Cisplatin

Katalognr.S1166 Batch:S116618

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Tekniska data

Formel

Cl2H6N2Pt
Molekylvikt 300.05 CAS-nr. 15663-27-1
Löslighet (25°C)* In vitro DMF 15 mg/mL (49.99 mM)
Water Insoluble
Ethanol Insoluble
In Vivo (Tillsätt lösningsmedel till produkten individuellt och i ordning.)
Clear solution
5%DMF 40%PEG300 5%Tween80 50%ddH2O

Validerad av Selleck-laboratorier. Om du behöver justeringar av denna formulering, kontakta vårt säljteam för skräddarsydd testning.

 0.750mg/ml (2.50mM) Taking the 1 mL working solution as an example, add 50 μL 15 mg/ml clarified DMF stock solution to 400 μL PEG300, mix evenly to clarify it; add 50 μL Tween80 to the above system, mix evenly to clarify it; then continue to add 500 μL ddH2O to adjust the volume to 1 mL. The mixed solution should be used immediately for optimal results. 
* <1 mg/ml betyder svårlösligt eller olösligt.
* Vänligen notera att Selleck testar lösligheten för alla förbindelser internt, och den faktiska lösligheten kan skilja sig något från publicerade värden. Detta är normalt och beror på små variationer mellan olika partier.
* Rumstempererad frakt (Stabilitetstester visar att denna produkt kan fraktas utan några kylåtgärder.)

Beredning av stamlösningar

Biologisk aktivitet

Beskrivning Cisplatin är ett oorganiskt platinakomplex, som kan hämma DNA synthesis genom att bilda DNA-addukter i tumörceller. Cisplatin aktiverar ferroptosis och inducerar autophagy.Lösningar är instabila och bör beredas färskt.DMSO rekommenderas inte för att lösa upp platinabaserade läkemedel, vilket lätt kan leda till inaktivering av läkemedlet.
Mål
DNA synthesis
(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.

This compound (30 μM) treated for 6 h induces an apparent activation of Erk in HeLa cells, which is sustained over the following 14 h period. It also shows an effective antineoplastic activity by inducing tumor cells death.

It 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.

This chemical (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. This compound (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.

Egenskaper Ett av de mest använda och mest potenta kemoterapeutiska medlen. Denna produkt rekommenderas inte att lösas i dimethylsulfoxide (DMSO).

Protokoll (från referens)

Cellanalys:

[3]
  • Cellinjer

    Leukemia L1210/0 cells

  • Koncentrationer

    7 μg/mL

  • Inkubationstid

    2 hours

  • Metod

    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 this compound as above are also diluted into 0.1% agar and allowed to grow for 2 weeks when colonies are counted.
Djurstudie:

[7]
  • Djurmodeller

    Female NMRI/Cpb (nuinu) mice

  • Doseringar

    5 mg/kg

  • Administrering

    i.v.

Referenser

  • https://pubmed.ncbi.nlm.nih.gov/14576837/
  • https://pubmed.ncbi.nlm.nih.gov/10993883/
  • https://pubmed.ncbi.nlm.nih.gov/3395999/
  • https://pubmed.ncbi.nlm.nih.gov/12065694/
  • https://pubmed.ncbi.nlm.nih.gov/8967349/
  • https://pubmed.ncbi.nlm.nih.gov/1563830/
  • https://pubmed.ncbi.nlm.nih.gov/24812268/
  • https://pubmed.ncbi.nlm.nih.gov/28494534/

Kundvalidering av produkt

<p>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.</p>

Data från [ Cancer Res , 2014 , 74(1), 298-308 ]

Data från [ PLoS One , 2013 , 8(1), e54595 ]

<p> </p><p>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. </p>

, 2013 , Dr. Edita Aksamitiene from Thomas Jefferson University

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).

Data från [ , , Curr Cancer Drug Targets, 2016, 16(7):631-8 ]

Sellecks Cisplatin Har citerats av 877 Publikationer

Regularized Single-Cell Imaging Enables Generalizable AI Models for Stain-Free Cell Viability Screening [ Small Methods, 2026, 10(4):e01369] PubMed: 41574984
Fra-2 controls the response to the KRAS inhibitor MRTX-1133 in pancreatic ductal adenocarcinoma [ Proc Natl Acad Sci U S A, 2026, 123(18):e2601788123] PubMed: 42054368
WEE1 stabilizes MYC to promote therapeutic resistance in esophageal adenocarcinoma [ Cancer Lett, 2026, 646:218418] PubMed: 41812823
Deciphering 14-3-3β-mediated phosphorylated alterations of cancer-related proteome in cisplatin resistance of gastric cancer [ Int J Biol Macromol, 2026, 358:151711] PubMed: 41905699
Preclinical evaluation of progesterone combined with EDP-M scheme in 2D and 3D models of adrenocortical carcinoma [ Biomed Pharmacother, 2026, 196:119090] PubMed: 41671730
Trefoil Factor-3 Is a Hypoxia-Triggered Pro-Tumorigenic Factor in Hepatoblastoma [ Liver Int, 2026, 46(4):e70592] PubMed: 41823075
A Comprehensive Adenoid Cystic Carcinoma-Derived Organoid Platform for Disease Modeling and Drug Screening Captures Interpatient Heterogeneity [ Cells, 2026, 15(4)383] PubMed: 41744826
Mathematical modeling of ribosome competition informs testable treatment strategies for drug-tolerant cancer persister cells [ iScience, 2026, 29(4):115493] PubMed: 42006289
KRAB Zinc-Finger Protein ZNF205 Promotes Hepatocellular Carcinoma via p53 Pathway Repression [ Cancer Sci, 2026, 117(4):1057-1071] PubMed: 41668275
Growth hormone receptor antagonism improves tumoral chemo-immunotherapy response in a mouse model of lung cancer [ Transl Oncol, 2026, 68:102787] PubMed: 42061046

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