Anti-Cancer Drug Top Quality Paclitaxel CAS 33069-62-4
|FOB Price:||US $100 / gram|
|Min. Order:||20 gram|
|Min. Order||FOB Price|
|20 gram||US $100/ gram|
|Port:||Hong Kong, Hong Kong|
|Payment Terms:||T/T, Western Union, Money Gram|
- Model NO.: CAS: 33069-62-4
- Customized: Customized
- Suitable for: Adult
- Purity: >99%
- Sample: Free
- Storage: Shading, Confined Preservation
- Trademark: JCJ
- Specification: White crystalline powder
- HS Code: 123456
- Powder: Yes
- Certification: ISO 9001
- State: Powder
- Appearance: Powder
- Color: White
- Market: Global
- Transport Package: Discreet and Safe Packages According to Different
- Origin: Made in China
Synonyms: N-BENZYL-BETA-PHENYLISOSERINE ESTER;PACLITAXEL, TAXUS BREVIFOLIA;PACLITAXEL, TAXUS SPECIES;PACLITAXOL;PACLITAXEL;TAXOL(TM);taxol a;TAXOL EQUIVALENT
Composition:Each 5 mL vial contains 30 mg paclitaxel and 49,7% v/v of dehydrated alcohol.
Paclitaxel powder is a chemotherapy drug that is given as a treatment for some types of cancer.
Paclitaxel powder is a mitotic inhibitor now used to treat patients with lung,ovarian,breast cancer, head and neck cancer, and advanced forms of Kaposi's sarcoma. Paclitaxel is also used for the prevention of restenosis.
Paclitaxel powder works by interfering with normal microtubule breakdown during cell division. Together with docetaxel, it forms the drug category of the taxanes. paclitaxel powder was the subject of a notable total synthesis by Robert A. Holton.
As well as offering substantial improvement in patient care, paclitaxel has been a relatively controversial drug.
Paclitaxel is an antimicrotubule agent that promotes the assembly of microtubules from tubulin dimers and stabilizes microtubules by preventing depolymerization. This stability results in the inhibition of the normal dynamic reorganisation of the microtubule network that is essential for vital interphase and mitotic cellular functions. In addition, paclitaxel induces abnormal arrays or bundles of microtubules throughout the cell cycle and multiple asters of microtubules during mitosis.
Following intravenous administration, paclitaxel exhibits a biphasic decline in plasma concentrations. The initial rapid decline represents distribution to the peripheral compartment and elimination; the later phase is due, in part, to a relatively slow efflux of paclitaxel from the peripheral compartment. In patients treated with doses of 135 and 175 mg/m² given as 3 and 24 hour infusions, mean terminal half-life has ranged from 3,0 to 52,7 hours. Mean values for total body clearance ranged from 11.6 to 24 L/h/m². Mean steady state volume of distribution has ranged from 198 to 688 L/m², indicating extensive extravascular distribution and/or tissue binding.
The pharmacokinetics of paclitaxel are non-linear. There is a disproportionately large increase in Cmax and AUC with increasing dose, accompanied by an apparent dose-related decrease in total body clearance. These findings are most readily observed in patients in whom, high plasma concentrations of paclitaxel are achieved. Saturable processes in distribution and elimination/metabolism may account for these findings.
There was no evidence of accumulation of paclitaxel with multiple treatment course.
In vitro studies of binding to human serum proteins, using paclitaxel concentrations ranging from 0,1 to 50 micrograms/mL, indicate that, on average, 89% of drug is bound. The presence of cimetidine, ranitidine, dexamethasone or diphenhydramine did not affect protein binding of paclitaxel.
The disposition of paclitaxel has not been fully elucidated in humans. After intravenous administration of paclitaxel, mean values of cumulative urinary recovery of unchanged drug ranged from 1.3 to 12.6% of the dose, indicating extensive non-renal clearance.
Hepatic metabolism and biliary clearance may be the principal mechanism for disposition of paclitaxel. Paclitaxel is metabolized primarily by cytochrome P450 enzymes. Hydroxylated metabolites have been demonstrated to be the principal metabolites. The formation of 6 alpha-hydroxypaclitaxel ,3'-p-hydroxypaclitaxel and 6 alpha,3'-p-dihydroxypaclitaxel is catalysed by CYP2C8, 3A4 and both 2C8 and 3A4 respectively. The effect of the renal or hepatic dysfunction on the disposition of paclitaxel has not been investigated. The clearance of paclitaxel was not affected by cimetidine pre-treatment. Ketoconazole may inhibit the metabolism of paclitaxel. Plasma levels of doxorubicin and doxorubicinol may be increased when paclitaxel and doxorubicin are used in combination.
1)he palliative treatment of stage 3 or 4 advanced local carcinoma of the ovary after surgical resection, in combination with cisplatin.
2)he palliative management of metastatic carcinoma of the ovary after failure of first line or subsequent chemotherapy.
3)he treatment of metastatic carcinoma of the breast after failure of combination chemotherapy or relapse within 6 months of adjuvant chemotherapy. Prior therapy should have included an anthracycline unless clinically contra-indicated.4. Palliative treatment of advanced non-small cell lung cancer in patients who are not candidates for potentially curative surgery and/or radiation therapy.
Primary treatment of ovarian carcinoma: a combination regimen consisting of Paclitaxel 135 mg/m² administered over 24 hours, followed by cisplatin 75 mg/m², every 3 weeks. Paclitaxel should be administered before cisplatin.
Indication 2 and 3:
Secondary treatment of ovarian carcinoma: Paclitaxel at a dose of 175 mg/m² administered intravenously over 3 hours every 3 weeks has been shown to be effective in patients with metastatic carcinoma of the ovary or breast after the failure of first line or subsequent chemotherapy.
Paclitaxel is contra-indicated in patients who have a history of severe hypersensitivity reactions to Paclitaxel or other drugs formulated with polyoxyethylated castor oil.
Paclitaxel should not be used in patients with baseline neutrophils <1 500/mm³.
Egnancy and Lactation
Paclitaxel has been shown to be embryotoxic, foetotoxic and to decrease fertility in animal studies.
There is no information on the use of Paclitaxel in pregnant women. Paclitaxelmay cause foetal harm when administered to pregnant women. Paclitaxelshould not be used during pregnancy. Women of childbearing potential should be advised to avoid becoming pregnant during therapy with Paclitaxel, and to inform the treating physician immediately should this occur.
It is not known whether Paclitaxel is excreted in human milk. Breast feeding should be discontinued for the duration of Paclitaxel therapy.
Store at room temperature not exceeding 25°C.
After first use any unused concentrate may be stored at room temperature not exceeding 25°C for up to 28 days.
Solutions for infusion prepared as recommended in bottles (glass, polypropylene) or plastic bags (polypropylene, polyolefin) and administered through polyethylene-lined administration sets, are stable at ambient temperature (approximately 25°C) and lighting conditions for up to 27 hours.
To be kept in outer container until required. Protect from light.
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