Name: Paclitaxel
Brand: BOC Sciences
Price: 199 USD
Availability: MadeToOrder

Synonyms

Docetaxel EP Impurity F; BMS 181339-01; BMS181339-01; BMS-181339-01; Taxol A; Abraxane; Paxene; Taxol

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

InChIKey

RCINICONZNJXQF-MZXODVADSA-N

Density

1.39 g/cm3

Solubility

DMSO, methanol, ethanol

Melting Point

213-216°C

Flash Point

532.6±34.3 °C

Index Of Refraction

1.637

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

PSA

221.29000

Vapor Pressure

0.0±0.3 mmHg at 25°C

Source

Taxus brevifolia ( a plant extract)

Appearance

White Solid

Quantity

Kilos

Quality Standard

USP

Shelf Life

≥360 days if stored properly

Shipping

-20°C (International: -20°C)

Storage

Store at -20°C (dark)

Pictograms

Irritant; Health Hazard; Corrosives

Signal Word

Danger

Boiling Point

957.1°C at 760 mmHg

Form

Powder

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.

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.

Pharmacology

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.

NCT Number	Condition Or Disease	Phase	Start Date	Sponsor	Status
NCT03779464	Pancreatic Cancer	Phase 2	2019-07-08	Wuhan Union Hospital, China	Unknown Verified July 2019 by Tao Zhang, Wuhan Union Hospital, China. Recruitment status was Recruiting
NCT03618758	Gastric Cancer Stage IV	Phase 1, Phase 2	2021-03-09	Seoul National University Bundang Hospital	Recruiting
NCT03872141	Breast Cancer		2021-05-03	Yale University	Completed
NCT04496544	Peripheral Arterial Disease		2020-08-03	Beth Israel Deaconess Medical Center	Active, not recruiting
NCT04159142	Triple Negative Breast Cancer	Phase 2	2019-11-12	Hebei Medical University Fourth Hospital	Recruiting

Paclitaxel is a microtubule-stabilizing natural product and a potent ADC cytotoxin employed as an ADC payload in antibody-drug conjugates. Its mechanism of action involves binding to β-tubulin subunits, promoting microtubule polymerization, stabilizing microtubules against depolymerization, and causing mitotic arrest in the G2/M phase. This results in inhibition of cell division and induction of apoptosis in proliferating tumor cells. The chemical structure of Paclitaxel allows covalent conjugation to monoclonal antibodies through cleavable or non-cleavable linkers, facilitating precise intracellular delivery in ADC applications.

Within antibody-drug conjugates, Paclitaxel is linked to antibodies using linker chemistries designed to ensure systemic stability and controlled intracellular payload release. The ADC remains inactive during circulation, minimizing off-target cytotoxicity. Upon receptor-mediated internalization into antigen-expressing tumor cells, enzymatic or chemical cleavage liberates the active Paclitaxel payload. Once released, it stabilizes microtubules, disrupts mitotic spindle formation, and triggers apoptosis. This targeted mechanism ensures cytotoxic effects are confined to tumor cells, enhancing the specificity and reproducibility of tumor-targeted therapy.

Applications of Paclitaxel include incorporation into ADCs targeting both solid tumors and hematologic malignancies with defined antigen expression. Its chemical compatibility with various linker chemistries allows optimization of conjugation efficiency, intracellular release kinetics, and pharmacokinetics. Paclitaxel demonstrates consistent cytotoxic activity in target-expressing tumor cells, supporting the development of ADCs with precise antimitotic activity. Its well-characterized mechanism of microtubule stabilization provides controlled apoptosis induction, making it suitable as a mechanistically robust payload for ADC design and targeted oncology therapy.

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.

HPLC

Catalog	Product Name	CAS	Inquiry
BADC-01447	Paclitaxel D5	1129540-33-5

What is Paclitaxel?

Paclitaxel is a well-known microtubule-stabilizing chemotherapeutic agent widely used as a payload in ADCs. It promotes apoptosis by inhibiting microtubule depolymerization, which arrests the cell cycle at the G2/M phase.

25/12/2021

We are interested in how Paclitaxel is used in ADC development.

Paclitaxel is conjugated to antibodies in ADCs to selectively target tumor cells, leveraging its cytotoxic mechanism while minimizing systemic toxicity. It is suitable for preclinical research and development of targeted therapeutics.

29/7/2019

Could you advise which linkers are compatible with Paclitaxel in ADCs?

Paclitaxel can be linked using cleavable or non-cleavable linkers, including peptide-based or ester linkers. Linker choice influences drug release, stability, and pharmacokinetics, which are key in ADC design.

12/8/2022

Dear team, may I ask if BOC Sciences provides Paclitaxel ADC customization?

BOC Sciences offers Paclitaxel ADC services including payload conjugation, linker optimization, and analytical support. Customized solutions enable precise ADC design for preclinical research and targeted therapy studies.

16/9/2018

Dear team, what safety precautions are necessary when handling Paclitaxel?

Paclitaxel is highly cytotoxic and requires strict laboratory safety practices, including PPE, containment, and adherence to handling protocols, to minimize risk during preparation, conjugation, and analysis.

23/12/2018

— Dr. Kevin Wallace, Senior Scientist (USA)

Paclitaxel from BOC Sciences arrived with outstanding purity, crucial for our ADC conjugation projects.

12/8/2022

— Dr. Daniel White, Senior Scientist (USA)

Paclitaxel batches from BOC Sciences consistently meet our purity standards, critical for reproducible ADC payload studies.

23/12/2018

— Ms. Annika Bauer, ADC Research Scientist (Germany)

We appreciated the detailed CoA and QC data accompanying Paclitaxel, which streamlined our laboratory workflow.

16/9/2018

— Dr. Oliver Grant, Biochemist (UK)

Paclitaxel delivered exceptional solubility and stability for conjugation, improving efficiency in our ADC development.