Cisplatin
(Synonyms: 顺铂; cis-Platinum; CDDP; cis-Diaminodichloroplatinum) 目录号 : GC11908
顺铂是最好的、最早的基于金属的化疗药物之一，用于治疗广泛的实体癌症，如睾丸癌、卵巢癌、膀胱癌、肺癌、宫颈癌、头颈部肿瘤和胃癌等。
Cas No.:15663-27-1
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >99.00%
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- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
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Cell lines |
H69 SCLC cells |
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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. |
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Applications |
The cells were 2- to 4-fold resistant to cisplatin, which could be used to further study the resistance mechanism. |
| Animal experiment [2]: | |
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Animal models |
Adult male Wistar rats, weighing 160-200 g |
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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. |
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Dosage form |
1.5 mg/kg |
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Applications |
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. |
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References: [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. |
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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]
References:
[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.
顺铂是最好的、最早的基于金属的化疗药物之一,用于治疗广泛的实体癌症,如睾丸癌、卵巢癌、膀胱癌、肺癌、宫颈癌、头颈部肿瘤和胃癌等。研究证实,顺铂通过攻击多个位置发挥其抗癌活性。通常情况下,顺铂与基因组DNA（gDNA）或线粒体DNA（mtDNA）结合形成DNA损伤,阻止DNA、mRNA和蛋白质的产生,阻滞DNA复制,并激活几条信号转导途径,最终导致坏死或凋亡。[1]
体外和体内实验表明,顺铂会导致细胞耐药性增强,给予顺铂的大鼠显示出肌酐、尿素和尿酸水平升高的现象,而这种影响比使用庆大霉素治疗的大鼠更为显著。
| Cas No. | 15663-27-1 | SDF | |
| 别名 | 顺铂; cis-Platinum; CDDP; cis-Diaminodichloroplatinum | ||
| 化学名 | azane;dichloroplatinum(2+) | ||
| Canonical SMILES | N.N.Cl[Pt+2]Cl | ||
| 分子式 | Cl2H6N2Pt | 分子量 | 300.05 |
| 溶解度 | 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) | 储存条件 | 4°C, protect from light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.3328 mL | 16.6639 mL | 33.3278 mL |
| 5 mM | 0.6666 mL | 3.3328 mL | 6.6656 mL |
| 10 mM | 0.3333 mL | 1.6664 mL | 3.3328 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
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.