Cisplatin

製品コードS1166

Cisplatin化学構造

分子量(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, compared with DMSO.

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文献中Selleckの製品使用例(189)

製品安全説明書

DNA/RNA Synthesis阻害剤の選択性比較

生物活性

製品説明 Cisplatin is an inorganic platinum complex, which is able to inhibit DNA synthesis by conforming DNA adducts in tumor cells. DMF is recommended, compared with DMSO.
特性 One of the most widely used and most potent chemotherapeutic agents.
ターゲット
DNA synthesis [1]
(Tumor cells)
体外試験

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]
細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
Human osteosarcoma cells (HOS, 143B, U2OS and MG‑63) NUDweplYS2WubDDjfYNt\SCjbnHsfZNqew>? NYrCU|I{OiEQvF2= MkP3OFghcA>? MXnDbZNxdGG2aX6geJJm[XSvZX70JI1iemunZHz5JIlv[3KnYYPl[EB1cGViR{KvUUBxd3C3bHH0bY9vKGmwIHHscEBk\WyuIHzpcoV{Ng>? MlvxN|ExPTlyOEO=
OVC cells (A2780, TOV-112D, and cis-A2780) MVHD[YxtKEO7dH;0c5hq[2m2eTDBd5NigQ>? MVWwMlUtKDFuIEKuOUwhPSxiMUCsJFIxNCCjbnSgOVAh|ryP MoHROFghcA>? NEPvOWxEd22kaX7heIlwdiCxZjDjbZNxdGG2aX6gZY5lKE2HSzDpcohq[mm2b4KgZ49jcW2ndHnubYIhMDFyIH7NLUBmdmijbnPld{Bk\WyuIHTlZZRpKGmwIITodoVmKG:4YYLpZY4h[2GwY3XyJINmdGxibHnu[ZMhMEF{N{iwMEBVV1ZvMUGySEwh[W6mIHPpd{1COjd6MDmu M4mx[|MyODV5NkGx
HCC cell lines HepG2 and Huh7 NUG5PFY6S2WubDD2bYFjcWyrdImgZZN{[Xl? MYCwMVMxKM7:TR?= M3HGbVQ5KGh? M3vXVWNFOTN|KzDIR2Mh[2WubIOg[ZhpcWKrdDDy[ZNqe3SjbnPlJJRwKGOrc4DsZZRqdi5? M4K5fFMyODV4NUOy

他の多くの細胞株試験データをご覧になる場合はこちらをクリックして下さい

アッセイ
Methods Test Index PMID
Western blot
ATF3; 

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.

FEN1; 

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
Immunofluorescence
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.

LC3B; 

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. 

26062553
体内試験 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]

お薦めの試験操作（参考用のみ）

細胞試験：

[3]
- 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.


    (参考用のみ)

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。

化学情報

分子量 300.05
化学式

Cl2H6N2Pt
CAS No. 15663-27-1
保管 粉
in solvent（毎回新しく調製した物を用意してください）
別名 N/A

便利ツール

モル濃度計算器

モル濃度計算器

求めたい質量、体積または濃度を計算してください。

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

モル濃度計算器方程式

  • 質量
    濃度
    体積
    分子量

*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA（製品ページで利用可能な）。

希釈計算器

希釈計算器

貯蔵液を準備するために必要な希釈率を計算してください。Selleck希釈計算器は、以下の方程式に基づきます：

開始濃度 x 開始体積 = 最終濃度 x 最終体積

希釈の計算式

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

  • C1
    V1
    C2
    V2

常に貯蔵液を準備するとき、小びんラベルとMSDS/COA（オンラインで利用できる）で見つかる製品のバッチに特有の分子量を使ってください。

連続希釈計算器方程式

  • 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):
分子量計算器

分子量计算器

そのモル質量と元素組成を計算するために、合成物の化学式を入力してください：

総分子量：g/mol

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

モル濃度計算器

質量 濃度 体積 分子量

臨床試験

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04000906 Not yet recruiting Drug: NAB paclitaxel|Drug: Cisplatin Peritoneal Carcinomatosis University Hospital Geneva September 2019 Phase 1
NCT03817970 Recruiting Drug: Granisetron|Drug: Ondansetron|Drug: Palonosetron Nephrotoxicity University of Colorado Denver|Memorial Sloan Kettering Cancer Center|Rutgers University|National Institute of General Medical Sciences (NIGMS) June 26 2019 Not Applicable
NCT03918382 Recruiting Other: Electronic Patient-Reported Outcome Head and Neck Cancer|Radiotherapy Side Effect Rigshospitalet Denmark|Danish Comprehensive Cancer Center|Danish Cancer Society|University of Copenhagen|Danish Head and Neck Cancer Group|Herlev Hospital|Zealand University Hospital|Odense University Hospital|Aalborg University Hospital|Aarhus University Hospital June 13 2019 Not Applicable
NCT03644589 Withdrawn Biological: Pembrolizumab|Drug: Cisplatin Estrogen Receptor Negative|HER2/Neu Negative|Metastatic Breast Cancer|Progesterone Receptor Negative|Recurrent Breast Carcinoma|Triple Negative Breast Cancer University of Washington|Merck Sharp & Dohme Corp. April 1 2019 Phase 2
NCT03773302 Recruiting Drug: BGJ398|Drug: Gemcitabine|Drug: Cisplatin Advanced Cholangiocarcinoma|FGFR2 Gene Mutation QED Therapeutics Inc. April 2019 Phase 3

技術サポート

ストックの作り方、阻害剤の保管方法、細胞実験や動物実験の際に注意すべき点など、製品を取扱う時に問い合わせが多かった質問に対しては取扱説明書でお答えしています。

Handling Instructions

他に質問がある場合は、お気軽にお問い合わせください。

  • * 必須

よくある質問（FAQ）

  • 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.

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Tags: Cisplatinを買う | Cisplatin ic50 | Cisplatin供給者 | Cisplatinを購入する | Cisplatin費用 | Cisplatin生産者 | オーダーCisplatin | Cisplatin化学構造 | Cisplatin分子量 | Cisplatin代理店
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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