Molecular Weight(MW): 300.05
Cisplatin is an inorganic platinum complex, which is able to inhibit DNA synthesis by conforming DNA adducts in tumor cells. DMF is recommended for dissolution.
Cited by 28 Publications
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Cell viabilities with increasing concentrations of cisplatin (CP) and doxorubicin (DOXO) under normoxic and hypoxic condition for 48 hours were determined by MTT assay. IC50 values are presented as the means ?SDs (n=4) and * denotes p<0.05.
Cancer Res 2014 74(1), 298-308. Cisplatin purchased from Selleck.
RH4 cells were stably transfected with STAT3-C vector. The expression of Flag-tagged STAT3 was examined in STAT3-C stably transfected RH4 and RH5 cells by western blot. (B) The inhibition of cell viability by cisplatin and doxorubicin in RH4 (B) cells was decreased in the presence of STAT3-C protein shown by MTT assay (*P<.05, ** P <.01, *** P <.001).
Curr Cancer Drug Targets, 2016, 16(7):631-8. Cisplatin purchased from Selleck.
Influence of miR-193a-5p and AP-2α on cisplatin sensitivity. UM-UC-3 cells were infected with lentiviral miR-193a-5p inhibitor or AP-2α gene. At 72h after transduction, cells were seeded on 96-well plates and treated with different concentration of cisplatin for 36 h. The cell viability was determined by MTT assay.
J Cancer, 2016, 7(12):1740-1746. Cisplatin purchased from Selleck.
Growth inhibitory effects of Cisplatin human pancreatic cancer cells. Capan-2 cells were plated in triplicates into 48-well plates at a density of 10,000 cells/ml. After 24 hours, complete culture medium was changed into fresh low-serum-containing medium (1% FBS) containing DMSO (control) or indicated doses of Cisplatin (Selleckchem). Cell viability 72 hours after treatment was determined by AlamarBlue assay (Invitrogen) according to manufacturer's instructions. Results are expressed as percentages of control, which was arbitrarily assigned 100% viability, and represented as the mean ± standard deviation (SD) of the tripicate wells.
2013 Dr. Edita Aksamitiene from Thomas Jefferson University. Cisplatin purchased from Selleck.
Purity & Quality Control
Choose Selective DNA/RNA Synthesis Inhibitors
|Description||Cisplatin is an inorganic platinum complex, which is able to inhibit DNA synthesis by conforming DNA adducts in tumor cells. DMF is recommended for dissolution.|
|Features||One of the most widely used and most potent chemotherapeutic agents.|
Cisplatin induces cytotoxic by interaction with DNA to form DNA adducts which activate several signal transduction pathways, including Erk, p53, p73, and MAPK, which culminates in the activation of apoptosis.  Cisplatin (30 μM) treated for 6 h induces an apparent activation of Erk in HeLa cells, which is sustained over the following 14 h period. Cisplatin also shows an effective antineoplastic activity by inducing tumor cells death. Cisplatin displays ability to cause renal proximal tubular cell (RPTC) apoptosis, 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.  Cisplatin (800 μM) causes typical features of necrosis of RPTC after treatment for 4 hr. 
|In vivo||Cisplatin has been demonstrated to be efficient in regression tumor growth in a wide variety of animal tumors models, including head and neck cancer xenografts, cervical squamous carcinoma xenografts, testicular carcinoma xenografts, ovarian cancer xenografts, breast carcinoma xenografts, colonic carcinoma, heterotransplanted hepatoblastoma, and so on. Cisplatin (5 mg/kg) given weekly i.v. at the day 1 and 7 induces a tumor growth inhibition (GI) of 77.5% and 85.1% of the serous xenografts Ov.Ri(C) and OVCAR-3, respectively. |
-  Siddik ZH. Oncogene, 2003, 22(47), 7265-7279.
-  Wang X, et al. J Biol Chem, 2000, 275(50), 39435-39443.
-  Sorenson CM, et al. Cancer Res, 1988, 48(16), 4484-4488.
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03673735||Not yet recruiting||Squamous Cell Head and Neck Carcinoma||European Organisation for Research and Treatment of Cancer - EORTC||March 2019||Phase 3|
|NCT03737994||Not yet recruiting||ALK Gene Rearrangement|ALK Positive|Non-Squamous Non-Small Cell Lung Carcinoma|Stage IV Lung Cancer AJCC v8|Stage IVA Lung Cancer AJCC v8|Stage IVB Lung Cancer AJCC v8||National Cancer Institute (NCI)||January 13 2019||Phase 2|
|NCT03700476||Not yet recruiting||Nasopharyngeal Neoplasms||Sun Yat-sen University|Innovent Biologics (Suzhou) Co. Ltd.||January 2019||Phase 3|
|NCT03619824||Not yet recruiting||Nasopharyngeal Neoplasms||Sun Yat-sen University|Innovent Biologics (Suzhou) Co. Ltd.||January 2019||Phase 2|
|NCT03631199||Not yet recruiting||Non-small Cell Lung Cancer||Novartis Pharmaceuticals|Novartis||January 14 2019||Phase 3|
|NCT03058094||Not yet recruiting||NSCLC||Hangzhou ACEA Pharmaceutical Research Co.Ltd.|Cancer Institute and Hospital Chinese Academy of Medical Sciences||December 2018||Phase 3|
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Frequently Asked Questions
What is the appropriate concentration of DMF for cell culture and animal study?
It depends on the cell type. The final concentration of DMF should be better limited to less than 0.1% if possible, or below 1%. Using saline as a vehicle for cisplatin at up to 3mg/ml is recommended. it's a suspension and can be administrated via oral gavage.