Home DNA Damage/DNA Repair DNA/RNA Synthesis chemical - Ferroptosis activator - Autophagy activator Cisplatin

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Cisplatin DNA Synthesis inhibitor

Cat.No.S1166

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 DNA/RNA Synthesis chemical Chemical Structure

Chemical Structure

Molecular Weight: 300.05

Jump to Mechanism of Action Cell Culture & Working Concentration Solubility Chemical Information, Storage & Stability Specificity

Quality Control

Products Often Used Together with Cisplatin

Ceralasertib (AZD6738)

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

Berzosertib (VE-822)

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

Elimusertib (BAY-1895344)

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

Cell Culture, Treatment & Working Concentration

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

Chemical Information, Storage & Stability

Molecular Weight 300.05 Formula

Cl2H6N2Pt

 Storage (From the date of receipt) 2 years 4°C(in the dark) powder
CAS No. 15663-27-1 Download SDF Storage of Stock Solutions Solutions are unstable. Prepare fresh or purchase small, pre-packaged sizes. Repackage upon receipt.
Synonyms NSC 119875, Cisplatinum, cis-diamminedichloroplatinum II, CDDP, cis DDP, DDP Smiles [NH2-].[NH2-].Cl[Pt+2]Cl

Solubility

In vitro
Batch:

DMF : 15 mg/mL

Water : Insoluble

Ethanol : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
Batch:

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)

mg/kg g μL

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% DMSO % % Tween 80 % ddH2O
%DMSO %

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Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such
as vortex, ultrasound or hot water bath can be used to aid dissolving.

Mechanism of Action

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/IC50/Ki
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]

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[2].

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. [4]

This chemical (800 μM) causes typical features of necrosis of RPTC after treatment for 4 hr. [5]
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. [6]
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/12065694/
  • [5] https://pubmed.ncbi.nlm.nih.gov/8967349/
  • [6] https://pubmed.ncbi.nlm.nih.gov/1563830/
  • [7] https://pubmed.ncbi.nlm.nih.gov/24812268/
  • [8] https://pubmed.ncbi.nlm.nih.gov/28494534/

Applications

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 S1166-WB1 20651982
Immunofluorescence H2A.X / RPA γ-H2A.X / 53BP1 N-cadherin / E-cadherin / Vimentin LC3B S1166-IF1 28993682
Growth inhibition assay Cell viability S1166-viability1 26062553

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT06356155 Not yet recruiting
Urothelial Carcinoma
University of Michigan Rogel Cancer Center
 October 2024 Phase 2
NCT06393816 Not yet recruiting
Large Cell Neuroendocrine Carcinoma of the Lung
Centre Leon Berard|Groupe Français de Pneumo-Cancérologie
 May 2024 Phase 2
NCT06406465 Not yet recruiting
Carcinoma Neuroendocrine|Tumor Neuroendocrine|Tumors Neuroendocrine|Neuroendocrine; Carcinoma|Small Cell; Receptors
National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)
 May 15 2024 Phase 2
NCT04915183 Recruiting
Hearing Loss|Head and Neck Cancer
National Institute on Deafness and Other Communication Disorders (NIDCD)|National Institutes of Health Clinical Center (CC)
 May 15 2024 Phase 2

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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 it at up to 3mg/ml is recommended. It's a suspension and can be administrated via oral gavage.

Signaling Pathway Map