Cisplatin - CAS 15663-27-1

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Category
APIs
Product Name
Cisplatin
Catalog Number
15663-27-1
CAS Number
15663-27-1
Molecular Weight
300.05
Molecular Formula
Cl2H6N2Pt
Quality Standard
USP
COA
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MSDS
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Structure
CAS 15663-27-1 Cisplatin
Specification
Purity
>95.0%(N)
Appearance
Orange or yellow crystalline powder
Related Products
Reference Reading
1. Analytical methodologies for metallomics studies of antitumor Pt-containing drugs
Diego Esteban-Fernandez, Estefanıa Moreno-Gordaliza, Gomez-Gomez*. Metallomics, 2010, 2, 19–38
Cisplatin interacts to a high extent with blood biomolecules remaining free only about 20% of the drug 24 h after its administration. This fact and the high saline content of blood prevent cisplatin from significantly evolving to the monoaqua form. Furthermore, the low amount of monoaqua derivative found in blood comes from the originally administered drug itself. The analysis of blood from patients, treated with cisplatin between 5 and 17 years before, showed levels of Pt which were between 2 and 3 orders of magnitude higher than basal. Such persistence is in agreement with the statement by some authors that the drug–protein adducts formed in blood act as an storage for the drug.
2. In situ analysis of cisplatin binding to DNA: the effects of physiological ionic conditions
Jin-Sung Park, Sook Ho Kim, Seok-Cheol Hong*. Phys. Chem. Chem. Phys., 2012, 14, 3128–3133
Understanding the mechanism of the action of anticancer drugs is the first step towards development of improved drug agents for the treatment of cancer. Cisplatin, one of the most successful anticancer drugs, is believed to exert its cytotoxic effects by binding to DNA. The interaction of cisplatin with DNA is a multi-stage process involving aquation of cisplatin, the pre-association of the aquated product with DNA, formation of a monofunctional adduct on DNA, and closure of the mono-functional adduct to a bifunctional adduct, which is the predominant end product from the reaction (Fig. 1). Since cisplatin can react with a wide range of biologically common substances, each stage of the process can be controlled and modified by various ions that are present in blood and cells.
3. In vitro studies on cisplatin focusing on kinetic aspects of intracellular chemistry by LC-ICP-MS
Gerrit Hermann, Petra Heffeter, Gunda Koellensperger*. Metallomics, 2013, 5, 636—647
In this way, cisplatin decay and cisplatin binding to cellular molecules could be monitored by NMR in a chemical surrounding, which was more representative for cancer cells than cell-mimicking physiological solutions. Surprisingly, no glutathione adducts could be observed, which is in strong contrast to the common hypothesis that glutathione is a major binding partner of cisplatin in the cell. For the first time, an intracellular half-life of 75 min was estimated. As a drawback, elevated cisplatin concentrations (due to sensitivity limitations) had to be used for these experiments.
4. Targeting and delivery of platinum-based anticancer drugs
Xiaoyong Wang* and Zijian Guo*. Chem.Soc.Rev., 2013, 42, 202—224
These efforts have brought five more drugs into clinical use, i.e. carboplatin, oxaliplatin, nedaplatin, lobaplatin, and heptaplatin, and about 10 other complexes are currently under clinical trials. Each of the latecomers shows some qualities that are not revealed by cisplatin. For example, nedaplatin displays less nephrotoxicity and neurotoxicity than cisplatin and carboplatin, and oxaliplatin demonstrates less toxicity and little or no cross resistance to cisplatin or carboplatin. However, since most of these drugs operate via a similar non-specific mechanism of action, some defects of cisplatin are consequently retained, albeit to a lesser extent.
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