Carboplatin (JM-8) is a cisplatin derivative, a DNA synthesis inhibitor. Carboplatin binds to DNA, inhibits replication and transcription, and induces cell death. Carboplatin has antitumor activity.

方法：5637 种细胞用 Carboplatin (0-10000 μM) 处理 4 h，使用 MTT 方法检测细胞活力。
结果：Carboplatin 存在剂量依赖性的细胞杀伤作用，IC50 值为 289.3±2.90 μM。[1]
方法：人 RB 肿瘤细胞 Y79 用 Carboplatin (20-80 μg/mL) 处理 2 天，使用 Flow Cytometry 检测细胞凋亡情况。
结果：Carboplatin 诱导细胞的早期凋亡率增加。[2]

方法：为检测体内抗肿瘤活性，将 Carboplatin (20 mg/kg) 尾静脉注射给携带人 RB 肿瘤 Y79 的 BALB/c (nu/nu) 小鼠，每三天一次，持续一周或两周。
结果：Carboplatin 在体内成功抑制人 RB 异种移植物的生长。[2]
方法：为检测体内抗肿瘤活性，将 Carboplatin (25-75 mg/kg) 腹腔注射给携带 EOC 异种移植瘤的免疫缺陷小鼠，每周一次，持续六周。
结果：OV1946 和 OV4453 对 Carboplatin 敏感，OV90 和 OV4485 显示出中等反应，TOV21G 和 TOV112D 具有耐药性。[3]

Radioligand binding studies on human AT1 receptors: A radioligand binding assay is performed by using human AT1 receptor-coated microplates containing 4.4 to 6.2 fmol of receptors/well (10 μg of membrane protein/well). Membrane-coated wells are incubated with 45 μL of assay buffer (50 mM Tris-HCl, 5 mM MgCl2, 1 mM EDTA, and 0.005% CHAPS, pH 7.4) containing various concentrations of Azilsartan at room temperature. After 90 minutes, 5 μL of 125I-Sar1-Ile8-AII (final concentration 0.6 nM) dissolved in assay buffer is added to the wells, and the plate is incubated for 5 hours. In each step, the plate is briefly and gently shaken on a plate shaker. In washout experiments, the membranes are incubated with Azilsartan for 90 minutes, then immediately washed twice with 200 μL/well of assay buffer to remove unbound compounds, and further incubated for 5 hours with 125I-Sar1-Ile8-AII. Membrane-bound radioactivity is counted using a TopCount Microplate Scintillation and Luminescence Counter. In the experiments to estimate the dissociation rate of Azilsartan from AT1 receptors, membranes are incubated for 90 minutes with Azilsartan at a concentration of 30 nM for Azilsartan. Azilsartan inhibits the specific binding of 125I-Sar1-Ile8-AII to human AT1 by approximately 90%. The membranes are then immediately washed twice with 200 μL/well of assay buffer and further incubated with 125I-Sar1-Ile8-AII for 240 minutes. Membrane-bound radioactivity is counted using the TopCount Microplate Scintillation and Luminescence Counterat 30 minutes, 60 minutes, 90 minutes, 120 minutes, 150 minutes, 180 minutes, or 240 minutes. Nonspecific binding of 125I-Sar1-Ile8-AII is estimated in the presence of 10 μM unlabeled AII. Unlabeled AII is added again after washout for the washout experiment. Specific binding is defined as total binding minus nonspecific binding.

3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide (MTT) assays: Exponentially growing A2780, SKOV3, IGROV-1 and HX62 ovarian cancer cells are plated in 96 well plates. A range of drug concentrations are added and the plates are incubated for 72 hours to allow for 3–4 doubling times. Each experiment is carried out in triplicate. Sulforhodamine B (SRB) assays: Exponentially growing A2780 cells are plated in 96 well microtitre plates. For experiments studying concomitant exposure, cells are exposed to increasing concentrations of both drugs for 96 hours. For experiments studying the effect of sequence of exposure to 17-AAG or carboplatin cells are exposed to increasing concentrations of 17-AAG or carboplatin for 24 hours. A period of 24-hour exposure to the first agent is chosen so that the A2780 cells would be exposed to the first drug for at least one doubling time (18-24 hours). The cells are then washed with sterile phosphate buffered saline and the medium is replenished. Following this, the second drug (to which the cells are not exposed to in the first 24 hours) or medium is added for 96 hours. All experiments are carried out in triplicate. The results of combination studies are analyzed using the well-established principles of median effect analysis method. The effects of the combination are calculated using an in-house spreadsheet. (Only for Reference)