Paclitaxel - CAS 33069-62-4

Paclitaxel - CAS 33069-62-4 Catalog number: BADC-00325

* Please be kindly noted products are not for therapeutic use. We do not sell to patients.

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.

ADCs Cytotoxin
Product Name
Catalog Number
Molecular Formula
Molecular Weight

Ordering Information

Catalog Number Size Price Quantity
BADC-00325 2 g $199
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.
BMS 181339-01; BMS181339-01; BMS-181339-01; Taxol A; Abraxane; Paxene; Taxol
[(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[,10.04,7]heptadec-13-en-2-yl] benzoate
Canonical SMILES
1.39 g/cm3
DMSO, methanol, ethanol
Melting Point
Flash Point
532.6±34.3 °C
Index Of Refraction
Optical Rotation
Specific optical rotation: -49 deg at 20 °C/D (methanol); UV max absorption 2 (methanol): 227, 273, nm (E= 29,800,1700);(c = 1, MeOH) [a]20D = -53 +- 20 degrees
Vapour Pressure
0.0±0.3 mmHg at 25°C
Mechanism Of Action
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.
Paclitaxel is a taxoid antineoplastic agent indicated as first-line and subsequent therapy for the treatment of advanced carcinoma of the ovary, and other various cancers including breast cancer. Paclitaxel is a novel 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 reorganization 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.
Toxicity (LD50)
Rat (ipr) LD50=32530 µg/kg. Symptoms of overdose include bone marrow suppression, peripheral neurotoxicity, and mucositis. Overdoses in pediatric patients may be associated with acute ethanol toxicity.
In Vitro
Paclitaxel at 0.1, 0.5, and 1 μM reduces the proliferation and survival of CCRF-HSB-2 cells in a dose-dependent fashion and that the IC50 value of taxol is about 0.25 μM. Paclitaxel directly associates with the endoplasmic reticulum to stimulate the release of calcium into the cytosol, contributing to the induction of apoptosis.
In Vivo
In a SCID mouse xenograft model, low dose metronomic Paclitaxel treatment decreases lung dissemination of EGI-1 cells without significantly affecting their local tumor growth. Low doses of paclitaxel promot liver metastasis in mouse xenografts, which correlats with changes in estrogen metabolism in the host liver. Paclitaxel (2 mg/kg per treatment, black circles) induces mechanical hypersensitivity in the glabrous skin of the hindpaw.
Clinical Trial Information
NCT NumberCondition Or DiseasePhaseStart DateSponsorStatus
NCT03779464Pancreatic CancerPhase 22019-07-08Wuhan Union Hospital, ChinaUnknown Verified July 2019 by Tao Zhang, Wuhan Union Hospital, China. Recruitment status was Recruiting
NCT03618758Gastric Cancer Stage IVPhase 1, Phase 22021-03-09Seoul National University Bundang HospitalRecruiting
NCT03872141Breast Cancer2021-05-03Yale UniversityCompleted
NCT04496544Peripheral Arterial Disease2020-08-03Beth Israel Deaconess Medical CenterActive, not recruiting
NCT04159142Triple Negative Breast CancerPhase 22019-11-12Hebei Medical University Fourth HospitalRecruiting
ADCs Cytotoxin
Taxus brevifolia ( a plant extract)
White Solid
Quality Standard
Shelf Life
≥360 days if stored properly
-20°C (International: -20°C)
Store at -20°C (dark)
Irritant; Health Hazard; Corrosives
Signal Word
Boiling Point
957.1°C at 760 mmHg
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.

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2




Send Inquiry

Verification code
Inquiry Basket