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Paclitaxel CAS 33069-62-4
Paclitaxel CAS 33069-62-4

Paclitaxel CAS 33069-62-4

Contact : Mr.Thyen-------------------------------- Email us at zhangyinglong@ycphar.com Whatsapp : +86 180 3817 6818

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Paclitaxel


Contact : Mr.Thyen

Email us at zhangyinglong@ycphar.com

Whatsapp : +86 180 3817 6818


Product Name: paclitaxels
Taxol paclitaxel CAS No: 33069-62-4
Taxol paclitaxel EINECS: 205-285-7 
Taxol paclitaxel Appearance:white crystalline powder
Taxol paclitaxel Molecular Formula:C47H51NO14
Taxol paclitaxel Molecular Weight:853.92
Taxol paclitaxel Herb Sourse:Taxus Chinensis Extract
Taxol paclitaxel Content:10~99%
Taxol paclitaxel Assay Method: HPLC
Taxol paclitaxel Specification:99% by HPLC
Taxol paclitaxel Shelf Life: 2 years when properly stored.
Taxol paclitaxel Storage: Cool and dry place,keep away from strong light & high temp
Taxol paclitaxel Package: 1kg, 5kg, aluminum foil vacuum bag.Or as per your requirement 


Product NamePaclitaxel
CAS33069-62-4
StandardUSP
Natural/SyntheticSynthesis
Extraction SourceAnti-tumor
LevelPharmaceutical Grade
Content99%
Appearancewhite powder
Packing10g/aluminum foil bag
CategoryPharmaceutical Raw Materials
FieldAnti-tumor > Breast Cancer
Deferred ProductsBreast Cancer, Uterine Cancer



Use: 1. This product is suitable for the treatment of first-line chemotherapy failure or repeated chemotherapy failure of patients with metastatic ovarian cancer. 2. This product is suitable for the treatment of metastatic breast cancer failure of comprehensive chemotherapy or recurrence of breast cancer within six months after adjuvant chemotherapy.


Pharmacogical Action:

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.
 
Dications:

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.
 

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