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.
Cited by 25 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.|
|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.
|In vitro||DMF||12 mg/mL (39.99 mM)|
|Ethanol||0.01 mg/mL (0.03 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01414608||Active not recruiting||Cervical Adenocarcinoma|Cervical Adenosquamous Carcinoma|Cervical Squamous Cell Carcinoma Not Otherwise Specified|Chemotherapeutic Agent Toxicity|Cognitive Side Effects of Cancer Therapy|Psychological Impact of Cancer|Radiation Toxicity|Sexual Dysfunction and Infertility|Stage IB Cervical Cancer|Stage IIA Cervical Cancer|Stage IIB Cervical Cancer|Stage IIIB Cervical Cancer|Stage IVA Cervical Cancer||Gynecologic Oncology Group|National Cancer Institute (NCI)||January 9 2012||Phase 3|
|NCT01454102||Active not recruiting||Non-small Cell Lung Cancer||Bristol-Myers Squibb||December 9 2011||Phase 1|
|NCT03101566||Recruiting||Biliary Tract Neoplasms||University of Michigan Cancer Center||September 8 2017||Phase 2|
|NCT03067181||Recruiting||Adult Germ Cell Tumor|Childhood Extracranial Germ Cell Tumor|Childhood Germ Cell Tumor|Extragonadal Embryonal Carcinoma|Grade 2 Immature Ovarian Teratoma|Grade 3 Immature Ovarian Teratoma|Malignant Germ Cell Tumor|Stage I Ovarian Choriocarcinoma|Stage I Ovarian Embryonal Carcinoma|Stage I Ovarian Teratoma|Stage I Ovarian Yolk Sac Tumor|Stage I Testicular Choriocarcinoma AJCC v6 and v7|Stage I Testicular Embryonal Carcinoma AJCC v6 and v7|Stage I Testicular Yolk Sac Tumor AJCC v6 and v7|Stage II Ovarian Choriocarcinoma|Stage II Ovarian Embryonal Carcinoma|Stage II Ovarian Yolk Sac Tumor|Stage II Testicular Choriocarcinoma AJCC v6 and v7|Stage II Testicular Embryonal Carcinoma AJCC v6 and v7|Stage II Testicular Yolk Sac Tumor AJCC v6 and v7|Stage III Ovarian Choriocarcinoma|Stage III Ovarian Embryonal Carcinoma|Stage III Ovarian Yolk Sac Tumor|Stage III Testicular Choriocarcinoma AJCC v6 and v7|Stage III Testicular Embryonal Carcinoma AJCC v6 and v7|Stage III Testicular Yolk Sac Tumor AJCC v6 and v7|Stage IV Ovarian Choriocarcinoma|Stage IV Ovarian Embryonal Carcinoma|Stage IV Ovarian Yolk Sac Tumor|Testicular Mixed Choriocarcinoma and Embryonal Carcinoma|Testicular Mixed Choriocarcinoma and Teratoma|Testicular Mixed Choriocarcinoma and Yolk Sac Tumor||Children''s Oncology Group|National Cancer Institute (NCI)||May 8 2017||Phase 3|
|NCT01042522||Recruiting||Ovarian Granulosa Cell Tumor|Ovarian Gynandroblastoma|Ovarian Sertoli-Leydig Cell Tumor|Ovarian Sex Cord Tumor With Annular Tubules|Ovarian Sex Cord-Stromal Tumor|Ovarian Sex Cord-Stromal Tumor of Mixed or Unclassified Cell Types|Ovarian Steroid Cell Tumor||Gynecologic Oncology Group|National Cancer Institute (NCI)||February 8 2010||Phase 2|
|NCT00248495||Completed||Lung Cancer||Roswell Park Cancer Institute||June 8 2005||Phase 2|
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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.
Your datasheet said that using DMF and DMSO as solvents to prepair stock solutions of cisplatin(Cat.No.S1166) is recommended. But using DMSO as the solvent would inactivate platinium complex as the paper reported?
DMSO will inactivate platin-containing compounds. DMF is a much better choice than DMSO so you can dissolve cisplatin in DMF at up to 12mg/ml. It can also be dissolve in water at 0.01mg/ml.