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Catalog No.: GC11908

Cisplatin is one of the best and first metal-based chemotherapeutic drugs, which is used for wide range of solid cancers such as testicular, ovarian, bladder, lung, cervical, head and neck cancer, gastric cancer and some other cancers.

Cisplatin Chemical Structure

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Cell experiment [1]:

Cell lines

H69 SCLC cells

Reaction Conditions

H69 SCLC cells were treated with100 ng/ml cisplatin, to produce the H69-CP or 200 ng/ml cisplatin to obtain the H69CIS200 cells. These doses are below an IC50 for cisplatin and are within the range achieved in the clinical use of cisplatin.


The cells were 2- to 4-fold resistant to cisplatin, which could be used to further study the resistance mechanism.

Animal experiment [2]:

Animal models

Adult male Wistar rats, weighing 160-200 g

Preparation Method

The rats were kept at 25 °C on a 12/12 h light/dark cycle, in single plastic cages with bedding, with access to standard rat food and water ad libitum. Rats were randomly assigned to one of three groups: 1) Control group, who received no intervention and maintained a regular diet; 2) Gentamicin group, who were administered 100 mg/kg BW IP gentamicin daily for 7 days; 3) Cisplatin group, who were administered 1.5 mg/kg BW IP cisplatin twice a week for 3 weeks.

Dosage form

1.5 mg/kg


Cisplatin and gentamicin could significantly elevate serum levels of creatinine, uric acid, and urea, with cisplatin showing higher elevation. Cisplatin could also significantly decrease the GSH and GPx levels.


[1]. Stordal B, et al. Understanding cisplatin resistance using cellular models. IUBMB Life. 2007 Nov;59(11):696-9.

[2]. Abouzed TK, et al. Assessment of gentamicin and cisplatin-induced kidney damage mediated via necrotic and apoptosis genes in albino rats. BMC Vet Res. 2021 Nov 16;17(1):350.


Cisplatin is one of the best and first metal-based chemotherapeutic drugs, which is used for wide range of solid cancers such as testicular, ovarian, bladder, lung, cervical, head and neck cancer, gastric cancer and some other cancers. Studies confirmed that cisplatin exerts its anticancer activity by attacking more than one place. Cisplatin generally binds with genomic DNA (gDNA) or mitochondrial DNA (mtDNA) to create DNA lesions, block the production of DNA, mRNA and proteins, arrest DNA replication, activate several transduction pathways which finally led to necrosis or apoptosis.[1]

In vitro and in vivo experiments indicated that cisplatin induced cell resistance and cisplatin administrated rats exhibited increased creatinine, urea, and uric acid and this effect was more pronounced than in rats treated with gentamicin.[1][2]

[1]. Stordal B, et al. Understanding cisplatin resistance using cellular models. IUBMB Life. 2007 Nov;59(11):696-9.
[2]. Abouzed TK, et al. Assessment of gentamicin and cisplatin-induced kidney damage mediated via necrotic and apoptosis genes in albino rats. BMC Vet Res. 2021 Nov 16;17(1):350.

Chemical Properties

Cas No. 15663-27-1 SDF
Synonyms CDDP
Chemical Name azane;dichloroplatinum(2+)
Canonical SMILES N.N.Cl[Pt+2]Cl
Formula Cl2H6N2Pt M.Wt 300.05
Solubility 5 mg/mL in DMF (16.66 mM; DMSO can inactivate Cisplatin's activity), 1 mg/mL in Water (3.33 mM; DMSO can inactivate Cisplatin's activity) Storage 4°C, protect from light
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

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Research Update

Cisplatin: The first metal based anticancer drug

Cisplatin or (SP-4-2)-diamminedichloridoplatinum(II) is one of the most potential and widely used drugs for the treatment of various solid cancers such as testicular, ovarian, head and neck, bladder, lung, cervical cancer, melanoma, lymphomas and several others. Cisplatin exerts anticancer activity via multiple mechanisms but its most acceptable mechanism involves generation of DNA lesions by interacting with purine bases on DNA followed by activation of several signal transduction pathways which finally lead to apoptosis. However, side effects and drug resistance are the two inherent challenges of cisplatin which limit its application and effectiveness. Reduction of drug accumulation inside cancer cells, inactivation of drug by reacting with glutathione and metallothioneins and faster repairing of DNA lesions are responsible for cisplatin resistance. To minimize cisplatin side effects and resistance, combination therapies are used and have proven more effective to defect cancers. This article highlights a systematic description on cisplatin which includes a brief history, synthesis, action mechanism, resistance, uses, side effects and modulation of side effects. It also briefly describes development of platinum drugs from very small cisplatin complex to very large next generation nanocarriers conjugated platinum complexes.

Cisplatin in cancer therapy: molecular mechanisms of action

Cisplatin, cisplatinum, or cis-diamminedichloroplatinum (II), is a well-known chemotherapeutic drug. It has been used for treatment of numerous human cancers including bladder, head and neck, lung, ovarian, and testicular cancers. It is effective against various types of cancers, including carcinomas, germ cell tumors, lymphomas, and sarcomas. Its mode of action has been linked to its ability to crosslink with the purine bases on the DNA; interfering with DNA repair mechanisms, causing DNA damage, and subsequently inducing apoptosis in cancer cells. However, because of drug resistance and numerous undesirable side effects such as severe kidney problems, allergic reactions, decrease immunity to infections, gastrointestinal disorders, hemorrhage, and hearing loss especially in younger patients, other platinum-containing anti-cancer drugs such as carboplatin, oxaliplatin and others, have also been used. Furthermore, combination therapies of cisplatin with other drugs have been highly considered to overcome drug-resistance and reduce toxicity. This comprehensive review highlights the physicochemical properties of cisplatin and related platinum-based drugs, and discusses its uses (either alone or in combination with other drugs) for the treatment of various human cancers. A special attention is paid to its molecular mechanisms of action, and its undesirable side effects.

Advances in Toxicological Research of the Anticancer Drug Cisplatin

Cisplatin is one of the most widely used chemotherapeutic agents for various solid tumors in the clinic due to its high efficacy and broad spectrum. The antineoplastic activity of cisplatin is mainly due to its ability to cross-link with DNA, thus blocking transcription and replication. Unfortunately, the clinical use of cisplatin is limited by its severe, dose-dependent toxic side effects. There are approximately 40 specific toxicities of cisplatin, among which nephrotoxicity is the most common one. Other common side effects include ototoxicity, neurotoxicity, gastrointestinal toxicity, hematological toxicity, cardiotoxicity, and hepatotoxicity. These side effects together reduce the life quality of patients and require lowering the dosage of the drug, even stopping administration, thus weakening the treatment effect. Few effective measures exist clinically against these side effects because the exact mechanisms of various side effects from cisplatin remain still unclear. Therefore, substantial effort has been made to explore the complicated biochemical processes involved in the toxicology of cisplatin, aiming to identify effective ways to reduce or eradicate its toxicity. This review summarizes and reviews the updated advances in the toxicological research of cisplatin. We anticipate to provide insights into the understanding of the mechanisms underlying the side effects of cisplatin and designing comprehensive therapeutic strategies involving cisplatin.

Is Autophagy Always a Barrier to Cisplatin Therapy?

Cisplatin has long been a first-line chemotherapeutic agent in the treatment of cancer, largely for solid tumors. During the course of the past two decades, autophagy has been identified in response to cancer treatments and almost uniformly detected in studies involving cisplatin. There has been increasing recognition of autophagy as a critical factor affecting tumor cell death and tumor chemoresistance. In this review and commentary, we introduce four mechanisms of resistance to cisplatin followed by a discussion of the factors that affect the role of autophagy in cisplatin-sensitive and resistant cells and explore the two-sided outcomes that occur when autophagy inhibitors are combined with cisplatin. Our goal is to analyze the potential for the combinatorial use of cisplatin and autophagy inhibitors in the clinic.

Can Cisplatin Therapy Be Improved? Pathways That Can Be Targeted

Cisplatin (cis-diamminedichloroplatinum (II)) is the oldest known chemotherapeutic agent. Since the identification of its anti-tumour activity, it earned a remarkable place as a treatment of choice for several cancer types. It remains effective against testicular, bladder, lung, head and neck, ovarian, and other cancers. Cisplatin treatment triggers different cellular responses. However, it exerts its cytotoxic effects by generating inter-strand and intra-strand crosslinks in DNA. Tumour cells often develop tolerance mechanisms by effectively repairing cisplatin-induced DNA lesions or tolerate the damage by adopting translesion DNA synthesis. Cisplatin-associated nephrotoxicity is also a huge challenge for effective therapy. Several preclinical and clinical studies attempted to understand the major limitations associated with cisplatin therapy, and so far, there is no definitive solution. As such, a more comprehensive molecular and genetic profiling of patients is needed to identify those individuals that can benefit from platinum therapy. Additionally, the treatment regimen can be improved by combining cisplatin with certain molecular targeted therapies to achieve a balance between tumour toxicity and tolerance mechanisms. In this review, we discuss the importance of various biological processes that contribute to the resistance of cisplatin and its derivatives. We aim to highlight the processes that can be modulated to suppress cisplatin resistance and provide an insight into the role of uptake transporters in enhancing drug efficacy.

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