Cisplatin (NSC 119875)

For research use only.

Catalog No.S1166 Synonyms: Cisplatinum, cis-diamminedichloroplatinum II, CDDP, cis DDP, DDP

447 publications

Cisplatin (NSC 119875) Chemical Structure

CAS No. 15663-27-1

Cisplatin (NSC 119875, Cisplatinum, cis-diamminedichloroplatinum II, CDDP, cis DDP, DDP) 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 best fresh-prepared.

Selleck's Cisplatin (NSC 119875) has been cited by 447 publications

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Description Cisplatin (NSC 119875, Cisplatinum, cis-diamminedichloroplatinum II, CDDP, cis DDP, DDP) 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 best fresh-prepared.
Features One of the most widely used and most potent chemotherapeutic agents. This product is not recommended to be dissolved in dimethylsulfoxide (DMSO).[7]
DNA synthesis [1]
(Tumor cells)
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 Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
Human osteosarcoma cells (HOS, 143B, U2OS and MG‑63) NXHjVWU6S2WubDDjfYNt\SCjbnHsfZNqew>? M1vXWVIh|ryP NGDYfmc1QCCq MmPmR4l{eGyjdHnuJJRz\WG2bXXueEBu[XKtZXTsfUBqdmO{ZXHz[YQhfGinIFeyM20heG:ydXzheIlwdiCrbjDhcIwh[2WubDDsbY5mey5? NG\zdFQ9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9|MUC1PVA5Oyd-M{GwOVkxQDN:L3G+
OVC cells (A2780, TOV-112D, and cis-A2780) M{n6b2NmdGxiQ4n0c5RwgGmlaYT5JGF{e2G7 M4niSFAvPSxiMTygNk42NCB3LDCxNEwhOjBuIHHu[EA2OCEQvF2= NGHodFU1QCCq M3G4e2NwdWKrbnH0bY9vKG:oIHPpd5Bt[XSrbjDhcoQhVUWNIHnubIljcXSxcjDjc4JqdWW2aX7pZkApOTBibl2pJIVvcGGwY3XzJINmdGxiZHXheIghcW5idHjy[YUhd3[jcnnhckBk[W6lZYKgZ4VtdCCuaX7ld{ApSTJ5OECsJHRQXi1zMULEMEBidmRiY3nzMWEzPzhyKT6= NIj0UHI9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9|MUC1O|YyOSd-M{GwOVc3OTF:L3G+
HCC cell lines HepG2 and Huh7 M2PHNWNmdGxidnnhZoltcXS7IHHzd4F6 MnTQNE0{OCEQvF2= M{mz[FQ5KGh? M4H3S2NFOTN|KzDIR2Mh[2WubIOg[ZhpcWKrdDDy[ZNqe3SjbnPlJJRwKGOrc4DsZZRqdi5? NXzye4p4RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxM{GwOVY2OzJpPkOxNFU3PTN{PD;hQi=>
Saos-2 cells NELpWlZyUFSVIH;mJJBm\GmjdILpZ{Bk[W6lZYKgZ4VtdCCuaX7ld{B1dyCrZHXueIlngSCvdXz0bZBt\SCxcIDvdpR2dmm2aXXzJIZweiCmcoXnJJJmeHW{cH;zbY5oQiCScnntZZJ6KHOlcnXlckBnd3JiU3Hvd{0zKGOnbHzz NETkVWk9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUSzOVE{QSd-Mkm0N|UyOzl:L3G+
OHS-50 cells MUXxTHRUKG:oIIDl[IlifHKrYzDjZY5k\XJiY3XscEBtcW6nczD0c{Bq\GWwdHnmfUBufWy2aYDs[UBweHCxcoT1col1cWW|IH\vdkBlenWpIILldJVzeG:|aX7nPkBRemmvYYL5JJNkemWnbjDmc5IhV0iVLUWwJINmdGy| NHX6Rmc9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUSzOVE{QSd-Mkm0N|UyOzl:L3G+
SK-N-MC cells MUDxTHRUKG:oIIDl[IlifHKrYzDjZY5k\XJiY3XscEBtcW6nczD0c{Bq\GWwdHnmfUBufWy2aYDs[UBweHCxcoT1col1cWW|IH\vdkBlenWpIILldJVzeG:|aX7nPkBRemmvYYL5JJNkemWnbjDmc5IhW0tvTj3NR{Bk\Wyucx?= NHT4TVM9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUSzOVE{QSd-Mkm0N|UyOzl:L3G+

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot

PubMed: 20651982     

ATF3 protein expression levels after treatment with low and cytotoxic doses of cisplatin (1 and 10 µg/ml) and carboplatin (27 and 270 µg/ml) in SKOV-3, MCF-7, PC3, A2780-cp, and A549 cell lines.


PubMed: 29541412     

MCF-7, BT-474, and MDA-MB-231 cells were treated with increasing concentrations of cisplatin for 24 h, and FEN1 protein expression was analyzed by western blotting.

PD-L1 / p-MEK / MEK / p-STAT3 / STAT3; 

PubMed: 29228662     

Expression of PD-L1, phosphor-MEK (p-MEK), total MEK, phosphor-STAT3 (p-STAT3), and total STAT3 in HNSCC cells was measured by western blotting. Cisplatin treatment increased PD-L1 and p-MEK expression.

LC3B-I / LC3B-II / Beclin-1; 

PubMed: 26715839     

Cells seeded and treated with 2 μg/mL cisplatin for 0 hours (h) (control), 24, 48, and 72 hours, then subjected to Western blot analysis of LC3B and Beclin-1 expression. β-Actin used as loading control. Data showed LC3B-II accumulation and Beclin-1 upregulation in a time-dependent manner.

p-AMPK / AMPK / p-mTOR / mTOR; 

PubMed: 26715839     

A549 cells treated with 2 μg/mL cisplatin for 0 hours (h) (control), 24, 48, and 72 hours; protein extracts were subjected to Western blot analysis of p-AMPK, AMPK, p-mTOR, mTOR, and β-actin. 

20651982 29541412 29228662 26715839
H2A.X / RPA; 

PubMed: 28993682     

Representative immunofluorescence of RPA and γH2A.X foci in cisplatin and/or olaparib treated cell CC cell lines along with PARP1 silenced cell treated with cisplatin.

γ-H2A.X / 53BP1; 

PubMed: 28993682     

Representative immunofluorescence of 53BP1 foci and γH2A.X foci in indicated treatment or siRNA transfection in CC cells. Cisplatin and olaparib both induce 53BP1 foci in CC cell line but combination of both drug or cisplatin treatment in PARP1 depleted cells produces higher number of 53BP1 foci and display more number of γH2A.X foci which co-localizes with each other.

N-cadherin / E-cadherin / Vimentin ; 

PubMed: 28105207     

Cell shape was observed by phase contrast microscopy and immunocytofluorescence. Staining of E-cadherin, N-cadherin and vimentin for the two groups of cells was observed by fluorescence microscope (magnification, ×400; Scale, 25 µm). Cells treated with cisplatin had higher N-cadherin expression.


PubMed: 26715839     

A549 cells were treated with 4 μg/mL cisplatin for 24 hours and stained by indirect immunofluorescence for LC3B. Distribution of endogenous LC3B was reviewed and scored under fluorescent microscope.

28993682 28105207 26715839
Growth inhibition assay
Cell viability; 

PubMed: 26062553     

Quercetin enhanced cisplatin sensitivity of 143B. 143B cells were treated with cisplatin at 0, 2, 4, 6, 8, 10, and 12 μM for 24 h. Quercetin was dissolved in water with 0.5 % (v/v) ethanol. Water with 0.5 % ethanol was used for the control. 143B cells co-treated with 5 μM quercetin and 5 μM cisplatin showed a cisplatin IC50 of 4.21 μM, while an IC50 of 6.12 μM was observed in cisplatin treatment. In “Cisplatin + quercetin” group, cells were treated with 5 μM quercetin for 12 h before cisplatin treatment. 

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]


Cell Research:


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  • 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.

    (Only for Reference)

Solubility (25°C)

In vitro DMSO 60 mg/mL (199.96 mM)
DMF 12 mg/mL (39.99 mM)
Water Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 300.05


CAS No. 15663-27-1
Storage 2 years 4°C(in the dark) powder
Synonyms Cisplatinum, cis-diamminedichloroplatinum II, CDDP, cis DDP, DDP
Smiles [NH2-].[NH2-].Cl[Pt+2]Cl

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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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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID