Cisplatin

Synonyms: NSC 119875, Cisplatinum, cis-diamminedichloroplatinum II, CDDP, cis DDP, DDP

Cisplatin is an inorganic platinum complex, which is able to inhibit DNA synthesis by conforming DNA adducts in tumor cells. Cisplatin activates ferroptosis and induces autophagy.Solutions are unstable and should be fresh-prepared.DMSO is not recommended to dissolve platinum-based drugs, which can easily lead to drug inactivation.

Cisplatin Chemical Structure

Cisplatin Chemical Structure

CAS: 15663-27-1

Selleck's Cisplatin has been cited by 680 publications

Purity & Quality Control

Batch: Purity: 99.84%
99.84

Products often used together with Cisplatin

Ceralasertib (AZD6738)


Explores the combined effect that potentiates the anti-tumor effects of cisplatin to resolve ATM-deficient non-small cell lung cancer in vivo

Vendetti FP, et al. Oncotarget. 2015 Dec 29; 6(42): 44289–44305.

Olaparib (AZD2281)


Cisplatin in combination with olaparib exhibits the significant synergistic effect in inhibiting the proliferation of the ovarian cancer cells.

Gao J, et al. Exp Ther Med. 2021;22(3):935.

Berzosertib (VE-822)


Berzosertib (VX-970), when given in combination with cisplatin, enhances the efficacy of cisplatin in patient-derived lung tumour xenografts.

Hall AB, et al. Oncotarget. 2014;5(14):5674-5685.

Durvalumab (anti-PD-L1)


Cisplatin in combination with durvalumab can show a synergistic effect in small-cell lung cancer (SCLC).

Tsvetkova D, et al. Molecules. 2022;27(8):2466. Published 2022 Apr 11.

Elimusertib (BAY-1895344)


Combination treatment with BAY 1895344 and cisplatin achieved strong synergistic activity on the proliferation of human HT-29 colorectal cancer cells in vitro.

Wengner AM, et al. Mol Cancer Ther. 2020 Jan;19(1):26-38.

Cisplatin Related Products

Choose Selective DNA/RNA Synthesis Inhibitors

Cell Data

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
Human osteosarcoma cells (HOS, 143B, U2OS and MG‑63) Cell cycle analysis 2 μM 48 h Cisplatin treatment markedly increased the G2/M population in all cell lines. 31059083
OVC cells (A2780, TOV-112D, and cis-A2780) Cell Cytotoxicity Assay 0.5, 1, 2.5, 5, 10, 20, and 50 μM 48 h Combination of cisplatin and MEK inhibitor cobimetinib (10 nM) enhances cell death in three ovarian cancer cell lines (A2780, TOV-112D, and cis-A2780). 31057611
HCC cell lines HepG2 and Huh7 Cell viability assay 0-30 μM 48 h CD133+ HCC cells exhibit resistance to cisplatin. 31056532
Saos-2 cells qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells 29435139
OHS-50 cells qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells 29435139
SK-N-MC cells qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells 29435139
Click to View More Cell Line Experimental Data

Biological Activity

Description Cisplatin is an inorganic platinum complex, which is able to inhibit DNA synthesis by conforming DNA adducts in tumor cells. Cisplatin activates ferroptosis and induces autophagy.Solutions are unstable and should be fresh-prepared.DMSO is not recommended to dissolve platinum-based drugs, which can easily lead to drug inactivation.
Features One of the most widely used and most potent chemotherapeutic agents. This product is not recommended to be dissolved in dimethylsulfoxide (DMSO).[7]
Targets
DNA synthesis [1]
(Tumor cells)
In vitro
In vitro

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. [1]

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[2].

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. [4]

Cisplatin (800 μM) causes typical features of necrosis of RPTC after treatment for 4 hr. [5]

Cell Research Cell lines Leukemia L1210/0 cells
Concentrations 7 μg/mL
Incubation Time 2 hours
Method

L1210/0 cells are maintained in an exponential suspension culture at 37 ℃ in a humidified atmosphere of 5% CO2 in McCoy's medium 5a (modified), supplemented with 15% calfserum, and Fungizone. L1210/0 cells are incubated in Cisplatin (7 μg/mL) for 2 hr at 37 ℃. To measure growth inhibition, the cells are centrifuged, washed once, resuspended in fresh medium at 30 × 103 to 50 × 103 cells/mL, and incubated for 3 days. Cell numbers are determined on a Coulter Counter. An aliquot of cells is diluted with an equal volume of 0.4% trypan blue. Viability is recorded as the percentage of cells that has excluded trypan blue. Cells incubated with Cisplatin as above are also diluted into 0.1% agar and allowed to grow for 2 weeks when colonies are counted.

Experimental Result Images Methods Biomarkers Images PMID
Western blot ATF3 FEN1 PD-L1 / p-MEK / MEK / p-STAT3 / STAT3 LC3B-I / LC3B-II / Beclin-1 p-AMPK / AMPK / p-mTOR / mTOR 20651982
Immunofluorescence H2A.X / RPA γ-H2A.X / 53BP1 N-cadherin / E-cadherin / Vimentin LC3B 28993682
Growth inhibition assay Cell viability 26062553
In Vivo
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. [6]

Animal Research Animal Models Female NMRI/Cpb (nuinu) mice
Dosages 5 mg/kg
Administration i.v.
NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT04915183 Not yet recruiting
Hearing Loss|Head and Neck Cancer
National Institute on Deafness and Other Communication Disorders (NIDCD)|National Institutes of Health Clinical Center (CC)
January 12 2024 Phase 3
NCT06086288 Not yet recruiting
Merkel Cell Carcinoma
Fondazione IRCCS Istituto Nazionale dei Tumori Milano
November 2023 Phase 2
NCT04402593 Withdrawn
Relapsed Germ Cell Cancer|Cisplatin Induced Tinnitus
Indiana University
September 2023 Not Applicable
NCT05946577 Not yet recruiting
Head Cancer|Neck Cancer
Assistance Publique - Hôpitaux de Paris
July 2023 --

Chemical Information & Solubility

Molecular Weight 300.05 Formula

Cl2H6N2Pt

CAS No. 15663-27-1 SDF Download Cisplatin SDF
Smiles [NH2-].[NH2-].Cl[Pt+2]Cl
Storage (From the date of receipt) 2 years 4°C(in the dark) powder Solutions are unstable. Prepare fresh or purchase small, pre-packaged sizes. Repackage upon receipt.

In vitro
Batch:

DMF : 15 mg/mL

Water : Insoluble

Ethanol : Insoluble


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In vivo
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Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

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Frequently Asked Questions

Question 1:
What is the appropriate concentration of DMF for cell culture and animal study?

Answer:
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.

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