»
«
Offline Showroom in USA
Post Offer Free
MOSINTER GROUP LIMITED
MOSINTER GROUP LIMITED

China Cisplatin CAS 15663-27-1 LEDERPLATIN BRIPLATIN DIAMMINEDICHLOROPLATINATE manufacturer

5th

Gold Index: 88356

You are here: home  > Pharmaceutical Chemicals API  > Antineoplastic Drugs API  > Cisplatin CAS 15663-27-1 LEDERPLATIN BRIPLATIN DIAMMINEDICHLOROPLATINATE

Cisplatin CAS 15663-27-1 LEDERPLATIN BRIPLATIN DIAMMINEDICHLOROPLATINATE 

Payment Terms: T/T,WU 
Place of Origin: Shandong, China (Mainland) 
inquire skype
Add to My Favorites
HiSupplier Escrow
Share |

Product Detail

Means of Transport: Ocean,Land,Air
Packing: s per request of clients
Brand: MOSINTER
Specification: CP/USP/EP
Molecular Weight: 300.05
Melting Point: 340 °C (dec.)(lit.)
Production Capacity: 50KG/YEAR
Delivery Date: within 7 days
Molecular Formula: Cl2H6N2Pt
Density: 3,7 g/cm3
Appearance: Yellow crystalline
Soluble: <0.1 g/100 mL at 19 ºC

Cisplatin is administered intravenously as short-term infusion in normal saline for treatment of solid malignancies.

Cisplatin (CAS: 15663-27-1)


Item

Index

Molecular Formula

Cl2H6N2Pt

Molecular Weight

300.05

Specification

CP/USP/EP

Appearance

Yellow crystalline

Melting point

340 °C (dec.)(lit.)

Density

3,7 g/cm3

Cisplatin, cisplatinum, or cis-diamminedichloroplatinum(II)(CDDP) is a chemotherapy drug. It was the first member of a class ofplatinum-containing anti-cancer  medicine, which now also includes carboplatin and oxaliplatin. These platinum complexes react in vivo, binding to and causing crosslinking of DNA, which ultimately triggers apoptosis (programmed cell death).

Usage

Cisplatin is administered intravenously as short-term infusion in normal saline for treatment of solid malignancies. It is used to treat various types of cancers, including sarcomas, some carcinomas (e.g. small cell lung cancer, and ovarian cancer), lymphomas, and germ cell tumors. It is used in combinations with bleomycin and vinblastine in testicular cancer.

Cisplatin is particularly effective against testicular cancer; the cure rate was improved from 10% to 85%.

In addition, Cisplatin is used in Auger therapy.

Mechanism of action

Following administration, one of the chloride ligands is slowly displaced by water (an aqua ligand), in a process termed aquation. The aqua ligand in the resulting [PtCl(H2O)(NH3)2]+ is itself easily displaced, allowing the platinum atom to bind to bases. Of the bases on DNA, guanine is preferred. Subsequent to formation of [PtCl(guanine-DNA)(NH3)2]+, crosslinking can occur via displacement of the other chloride ligand, typically by another guanine. Cisplatin crosslinks DNA in several different ways, interfering with cell division by mitosis. The damaged DNA elicits DNA repair mechanisms, which in turn activate apoptosis when repair proves impossible. In 2008, researchers were able to show that the apoptosis induced by cisplatin on human colon cancer cells depends on the mitochondrial serine-protease Omi/Htra2. Since this was only demonstrated for colon carcinoma cells, it remains an open question if the Omi/Htra2 protein participates in the cisplatin-induced apoptosis in carcinomas from other tissues.

Most notable among the changes in DNA are the 1,2-intrastrand cross-links with purine bases. These include 1,2-intrastrand d(GpG) adducts which form nearly 90% of the adducts and the less common 1,2-intrastrand d(ApG) adducts. 1,3-intrastrand d(GpXpG) adducts occur but are readily excised by the nucleotide excision repair (NER). Other adducts include inter-strand crosslinks and nonfunctional adducts that have been postulated to contribute to cisplatin's activity. Interaction with cellular proteins, particularly HMG domain proteins, has also been advanced as a mechanism of interfering with mitosis, although this is probably not its primary method of action.

Note that although cisplatin is frequently designated as an alkylating agent, it has no alkyl group and so cannot carry out alkylating reactions. It is correctly classified as alkylating-like.

Cisplatin resistance

Cisplatin combination chemotherapy is the cornerstone of treatment of many cancers. Initial platinum responsiveness is high but the majority of cancer patients will eventually relapse with cisplatin-resistant disease. Many mechanisms of cisplatin resistance have been proposed including changes in cellular uptake and efflux of the drug, increased detoxification of the drug, inhibition of apoptosis and increased DNA repair.Oxaliplatin is active in highly cisplatin-resistant cancer cells in the laboratory; however, there is little evidence for its activity in the clinical treatment of patients with cisplatin-resistant cancer.The drug paclitaxel may be useful in the treatment of cisplatin-resistant cancer; the mechanism for this activity is unknown.

Transplatin

Transplatin, the trans stereoisomer of cisplatin, has formula trans-[PtCl2(NH3)2] and does not exhibit a comparably useful pharmacological effect. Its low activity is generally thought to be due to rapid deactivation of the drug before it can arrive at the DNA.[citation needed] It is toxic, and it is desirable to test batches of cis-platin for the absence of the trans isomer. In a procedure by Woollins et al., which is based on the classic 'Kurnakov test', thiourea reacts with the sample to give derivatives which can easily be separated and detected byHPLC.

Side effects

Cisplatin has a number of side-effects that can limit its use:

  • Nephrotoxicity (kidney damage) is a major concern. The dose is reduced when the patient's creatinine clearance (a measure of renal function) is reduced. Adequate hydration and diuresisis used to prevent renal damage. The nephrotoxicity of platinum-class  medicine seems to be related to reactive oxygen species and in animal models can be ameliorated by free radicalscavenging agents (e.g., amifostine). Nephrotoxicity is a dose-limiting side effect.

  • Neurotoxicity (nerve damage) can be anticipated by performing nerve conduction studies before and after treatment. Common neurological side effects of Cisplatin include visual perception and hearing disorder, which can occur soon after treatment begins. While triggering apoptosis through interfering with DNA replication remains the primary mechanism of Cisplatin, this has not been found to contribute to neurological side effects. Recent studies have shown that Cisplatin noncompetitively inhibits an archetypal, membrane-bound mechanosensitive sodium-hydrogen ion transporter known as NHE-1. It is primarily found on cells of the peripheral nervous system, which are aggregated in large numbers near the ocular and aural stimuli-receiving centers. This noncompetitive interaction has been linked to hydroelectrolytic imbalances and cytoskeleton alterations, both of which have been confirmed in vitro and in vivo. However, NHE-1 inhibition has been found to be both dose-dependent (half-inhibition = 30 µg/mL) and reversible.

  • Nausea and vomiting: cisplatin is one of the most emetogenic chemotherapy agents, but this symptom is managed with prophylactic antiemetics (ondansetron, granisetron, etc.) in combination with corticosteroids. Aprepitant combined with ondansetron and dexamethasone has been shown to be better for highly emetogenic chemotherapy than just ondansetron anddexamethasone.

  • Ototoxicity (hearing loss): there is at present no effective treatment to prevent this side effect, which may be severe. Audiometric analysis may be necessary to assess the severity of ototoxicity. Other  medicine (such as the aminoglycoside antibiotic class) may also cause ototoxicity, and the administration of this class of antibiotics in patients receiving cisplatin is generally avoided. The ototoxicity of both the aminoglycosides and cisplatin may be related to their ability to bind to melanin in the stria vascularis of the inner ear or the generation of reactive oxygen species.

  • Electrolyte disturbance: Cisplatin can cause hypomagnesaemia, hypokalaemia and hypocalcaemia. The hypocalcaemia seems to occur in those with low serum magnesium secondary to cisplatin, so it is not primarily due to the Cisplatin.

  • Myelotoxicity: This agent can also cause profound bone marrow suppression.

  • Hemolytic anemia can be developed after several courses of cisplatin. It is suggested that an antibody reacting with a cisplatin-red-cell membrane is responsible for hemolysis.

  • Approved for clinical use by the United States Food and Drug Administration (FDA) in 1978, it revolutionized the treatment of certain cancers. Detailed studies on its molecularmechanism of action, using a variety of spectroscopic methods including X-ray, NMR spectroscopy, and other physico-chemical methods, revealed its ability to form irreversible crosslinks with bases in DNA.

bigPhoto
skype Mr. Fedor

Tel: +86-574-89212210
Fax: +86-574-89212215
Mobile: 86- 189 8930 5995
Contact to this supplier

Didn't find what you're looking for? Post Buying Lead or contact HiSupplier Customer Service Center  for help!

Related Search

Find more related products in following catalogs on Hisupplier.com

Other products from this supplier

Company Info

MOSINTER GROUP LIMITED [China (Mainland)]

sgs ico Offline Showroom in USA

Business Type:Manufacturer, Trading Company
City: Ningbo
Province/State: Zhejiang
Country/Region: China (Mainland)

Follow Us: Follow us on facebook Follow us on linkedin

Fedor:   skype

You May Like: