Cisplatin (NSC 119875)

For research use only. Not for use in humans.

製品コードS1166 別名:Cisplatinum, cis-diamminedichloroplatinum II, CDDP, cis DDP, DDP

Cisplatin (NSC 119875)化学構造

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.

サイズ 価格(税別)  
JPY 12000
JPY 16200
JPY 34900

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DNA/RNA Synthesis阻害剤の選択性比較


製品説明 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.
特性 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)

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 Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
Human osteosarcoma cells (HOS, 143B, U2OS and MG‑63) NGTDfmZE\WyuIHP5Z4xmKGGwYXz5d4l{ M{i0TFIh|ryP NVvjZm01PDhiaB?= NFuzSFJEcXOybHH0bY4hfHKnYYTt[Y51KG2jcnvl[Ix6KGmwY4LlZZNm\CC2aHWgS|IwVSCyb4D1cIF1cW:wIHnuJIFtdCClZXzsJIxqdmW|Lh?= MV[8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8{OTB3OUC4N{c,OzFyNUmwPFM9N2F-
OVC cells (A2780, TOV-112D, and cis-A2780) NFL1dXJE\WyuIFP5eI91d3irY3n0fUBCe3OjeR?= M{TEZlAvPSxiMTygNk42NCB3LDCxNEwhOjBuIHHu[EA2OCEQvF2= MWK0PEBp MmDxR49u[mmwYYTpc44hd2ZiY3nzdIxifGmwIHHu[EBOTUtiaX7obYJqfG:{IHPvZolu\XSrbnniJEgyOCCwTTmg[Y5p[W6lZYOgZ4VtdCCmZXH0bEBqdiC2aILl[UBwfmG{aXHuJINidmOncjDj[YxtKGyrbnXzJEhCOjd6MDygWG9XNTFzMlSsJIFv\CClaYOtRVI4QDBrLh?= NGXw[pI9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9|MUC1O|YyOSd-M{GwOVc3OTF:L3G+
HCC cell lines HepG2 and Huh7 NFvUZYNE\WyuII\pZYJqdGm2eTDhd5NigQ>? M3r6cVAuOzBizszN NIK5e|Y1QCCq M{\LXGNFOTN|KzDIR2Mh[2WubIOg[ZhpcWKrdDDy[ZNqe3SjbnPlJJRwKGOrc4DsZZRqdi5? Mkj0QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOzFyNU[1N|IoRjNzMEW2OVMzRC:jPh?=
Saos-2 cells M{e2[5FJXFNib3[gdIVlcWG2cnnjJINidmOncjDj[YxtKGyrbnXzJJRwKGmmZX70bYZ6KG23bITpdIxmKG:ycH;yeJVvcXSrZYOg[o9zKGS{dXegdoVxfXKyb4Ppcoc7KFC{aX3hdpkhe2O{ZXXuJIZweiCVYX;zMVIh[2WubIO= MW[8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTR|NUGzPUc,Ojl2M{WxN|k9N2F-
OHS-50 cells NVi5OYJNeUiWUzDv[kBx\WSrYYTybYMh[2GwY3XyJINmdGxibHnu[ZMhfG9iaXTlcpRq\nlibYXseIlxdGVib4Dwc5J1fW6rdHnld{Bnd3JiZIL1[{Bz\XC3coDvd4lv\zpiUILpcYFzgSC|Y4Ll[Y4h\m:{IF;IV{02OCClZXzsdy=> NHPjR4g9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUSzOVE{QSd-Mkm0N|UyOzl:L3G+
SK-N-MC cells MlLpdWhVWyCxZjDw[YRq[XS{aXOgZ4Fv[2W{IHPlcIwhdGmwZYOgeI8hcWSnboTp[pkhdXWudHnwcIUhd3Cyb4L0eY5qfGmnczDmc5Ih\HK3ZzDy[ZB2enCxc3nu[|ohWHKrbXHyfUB{[3KnZX6g[o9zKFONLV6tUWMh[2WubIO= M4jwVVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7NEO1NVM6Lz5{OUSzOVE{QTxxYU6=


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. 


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]




- 合併
  • 細胞株: Leukemia L1210/0 cells
  • 濃度: 7 μg/mL
  • 反応時間: 2 hours
  • 実験の流れ:

    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.


溶解度 (25°C)

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

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程で起きる正常な現象ですからご安心ください。


分子量 300.05


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


投与量 mg/kg 動物平均体重 g 投与体積(動物毎) ul 動物数
% DMSO % % Tween 80 % ddH2O





質量 (mg) = 濃度 (mM) x 体積 (mL) x 分子量 (g/mol)


  • 質量





開始濃度 x 開始体積 = 最終濃度 x 最終体積


この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 入力 出力 )

  • C1



  • 連続希釈剤

  • 計算結果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):




チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2


質量 濃度 体積 分子量



Handling Instructions


  • * 必須


  • 質問1:

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

  • 回答:

    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.

DNA/RNA Synthesisシグナル伝達経路

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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID