Paclitaxel
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| Category | Antineoplastic |
| Catalog number | BBF-04014 |
| CAS | 33069-62-4 |
| Molecular Weight | 853.91 |
| Molecular Formula | C47H51NO14 |
| Purity | >98% |
Ordering Information
| Catalog Number | Size | Price | Stock | Quantity |
|---|---|---|---|---|
| BBF-04014 | 2 g | $199 | In stock |
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Paclitaxel is a compound with anti-tumor activity extracted from the Pacific yew tree Taxus brevifolia. Paclitaxel is a microtubule polymer stabilizer with IC50 of 0.1 pM in human endothelial cells.
Specification
| Related CAS | 117527-50-1 (Succinate) |
| Synonyms | Docetaxel EP Impurity F; BMS 181339-01; BMS181339-01; BMS-181339-01; Taxol A; Abraxane; Paxene; Taxol |
| Shelf Life | ≥360 days if stored properly |
| Storage | Store at -20°C (dark) |
| IUPAC Name | [(1S,2S,3R,4S,7R,9S,10S,12R,15S)-4,12-diacetyloxy-15-[(2R,3S)-3-benzamido-2-hydroxy-3-phenylpropanoyl]oxy-1,9-dihydroxy-10,14,17,17-tetramethyl-11-oxo-6-oxatetracyclo[11.3.1.03,10.04,7]heptadec-13-en-2-yl] benzoate |
| Canonical SMILES | CC1=C2C(C(=O)C3(C(CC4C(C3C(C(C2(C)C)(CC1OC(=O)C(C(C5=CC=CC=C5)NC(=O)C6=CC=CC=C6)O)O)OC(=O)C7=CC=CC=C7)(CO4)OC(=O)C)O)C)OC(=O)C |
| InChI | InChI=1S/C47H51NO14/c1-25-31(60-43(56)36(52)35(28-16-10-7-11-17-28)48-41(54)29-18-12-8-13-19-29)23-47(57)40(61-42(55)30-20-14-9-15-21-30)38-45(6,32(51)22-33-46(38,24-58-33)62-27(3)50)39(53)37(59-26(2)49)34(25)44(47,4)5/h7-21,31-33,35-38,40,51-52,57H,22-24H2,1-6H3,(H,48,54)/t31-,32-,33+,35-,36+,37+,38-,40-,45+,46-,47+/m0/s1 |
| InChI Key | RCINICONZNJXQF-MZXODVADSA-N |
| Source | Taxus brevifolia ( a plant extract) |
Properties
| Appearance | White Solid |
| Application | ADCs Cytotoxin |
| Antibiotic Activity Spectrum | neoplastics (Tumor) |
| Boiling Point | 957.1°C at 760 mmHg |
| Melting Point | 213-216°C |
| Flash Point | 532.6±34.3 °C |
| Density | 1.39 g/cm3 |
| Solubility | DMSO, methanol, ethanol |
| LogP | 3 |
Toxicity
| Carcinogenicity | No indication of carcinogenicity to humans (not listed by IARC). |
| Mechanism Of Toxicity | Paclitaxel interferes with the normal function of microtubule growth. Whereas drugs like colchicine cause the depolymerization of microtubules in vivo, paclitaxel arrests their function by having the opposite effect; it hyper-stabilizes their structure. This destroys the cell's ability to use its cytoskeleton in a flexible manner. Specifically, paclitaxel binds to the β subunit of tubulin. Tubulin is the 'building block' of mictotubules, and the binding of paclitaxel locks these building blocks in place. The resulting microtubule/paclitaxel complex does not have the ability to disassemble. This adversely affects cell function because the shortening and lengthening of microtubules (termed dynamic instability) is necessary for their function as a transportation highway for the cell. Chromosomes, for example, rely upon this property of microtubules during mitosis. Further research has indicated that paclitaxel induces programmed cell death (apoptosis) in cancer cells by binding to an apoptosis stopping protein called Bcl-2 (B-cell leukemia 2) and thus arresting its function. |
| Toxicity | LD50 = 32530 microg/kg (Rat). |
Reference Reading
1.Discovery of a Highly Selective STK16 Kinase Inhibitor.
Liu F, Wang J, Yang X, Li B, Wu H, Qi S, Chen C, Liu X, Yu K, Wang W, Zhao Z, Wang A, Chen YF, Wang L, Gray NS, Liu J, Zhang X, Liu Q. ACS Chem Biol. 2016 Apr 15. [Epub ahead of print]
STK16, a serine/threonine protein kinase, is ubiquitously expressed and is conserved among all eukaryotes. STK16 has been implicated to function in a variety of cellular processes such as VEGF and cargo secretion but the pathways through which these effects are mediated remain to be elucidated. Through screening of our focused library of kinase inhibitors we discovered a highly selective ATP competitive inhibitor, STK16-IN-1, which exhibits potent inhibitory activity against STK16 kinase (IC50: 0.295 M) with excellent selective across the kinome as assessed using the KinomeScanTM profiling assay (S score (1)=0.0). In MCF-7 cells, treatment with STK16-IN-1 results in a reduction in cell number and accumulation of binucleated cells, which can be recapitulated by RNAi knockdown of STK16. Co-treatment of STK16-IN-1 with chemotherapeutics such as cisplatin, doxorubicin, cochicine and paclitaxel results in a slight potentiation of the anti-proliferative effects of the chemotherapeutics.
2.Mucinous ovarian cancer: A therapeutic review.
Xu W1, Rush J2, Rickett K3, Coward JI4. Crit Rev Oncol Hematol. 2016 Mar 19. pii: S1040-8428(16)30056-7. doi: 10.1016/j.critrevonc.2016.03.015. [Epub ahead of print]
Mucinous ovarian cancer represents approximately 3% of epithelial ovarian cancers (EOC). Despite this seemingly low prevalence, it remains a diagnostic and therapeutic conundrum that has resulted in numerous attempts to adopt novel strategies in managing this disease. Anecdotally, there has been a prevailing notion that established gold standard systemic regimens should be substituted for those utilised in cancers such as gastrointestinal (GI) malignancies; tumours that share more biological similarities than other EOC subtypes. This review summarises the plethora of small studies which have adopted this philosophy and influenced the design of the multinational GOG142 study, which was ultimately terminated due to poor accrual. To date, there is a paucity of evidence to support delivering 'GI style' chemotherapy for mucinous ovarian cancer over and above carboplatin-paclitaxel doublet therapy. Hence there is an urge to develop studies focused on targeted therapeutic agents driven by refined mutational analysis and conducted within the context of harmonised international collaborations.
3.A tunable delivery platform to provide local chemotherapy for pancreatic ductal adenocarcinoma.
Indolfi L1, Ligorio M2, Ting DT3, Xega K4, Tzafriri AR5, Bersani F4, Aceto N4, Thapar V4, Fuchs BC4, Deshpande V4, Baker AB6, Ferrone CR4, Haber DA7, Langer R8, Clark JW4, Edelman ER9. Biomaterials. 2016 Mar 31;93:71-82. doi: 10.1016/j.biomaterials.2016.03.044. [Epub ahead of print]
Pancreatic ductal adenocarcinoma (PDAC) is one of the most devastating and painful cancers. It is often highly resistant to therapy owing to inherent chemoresistance and the desmoplastic response that creates a barrier of fibrous tissue preventing transport of chemotherapeutics into the tumor. The growth of the tumor in pancreatic cancer often leads to invasion of other organs and partial or complete biliary obstruction, inducing intense pain for patients and necessitating tumor resection or repeated stenting. Here, we have developed a delivery device to provide enhanced palliative therapy for pancreatic cancer patients by providing high concentrations of chemotherapeutic compounds locally at the tumor site. This treatment could reduce the need for repeated procedures in advanced PDAC patients to debulk the tumor mass or stent the obstructed bile duct. To facilitate clinical translation, we created the device out of currently approved materials and drugs.
4.Outcomes of Patients With Surgically and Pathologically Staged IIIA-IVB Pure Endometrioid-type Endometrial Cancer: A Taiwanese Gynecology Oncology Group (TGOG-2005) Retrospective Cohort Study (A STROBE-Compliant Article).
Chen JR1, Chang TC, Fu HC, Lau HY, Chen IH, Ke YM, Liang YL, Chiang AJ, Huang CY, Chen YC, Hong MK, Wang YC, Huang KF, Hsiao SM, Wang PH. Medicine (Baltimore). 2016 Apr;95(15):e3330. doi: 10.1097/MD.0000000000003330.
In the management of patients with advanced-stage pure endometrioid-type endometrial cancer (E-EC), such as positive lymph nodes (stage III) or stage IV, treatment options are severely limited. This article aims to investigate the outcome of women with FIGO III-IV E-EC (based on FIGO 2009 system).The retrospective cohort study, based on the Taiwanese Gynecologic Oncology Group (TGOG-2005), enrolled patients undergoing staging surgery to have a pathologically confirmed FIGO III-IV E-EC from 22-member hospitals between 1991 and 2010.This cohort included 541 patients (stage III, n = 464; stage IV, n = 77). Five-year overall survival (OS) was 70.4%. Median progression-free survival (PFS) was 43 months (range 0-258 months) and median OS was 52 months (range 1-258 months). Multivariate analysis showed that FIGO stage, >1/2 myometrial invasion (hazard ratio [HR] 1.53, 95% confidence interval [CI] 1.12-2.09; P = 0.007), histological grade 3 (HR 2.
Spectrum
LC-MS/MS Spectrum - , positive
Predicted LC-MS/MS Spectrum - 10V, Positive
Experimental Conditions
Ionization Mode: Positive
Collision Energy: 10 eV
Instrument Type: QTOF (generic), spectrum predicted by CFM-ID
Mass Resolution: 0.0001 Da
Molecular Formula: C47H51NO14
Molecular Weight (Monoisotopic Mass): 853.331 Da
Molecular Weight (Avergae Mass): 853.9061 Da
Collision Energy: 10 eV
Instrument Type: QTOF (generic), spectrum predicted by CFM-ID
Mass Resolution: 0.0001 Da
Molecular Formula: C47H51NO14
Molecular Weight (Monoisotopic Mass): 853.331 Da
Molecular Weight (Avergae Mass): 853.9061 Da
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
