治疗NOD-SCID异种移植小鼠，与帕比司他（panobinostat）联合使用显著抑制了肿瘤的生长，显示出协同抗癌效果[7]。