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Cisplatin Inhibits DNA synthesis,chemotherapy drug

Catalog No.A8321
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Sample solution is provided at 25 µL, 10mM.

Product Citations

1. Wu Q, Wei X, et al. "Bionic 3D spheroids biosensor chips for high-throughput and dynamic drug screening." Biomed Microdevices. 2018 Sep 15;20(4):82. PMID:30220069
2. Yeo SK, Paul R, et al. "Improved efficacy of mitochondrial disrupting agents upon inhibition of autophagy in a mouse model of BRCA1-deficient breast cancer." Autophagy. 2018;14(7):1214-1225. PMID:29938573
3. Sharma K, Vu TT, et al. "p53-independent Noxa induction by cisplatin is regulated by ATF3/ATF4 in head and neck squamous cell carcinoma cells." Mol Oncol. 2018 Jan 19. PMID:29352505
4. Lochmann TL, Floros KV, et al. "Venetoclax Is Effective in Small-Cell Lung Cancers with High BCL-2 Expression." Clin Cancer Res. 2018 Jan 15;24(2):360-369. PMID:29118061

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Chemical structure


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Related Biological Data


Related Biological Data


Related Biological Data


Related Biological Data


Biological Activity

Description Cisplatin is a highly effective and broad-spectrum chemotherapeutic agent.


Cell experiment [1]:

Cell lines

L1210/0 cells

Preparation method

The solubility of this compound in DMF is >12.5 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.

Reaction Conditions

0, 0.5, 1, 2, 4 and 8 μg/mL; 2 hrs


At low concentrations, Cisplatin induced minimal cell death. At higher concentrations, cell death was obvious with only 4% viability. By 10 days after incubation, these few survivors begun to grow and became the predominant cells in the population.

Animal experiment [2]:

Animal models

Nude mice bearing human ovarian cancer OVCAR-3 cell xenografts

Dosage form

5 mg/kg, i.v.; at day 0 and day 7


Cisplatin (5 mg/kg) given at the day 0 and 7 induced a tumor growth inhibition (GI) (85.1%) of the OVCAR-3 cell xenografts.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.


[1]. Sorenson CM, Eastman A. Mechanism of cis-diamminedichloroplatinum(II)-induced cytotoxicity: role of G2 arrest and DNA double-strand breaks. Cancer Res. 1988 Aug 15;48(16):4484-8.

[2]. Molthoff CF, Pinedo HM, Schlüper HM, Rutgers DH, Boven E. 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.

Cisplatin Dilution Calculator

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Cisplatin Molarity Calculator



Chemical Properties

Cas No. 15663-27-1 SDF Download SDF
Synonyms CDDP
Chemical Name azane;dichloroplatinum(2+)
Canonical SMILES N.N.Cl[Pt+2]Cl
Formula Cl2H6N2Pt M.Wt 300.05
Solubility ≥12.5mg/mL in DMF
Cisplatin cannot be dissolved in DMSO (DMSO will inactivate platinum-containing compounds)
Storage Store at RT
It is recommended to store in the form of powder in the dark, the solution is very unstable (Prepare Solution fresh and use at room temperature)
Shipping Condition Evaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.


Cisplatin is a highly effective and broad-spectrum chemotherapeutic agent [1].

Cisplatin is an anticancer agent with some side effects. It is believed to induce apoptosis through several mechanisms. The traditional mechanism is that cisplatin enters the cell, interacts with the DNA guanine bases and forms the inter- or intra-strand chain cross-linking, then prevents the replication of DNA. This formation can also induce apoptosis by activating p53. Cisplatin was also found to cause ROS generation and increase lipid peroxidation, which leads cells to the apoptotic pathway. In addition, cisplatin induces apoptosis with the caspase-dependent pathway. In cochlear cells, cisplatin treatment results in the increase of caspases-3 and -9 and causes the cochlear damage side effect [1].

[1] Casares C, Ramírez-Camacho R, Trinidad A, et al. Reactive oxygen species in apoptosis induced by cisplatin: review of physiopathological mechanisms in animal models. European Archives of Oto-Rhino-Laryngology, 2012, 269(12): 2455-2459.