Cisplatin

产品编号 T1564   CAS 15663-27-1
别名: cis-Diaminodichloroplatinum, CDDP

Cisplatin, a DNA-crosslinking agent, is able to suppress DNA synthesis by conforming DNA adducts in cancer cells.

Cisplatin结构式
Cisplatin , CAS 15663-27-1
规格 库存 价格/RMB 数量
100 mg 上海现货 410.00
500 mg 上海现货 1020.00
1 g 上海现货 1715.00
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纯度 99.62%
纯度 98.11%
纯度 98.00%
纯度 98.00%
纯度 99.60%
生物活性
化学信息
存储 & 溶解度
配制溶液
产品描述 Cisplatin, a DNA-crosslinking agent, is able to suppress DNA synthesis by conforming DNA adducts in cancer cells.
靶点活性 Caspase-3   Caspase-9   DNA synthesis
体外活性 Cisplatin (50 μM) produced time-dependent apoptosis in RPTCs, causing cell shrinkage, a 50-fold increase in caspase 3 activity, a 4-fold increase in phosphatidylserine externalization, and 5- and 15-fold increases in chromatin condensation and DNA hypoploidy, respectively. Mitochondrial membrane potential and ATP levels did not change at any time during cisplatin exposure [1]. High concentrations of cisplatin (800 μM) led to necrotic cell death over a few hours. Much lower concentrations of cisplatin (8 microM) led to apoptosis, which caused loss of the cell monolayer over several days. DNA electrophoresis of cells exposed to 800 μM cisplatin yielded a "smear" pattern, due to random DNA degradation [2].
体内活性 In melanoma-bearing mice, cisplatin (4 mg/kg B.W.) reduced the size and weight of the solid tumors, and HemoHIM supplementation with cisplatin enhanced the decrease of both the tumor size and weight. In melanoma-bearing mice treated with cisplatin, HemoHIM administration also increased the activity of NK cells and Tc cells and the IL-2 and IFN-gamma secretion from splenocytes [3]. The maximum tolerated dose of cisplatin given weekly i.v. x 2 induced a tumor growth inhibition (GI) of 77.5% and 85.1% of the serous xenografts Ov.Ri(C) and OVCAR-3, respectively. The mucinous xenograft Ov.Pe was relatively resistant to cisplatin. The maximum tolerated dose of CTX, given i.p. x 2 with a 2-week interval, induced a GI between 52.9% and 59.7% for each of the 3 xenografts [4].
细胞实验 Rabbit renal proximal tubules were isolated using the iron oxide perfusion method and grown in 35-mm tissue culture dishes under improved conditions as described previously. The cell culture medium was a 1:1 mixture of Dulbecco’s modified Eagle’s medium/Ham’s F-12 (without D-glucose, phenol red, or sodium pyruvate) supplemented with 15 mM HEPES buffer, 2.5 mM L-glutamine, 1 μM pyridoxine HCl, 15 mM sodium bicarbonate, and 6 mM lactate. Hydrocortisone (50 nM), selenium (5 ng/ml), human transferrin (5 μg/ml), bovine insulin (10 nM), and L-ascorbic acid-2-phosphate (50 μM) were added to fresh culture medium immediately before daily media change. In general, confluent RPTCs were treated with inhibitors or diluent control [typically DMSO at 0.1% (v/v)] for 30 min before treatment with cisplatin. Aliquots of RPTCs were used for various assays as detailed below [1]. Cell lines: Leukemia L1210/0 cells
动物实验 Mice were divided randomly into three groups (Control, Cisplatin and Cisplatin+HemoHIM), and each group consisted of twenty mice. B16F0 melanoma (5 × 10^5 cells/mouse) was inoculated into subcutaneous femoral left region of mice at 3 days before an initial injection of cisplatin. Cisplatin was injected intraperitoneally at 4 mg/kg body weight (B.W.) on day 0, 7 and 14 (total three injections). Experimental group was intubated with HemoHIM at a final concentration of 100 mg/kgB.W. by everyday from day -1 to day 16, while the control group received only water. On day 17 after initial injection of cisplatin, all mice of each group were experimented, respectively, to evaluate tumor weight or tumor size. The tumor size was calculated as follows: tumor size = ab^2/2, where a and b are the larger and smaller diameters, respectively [3].
别名 cis-Diaminodichloroplatinum , CDDP
纯度 99.62%
分子量 300.05
分子式 H6Cl2N2Pt
CAS No. 15663-27-1

存储

0-4℃ for short term (days to weeks), or -20℃ for long term (months).

溶解度

DMF: 3 mg/mL

( < 1 mg/ml refers to the product slightly soluble or insoluble )

溶液 1

Saline: 3mg/mL

文献引用

参考文献
1. Cummings BS, et al. Cisplatin-induced renal cell apoptosis: caspase 3-dependent and -independent pathways. J Pharmacol Exp Ther. 2002 Jul;302(1):8-17. 2. Lieberthal W, et al. Mechanisms of death induced by cisplatin in proximal tubular epithelial cells: apoptosis vs. necrosis. Am J Physiol. 1996 Apr;270(4 Pt 2):F700-8. 3. Park HR, et al. Enhanced antitumor efficacy of cisplatin in combination with HemoHIM in tumor-bearing mice. BMC Cancer. 2009 Mar 17;9:85. 4. Molthoff CF, et al. Comparison of 131I-labelled anti-episialin 139H2 with cisplatin, cyclophosphamide or external-beam radiation for anti-tumor efficacy in human ovarian cancer xenografts. Int J Cancer. 1992 Apr 22;51(1):108-15. 5. Xu C, Zhao W, Huang X, et al. TORC2/3-mediated DUSP1 upregulation is essential for human decidualization[J]. Reproduction. 2021, 1(aop). 6. Shao C S, Zhou X H, Zheng X X, et al. Ganoderic acid D induces synergistic autophagic cell death except for apoptosis in ESCC cells[J]. Journal of Ethnopharmacology. 2020, 262: 113213. 7. Wu Y, Zhou L, Wang Z, et al. Systematic screening for potential therapeutic targets in osteosarcoma through a kinome-wide CRISPR-Cas9 library[J]. Cancer Biology & Medicine. 2020, 17(3): 782. 8. Wang C, Xiong M, Yang C, et al. PEGylated and Acylated Elabela Analogues Show Enhanced Receptor Binding, Prolonged Stability, and Remedy of Acute Kidney Injury[J]. Journal of Medicinal Chemistry. 2020 9. Kang C L, Qi B, Cai Q Q, et al. LncRNA AY promotes hepatocellular carcinoma metastasis by stimulating ITGAV transcription. Theranostics. 2019, 9(15): 4421. 10. Liu L, Liu S, Deng P, et al. Targeting the IRAK1-S100A9 Axis Overcomes Resistance to Paclitaxel in Nasopharyngeal Carcinoma[J]. Cancer Research.

相关化合物库

该产品包含在如下化合物库中:
Approved Drug Library Bioactive Compound Library Inhibitor Library Anti-Cancer Compound Library Clinical Compound Library Epigenetics Compound Library FDA-Approved Drug Library DNA Damage & Repair Compound Library Anti-Cancer Approved Drug Library Anti-Cancer Clinical Compound Library Cardiotoxicity Compound Library Toxic Compound Library Anti-Cancer Active Compound Library Anti-Cancer Drug Library Drug Repurposing Compound Library Ferroptosis Compound Library Drug-induced Liver Injury (DILI) Compound Library NMPA-Approved Drug Library FDA-Approved & Pharmacopeia Drug Library Anti-Pancreatic Cancer Compound Library

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