Potent anticancer agent that blocks DNA synthesis. Induces apoptosis via p53-dependent and -independent mechanisms. Inhibits X-linked inhibitor of apoptosis protein (XIAP) expression and activates caspase-3. In certain glioma cell lines, sensitizes cells to TNF-α-induced apoptosis.
|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
|water||1.5||5 with gentle warming|
Preparing Stock Solutions
The following data is based on the product molecular weight 300.05. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||3.33 mL||16.66 mL||33.33 mL|
|5 mM||0.67 mL||3.33 mL||6.67 mL|
|10 mM||0.33 mL||1.67 mL||3.33 mL|
|50 mM||0.07 mL||0.33 mL||0.67 mL|
References are publications that support the biological activity of the product.
Seki et al (2000) Cisplatin (CDDP) specifically induces apoptosis via sequential activation of caspase-8, -3 and -6 in osteosarcoma. Cancer Chemother.Pharmacol. 45 199 PMID: 10663637
Duan et al (2004) Impairment of both apoptotic and cytoprotective signalings in glioma cells resistant to the combined use of cisplatin and tumor necrosis factor α. Clin.Cancer Res. 10 234 PMID: 14734475
Nomura et al (2004) Cisplatin inhibits the expression of X-linked inhibitor of apoptosis protein in human LNCaP cells. Urol.Oncology 22 453
If you know of a relevant reference for Cisplatin, please let us know.
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Keywords: Cisplatin, Cisplatin supplier, Potent, proapoptotic, anticancer, agent, activates, caspase-3, DNA-alkylating, antitumor, Caspases, Apoptosis, Inducers, Proteinases, Proteases, chemotherapeutics, CDDP, 2251, Tocris Bioscience
19 Citations for Cisplatin
Citations are publications that use Tocris products. Selected citations for Cisplatin include:
Szabova et al (2014) Pathway-specific engineered mouse allograft models functionally recapitulate human serous epithelial ovarian cancer. Cell Rep 9 e95649 PMID: 24748377
Chia et al (2017) Phenotype-driven precision oncology as a guide for clinical decisions one patient at a time. Nat Commun 8 435 PMID: 28874669
Zhang (2017) The BTK Inhibitor, Ibrutinib (PCI-32765) Overcomes Paclitaxel Resistance in ABCB1 and ABCC10 Overexpressing Cells and Tumors. Mol Cancer Ther 16 1021 PMID: 28265007
Liu and Kwiatkowski (2015) Combined CDKN1A/TP53 mutation in bladder cancer is a therapeutic target. Mol Cancer Ther 14 174 PMID: 25349305
Kathawala et al (2014) Masitinib antagonizes ATP-binding cassette subfamily C member 10-mediated paclitaxel resistance: a preclinical study. Mol Cancer Ther 13 714 PMID: 24431074
Kathawala et al (2014) Masitinib antagonizes ATP-binding cassette subfamily G member 2-mediated multidrug resistance. Int J Oncol 44 1634 PMID: 24626598
Guindon et al (2014) Optimization of a cisplatin model of chemotherapy-induced peripheral neuropathy in mice: use of vitamin C and sodium bicarbonate pretreatments to reduce nephrotoxicity and improve animal health status. Mol Pain 10 56 PMID: 25189223
Kim et al (2016) Identification of therapeutic targets applicable to clinical strategies in ovarian cancer. BMC Cancer 16 678 PMID: 27558154
Guindon et al (2013) Alterations in endocannabinoid tone following chemotherapy-induced peripheral neuropathy: effects of endocannabinoid deactivation inhibitors targeting fatty-acid amide hydrolase and monoacylglycerol lipase in comparison to reference analgesics following c Pharmacol Res 67 94 PMID: 23127915
Ibáñez et al (2012) A high throughput scintillation proximity imaging assay for protein methyltransferases. Comb Chem High Throughput Screen 15 359 PMID: 22256970
Natrajan et al (2012) Functional characterization of the 19q12 amplicon in grade III breast cancers. Breast Cancer Res 14 R53 PMID: 22433433
Kathawala et al (2015) The small molecule tyrosine kinase inhibitor NVP-BHG712 antagonizes ABCC10-mediated paclitaxel resistance: a preclinical and pharmacokinetic study. Oncotarget 6 510 PMID: 25402202
Deng et al (2012) The maintenance of cisplatin- and paclitaxel-induced mechanical and cold allodynia is suppressed by cannabinoid CB? receptor activation and independent of CXCR4 signaling in models of chemotherapy-induced peripheral neuropathy. Mol Pain 8 71 PMID: 22998838
Marcus et al (2015) Tolerance to the antinociceptive effects of chronic morphine requires c-Jun N-terminal kinase. Mol Pain 11 34 PMID: 26065412
Robinson et al (2013) RB1 status in triple negative breast cancer cells dictates response to radiation treatment and selective therapeutic drugs. PLoS One 8 e78641 PMID: 24265703
Fard et al (2013) The heterogenic final cell cycle of chicken retinal Lim1 horizontal cells is not regulated by the DNA damage response pathway. Cell Cycle 13 408 PMID: 24247150
Saja et al (2015) Triglyceride-Rich Lipoproteins Modulate the Distribution and Extravasation of Ly6C/Gr1(low) Monocytes. Cell Death Dis 12 1802 PMID: 26344769
Sun et al (2015) SOX4 contributes to the progression of cervical cancer and the resistance to the chemotherapeutic drug through ABCG2. Korean J Pain 6 e1990 PMID: 26583330
Lin et al (2015) A New Rat Model of Cisplatin-induced Neuropathic Pain. Oncotarget 28 236 PMID: 26495078
Do you know of a great paper that uses Cisplatin from Tocris? Please let us know.
Reviews for Cisplatin
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Determined the optimal dose to identify the chemoresistant population in our cell line. Cells were treated with escalating doses of cisplatin (0.01-100uM) and viability determined 4 days post treatment.
Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Cell Cycle & DNA Damage Repair Poster
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Huntington's Disease Poster
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Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.