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MedKoo CAT#: 100690

CAS#: 33069-62-4 (free base)

Description: Paclitaxel is a compound with antineoplastic activity extracted from the Pacific yew tree Taxus brevifolia. Paclitaxel binds to tubulin and inhibits the disassembly of microtubules, thereby inhibiting cell division. This agent also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein Bcl-2 (B-cell Leukemia 2).

Chemical Structure

CAS# 33069-62-4 (free base)

Theoretical Analysis

MedKoo Cat#: 100690
Name: Paclitaxel
CAS#: 33069-62-4 (free base)
Chemical Formula: C47H51NO14
Exact Mass: 853.33096
Molecular Weight: 853.91
Elemental Analysis: C, 66.11; H, 6.02; N, 1.64; O, 26.23

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1.0g USD 150.0 Ready to ship
2.0g USD 250.0 Ready to ship
5.0g USD 550.0 Ready to ship
10.0g USD 950.0 Ready to ship
20.0g USD 1750.0 Ready to ship
50.0g USD 3650.0 Ready to ship
100.0g USD 5850.0 Ready to ship
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Related CAS #: 186040-50-6 (ceribate); 33069-62-4 (free base)  

Synonym: BMS 181339-01; BMS181339-01; BMS-181339-01; Brand name: Taxol; Anzatax; Asotax; Bristaxol; Praxel; Taxol Konzentrat. TAX.

IUPAC/Chemical Name: (2aR,4S,4aS,6R,9S,11S,12S,12aR,12bS)-9-(((2R,3S)-3-benzamido-2-hydroxy-3-phenylpropanoyl)oxy)-12-(benzoyloxy)-4,11-dihydroxy-4a,8,13,13-tetramethyl-5-oxo-2a,3,4,4a,5,6,9,10,11,12,12a,12b-dodecahydro-1H-7,11-methanocyclodeca[3,4]benzo[1,2-b]oxete-6,12b-diyl diacetate


InChi Code: 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

SMILES Code: O=C1[C@H](OC(C)=O)C(C2(C)C)=C(C)[C@@H](OC([C@H](O)[C@@H](NC(C3=CC=CC=C3)=O)C4=CC=CC=C4)=O)C[C@@]2(O)[C@@H](OC(C5=CC=CC=C5)=O)[C@@]6([H])[C@@]1(C)[C@@H](O)C[C@@]7([H])OC[C@]76OC(C)=O

Appearance: white solid powder

Purity: >98% (or refer to the Certificate of Analysis)

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.

Storage Condition: Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

Solubility: Soluble in DMSO, not in water

Shelf Life: >2 years if stored properly

Drug Formulation: This drug may be formulated in DMSO

Stock Solution Storage: 0 - 4 C for short term (days to weeks), or -20 C for long term (months).

HS Tariff Code: 2934.99.9001

Biological target: Antineoplastic agent that stabilizes tubulin polymerization.
In vitro activity: PTX (Paclitaxel) or PTX-Tf-NPs (Paclitaxel transferrin nanoparticles) reduce the viability of rat glioblastoma C6 cells in a dosedependent manner, but PTX-Tf-NPs exhibit a stronger inhibitory effect at higher concentrations compared with PTX. Rat glioblastoma C6 cells were treated with Tf-NPs, PTX or PTX-Tf-NPs for 48 h, and cell viability was detected using the MTT assay. The percentages of cell viability are presented in Fig. 1 and Table I. The results indicated that treatment with Tf-NPs at concentrations of 0.0032 or 0.016 µg/ml did not inhibit C6 cell viability, whereas Tf-NP treatment at concentrations of 0.08, 0.4, 2 and 10 µg/ml resulted in a cell viability of 92, 97, 97 and 88% in C6 cells, respectively, compared with control cells, indicating that Tf-NPs alone cause a low cytotoxicity in C6 cells. Both PTX and PTX-Tf-NPs exhibited a dose-dependent effect on cell viability in C6 cells. Following PTX treatment at concentrations of 0.0032, 0.016 and 0.08 µg/ml, C6 cell viability was 91, 87 and 83%, respectively, while following PTX-Tf-NP treatment, cell viability was 95, 91 and 83%, respectively. Statistical analysis revealed that at a concentration of ≤0.08 µg/ml, no significant difference in cell viability by treatment with either PTX or PTX-Tf-NPs was observed, indicating that PTX and PTX-Tf-NPs exhibit similar cell viability inhibitory effects at these concentrations. Nevertheless, at concentrations of 0.4, 2 and 10 µg/ml, C6 cells treated with PTX exhibited an average viability of 81, 74 and 62%, respectively, but C6 cells treated with PTX-Tf-NPs exhibited significantly lower viability compared with cells treated with PTX (78, 69 and 56%, respectively). This suggested that PTX-Tf-NPs were more potent compared with PTX in reducing the viability of C6 glioblastoma cells at higher concentrations. Reference: Exp Ther Med. 2021 Apr; 21(4): 292.
In vivo activity: The blank and the PCX(Paclitxel)-loaded CD nanoparticles were administered to the tumor-bearing mice, and the change in tumor size was followed for 14 days (Figure 8 and Figure 9). On day 5, compared to the control groups that received physiological saline or blank CD nanoparticles, an approximately 25% reduction was observed in the tumor size of the mice treated with PCX-loaded nanoparticle or PCX solution (Figure 8). The most significant difference between the groups was achieved on day 8 in which the tumors continued to grow in the physiological saline control group; on the other hand, either the blank or the PCX-loaded CD nanoparticles reduced the tumor burden. In general, the PCX-loaded positively charged nanoparticles were the most efficient antitumor formulation, albeit not reaching the level of statistical significance (Figure 8). On day 14, the tumor size was reduced by 50% in all groups that were treated with blank or PCX-loaded CD formulations, or PCX solution. Collectively, the antitumor effect of the PCX-loaded amphiphilic CD nanoparticles was observed earlier than the PCX solution. Interestingly, in the long run, the blank CD nanoparticles were also capable of hindering the tumor growth (Figure 8 and Figure 9). Accordingly, Erdogar et al. showed that folatetargeted CD nanoparticles were better tolerated by animals and localized in the tumor area than PCX solution in Cremophor®EL. These results support that the CD nanoparticles can be a good candidate for increasing the efficacy and safety of PCX therapy in breast cancer. Reference: Nanomaterials (Basel). 2021 Feb; 11(2): 515.

Solubility Data

Solvent Max Conc. mg/mL Max Conc. mM
Cloroform 1.0 1.17
DMF 5.0 5.86
DMSO 77.85 91.17
DMSO:PBS (pH 7.2) (1:10) 0.1 0.12
Ethanol 14.33 16.78
Methanol 5.0 5.86

Preparing Stock Solutions

The following data is based on the product molecular weight 853.91 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Recalculate based on batch purity %
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 1.15 mL 5.76 mL 11.51 mL
5 mM 0.23 mL 1.15 mL 2.3 mL
10 mM 0.12 mL 0.58 mL 1.15 mL
50 mM 0.02 mL 0.12 mL 0.23 mL
Formulation protocol: 1. Wang L, Liu C, Qiao F, Li M, Xin H, Chen N, Wu Y, Liu J. Analysis of the cytotoxic effects, cellular uptake and cellular distribution of paclitaxel-loaded nanoparticles in glioblastoma cells in vitro. Exp Ther Med. 2021 Apr;21(4):292. doi: 10.3892/etm.2021.9723. Epub 2021 Jan 27. PMID: 33717235; PMCID: PMC7885080. 2. Yang X, Qin J, Gong C, Yang J. Propofol enhanced the cell sensitivity to paclitaxel (PTX) in prostatic cancer (PC) through modulation of HOTAIR. Genes Genomics. 2021 Apr 23. doi: 10.1007/s13258-021-01093-0. Epub ahead of print. PMID: 33893626. 3. Varan G, Varan C, Öztürk SC, Benito JM, Esendağlı G, Bilensoy E. Therapeutic Efficacy and Biodistribution of Paclitaxel-Bound Amphiphilic Cyclodextrin Nanoparticles: Analyses in 3D Tumor Culture and Tumor-Bearing Animals In Vivo. Nanomaterials (Basel). 2021 Feb 18;11(2):515. doi: 10.3390/nano11020515. PMID: 33670527; PMCID: PMC7922126. 4. Gui G, Fan Z, Ning Y, Yuan C, Zhang B, Xu Q. Optimization, Characterization and in vivo Evaluation of Paclitaxel-Loaded FolateConjugated Superparamagnetic Iron Oxide Nanoparticles. Int J Nanomedicine. 2021 Mar 19;16:2283-2295. doi: 10.2147/IJN.S287434. PMID: 33776433; PMCID: PMC7992116.
In vitro protocol: 1. Wang L, Liu C, Qiao F, Li M, Xin H, Chen N, Wu Y, Liu J. Analysis of the cytotoxic effects, cellular uptake and cellular distribution of paclitaxel-loaded nanoparticles in glioblastoma cells in vitro. Exp Ther Med. 2021 Apr;21(4):292. doi: 10.3892/etm.2021.9723. Epub 2021 Jan 27. PMID: 33717235; PMCID: PMC7885080. 2. Yang X, Qin J, Gong C, Yang J. Propofol enhanced the cell sensitivity to paclitaxel (PTX) in prostatic cancer (PC) through modulation of HOTAIR. Genes Genomics. 2021 Apr 23. doi: 10.1007/s13258-021-01093-0. Epub ahead of print. PMID: 33893626.
In vivo protocol: 1. Varan G, Varan C, Öztürk SC, Benito JM, Esendağlı G, Bilensoy E. Therapeutic Efficacy and Biodistribution of Paclitaxel-Bound Amphiphilic Cyclodextrin Nanoparticles: Analyses in 3D Tumor Culture and Tumor-Bearing Animals In Vivo. Nanomaterials (Basel). 2021 Feb 18;11(2):515. doi: 10.3390/nano11020515. PMID: 33670527; PMCID: PMC7922126. 2. Gui G, Fan Z, Ning Y, Yuan C, Zhang B, Xu Q. Optimization, Characterization and in vivo Evaluation of Paclitaxel-Loaded FolateConjugated Superparamagnetic Iron Oxide Nanoparticles. Int J Nanomedicine. 2021 Mar 19;16:2283-2295. doi: 10.2147/IJN.S287434. PMID: 33776433; PMCID: PMC7992116.

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1: Carbognin L, Sperduti I, Nortilli R, Brunelli M, Vicentini C, Pellini F, Pollini GP, Giannarelli D, Tortora G, Bria E. Balancing activity and tolerability of neoadjuvant paclitaxel- and docetaxel-based chemotherapy for HER2-positive early stage breast cancer: sensitivity analysis of randomized trials. Cancer Treat Rev. 2015 Mar;41(3):262-70. doi: 10.1016/j.ctrv.2015.02.003. Epub 2015 Feb 9. Review. PubMed PMID: 25683304.

2: Onishi Y, Eshita Y, Ji RC, Onishi M, Kobayashi T, Mizuno M, Yoshida J, Kubota N. Anticancer efficacy of a supramolecular complex of a 2-diethylaminoethyl-dextran-MMA graft copolymer and paclitaxel used as an artificial enzyme. Beilstein J Nanotechnol. 2014 Dec 1;5:2293-307. doi: 10.3762/bjnano.5.238. eCollection 2014. Review. PubMed PMID: 25551057; PubMed Central PMCID: PMC4273266.

3: Liu H, Chen X, Sun J, Gao P, Song Y, Zhang N, Lu X, Xu H, Wang Z. The efficacy and toxicity of paclitaxel plus S-1 compared with paclitaxel plus 5-FU for advanced gastric cancer: a PRISMA systematic review and meta-analysis of randomized controlled trials. Medicine (Baltimore). 2014 Nov;93(25):e164. doi: 10.1097/MD.0000000000000164. Review. PubMed PMID: 25437030.

4: Slaughter KN, Moore KN, Mannel RS. Anti-angiogenic therapy versus dose-dense paclitaxel therapy for frontline treatment of epithelial ovarian cancer: review of phase III randomized clinical trials. Curr Oncol Rep. 2014 Nov;16(11):412. doi: 10.1007/s11912-014-0412-2. Review. PubMed PMID: 25292279.

5: Blais N, Hirsh V. Chemotherapy in Metastatic NSCLC - New Regimens (Pemetrexed, Nab-Paclitaxel). Front Oncol. 2014 Jul 21;4:177. doi: 10.3389/fonc.2014.00177. eCollection 2014. Review. Erratum in: Front Oncol. 2014;4:300. PubMed PMID: 25101242; PubMed Central PMCID: PMC4104641.

6: Tofthagen C, McAllister RD, Visovsky C. Peripheral neuropathy caused by Paclitaxel and docetaxel: an evaluation and comparison of symptoms. J Adv Pract Oncol. 2013 Jul;4(4):204-15. Review. PubMed PMID: 25032002; PubMed Central PMCID: PMC4093436.

7: Litsky J, Chanda A, Stilp E, Lansky A, Mena C. Critical evaluation of stents in the peripheral arterial disease of the superficial femoral artery - focus on the paclitaxel eluting stent. Med Devices (Auckl). 2014 May 28;7:149-56. doi: 10.2147/MDER.S45472. eCollection 2014. Review. PubMed PMID: 24920940; PubMed Central PMCID: PMC4045256.

8: Borazanci E, Von Hoff DD. Nab-paclitaxel and gemcitabine for the treatment of patients with metastatic pancreatic cancer. Expert Rev Gastroenterol Hepatol. 2014 Sep;8(7):739-47. doi: 10.1586/17474124.2014.925799. Epub 2014 May 31. Review. PubMed PMID: 24882381.

9: Li P, Liu JP. Long-term risk of late and very late stent thrombosis in patients treated with everolimus against paclitaxel-eluting stents: an updated meta-analysis. Coron Artery Dis. 2014 Aug;25(5):369-77. doi: 10.1097/MCA.0000000000000109. Review. PubMed PMID: 24818639.

10: Glück S. nab-Paclitaxel for the treatment of aggressive metastatic breast cancer. Clin Breast Cancer. 2014 Aug;14(4):221-7. doi: 10.1016/j.clbc.2014.02.001. Epub 2014 Feb 20. Review. PubMed PMID: 24806278.

11: Neesse A, Michl P, Tuveson DA, Ellenrieder V. nab-Paclitaxel: novel clinical and experimental evidence in pancreatic cancer. Z Gastroenterol. 2014 Apr;52(4):360-6. doi: 10.1055/s-0034-1366002. Epub 2014 Mar 31. Review. PubMed PMID: 24687799.

12: Al-Batran SE, Geissler M, Seufferlein T, Oettle H. Nab-paclitaxel for metastatic pancreatic cancer: clinical outcomes and potential mechanisms of action. Oncol Res Treat. 2014;37(3):128-34. doi: 10.1159/000358890. Epub 2014 Feb 7. Review. PubMed PMID: 24685917.

13: De Luca G, Wirianta J, Lee JH, Kaiser C, Di Lorenzo E, Suryapranata H. Sirolimus-eluting versus paclitaxel-eluting stent in primary angioplasty: a pooled patient-level meta-analysis of randomized trials. J Thromb Thrombolysis. 2014 Oct;38(3):355-63. Review. PubMed PMID: 24659172.

14: Roy A, Bhattacharyya M, Ernsting MJ, May JP, Li SD. Recent progress in the development of polysaccharide conjugates of docetaxel and paclitaxel. Wiley Interdiscip Rev Nanomed Nanobiotechnol. 2014 Jul-Aug;6(4):349-68. doi: 10.1002/wnan.1264. Epub 2014 Mar 20. Review. PubMed PMID: 24652678; PubMed Central PMCID: PMC4057951.

15: de Weger VA, Beijnen JH, Schellens JH. Cellular and clinical pharmacology of the taxanes docetaxel and paclitaxel--a review. Anticancer Drugs. 2014 May;25(5):488-94. doi: 10.1097/CAD.0000000000000093. Review. Erratum in: Anticancer Drugs. 2015 Feb;26(2):240. PubMed PMID: 24637579.

16: Howat S, Park B, Oh IS, Jin YW, Lee EK, Loake GJ. Paclitaxel: biosynthesis, production and future prospects. N Biotechnol. 2014 May 25;31(3):242-5. doi: 10.1016/j.nbt.2014.02.010. Epub 2014 Mar 11. Review. PubMed PMID: 24614567.

17: Zhang D, Yang R, Wang S, Dong Z. Paclitaxel: new uses for an old drug. Drug Des Devel Ther. 2014 Feb 20;8:279-84. doi: 10.2147/DDDT.S56801. eCollection 2014. Review. PubMed PMID: 24591817; PubMed Central PMCID: PMC3934593.

18: Megerdichian C, Olimpiadi Y, Hurvitz SA. nab-Paclitaxel in combination with biologically targeted agents for early and metastatic breast cancer. Cancer Treat Rev. 2014 Jun;40(5):614-25. doi: 10.1016/j.ctrv.2014.02.001. Epub 2014 Feb 12. Review. PubMed PMID: 24560997.

19: Cecco S, Aliberti M, Baldo P, Giacomin E, Leone R. Safety and efficacy evaluation of albumin-bound paclitaxel. Expert Opin Drug Saf. 2014 Apr;13(4):511-20. doi: 10.1517/14740338.2014.893293. Epub 2014 Feb 22. Review. PubMed PMID: 24559090.

20: Al-Hajeili M, Azmi AS, Choi M. Nab-paclitaxel: potential for the treatment of advanced pancreatic cancer. Onco Targets Ther. 2014 Feb 4;7:187-92. doi: 10.2147/OTT.S40705. eCollection 2014. Review. PubMed PMID: 24523592; PubMed Central PMCID: PMC3921002.

Additional Information

Paclitaxel is a mitotic inhibitor used in cancer chemotherapy. It was discovered in a National Cancer Institute program at the Research Triangle Institute in 1967 when Monroe E. Wall and Mansukh C. Wani isolated it from the bark of the Pacific Yew tree, Taxus brevifolia and named it 'taxol'. When it was developed commercially by Bristol-Myers Squibb (BMS) the generic name was changed to 'paclitaxel' and the BMS compound is sold under the trademark 'TAXOL'. In this formulation, paclitaxel is dissolved in Cremophor EL and ethanol, as a delivery agent. A newer formulation, in which paclitaxel is bound to albumin, is sold under the trademark Abraxane. Paclitaxel is 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 stabilizes microtubules and as a result, interferes with the normal breakdown of microtubules during cell division. Together with docetaxel, it forms the drug category of the taxanes. It 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. There was originally concern because of the environmental impact of its original sourcing, no longer used, from the Pacific yew. In addition, the assignment of rights, and even the name itself, to Bristol-Myers Squibb were the subject of public debate and Congressional hearings.
According to, In 1955 the National Cancer Institute (NCI) set up the Cancer Chemotherapy National Service Center (CCNSC) to act as a public screening center for anti-cancer activity in compounds submitted by external institutions and companies. Although the majority of compounds screened were of synthetic origin, one chemist, Jonathan Hartwell, who was employed there from 1958 onwards, had had experience of natural product derived compounds and began a plant screening operation. After some years of informal arrangements, in July 1960 the NCI commissioned USDA botanists to collect samples from about 1000 plant species per year. On August 21, 1962, one of those botanists, Arthur S. Barclay, collected bark from a single Pacific yew tree, Taxus brevifolia, in a forest north of the town of Packwood, Washington as part of a four month trip collecting material from over 200 different species. The material was then processed by a number of specialist CCNSC subcontractors and one of the Taxus samples was found to be cytotoxic in a cellular assay on May 22, 1964. Accordingly, in late 1964 or early 1965, the fractionation and isolation laboratory run by Monroe E. Wall in Research Triangle Park, North Carolina, began work on fresh Taxus samples, isolating the active ingredient in September 1966 and announcing their findings at an April 1967 American Chemical Society meeting in Miami Beach. They named the pure compound 'taxol' in June 1967.  Wall and his colleague Wani published their results, including the chemical structure, in 1971. The NCI continued to commission work to collect more Taxus bark and to isolate increasing quantities of taxol. By 1969 28 kg of crude extract had been isolated from almost 1,200 kg of bark, although this ultimately yielded only 10g of pure material.But for several years no use was made of the compound by the NCI. In 1975 it was shown to be active in another in vitro system ; two years later a new department head reviewed the data and finally recommended that taxol be moved on to the next stage in the discovery process. This required increasing quantities of purified taxol, up to 600g, and in 1977 a further request for 7,000 lbs of bark was made. In 1978, two NCI researchers published a report showing that taxol was mildly effective in leukaemic mice. In November 1978, taxol was shown to be effective in xenograft studies.Meanwhile taxol began to be well known in the cell biology, as well as the cancer community, with a publication in early 1979 by Susan B. Horwitz, a molecular pharmacologist at Albert Einstein College of Medicine, that showed that taxol had a previously unknown mechanism of action involving the stabilization of microtubules. Together with formulation problems, this increased interest from researchers meant that by 1980 the NCI envisaged needing to collect 20,000 lbs of bark. Animal toxicology studies were complete by June 1982, and in November NCI applied for the IND necessary to begin clinical trials in humans.
Production of Paclitaxel
From 1967 to 1993, almost all paclitaxel produced was derived from bark from the Pacific yew, the harvesting of which kills the tree in the process. The processes used were descendants of the original isolation method of Wall and Wani; by 1987 the NCI had contracted Hauser Chemical Research of Boulder, Colorado to handle bark on the scale needed for Phase II and III trials. While there was considerable uncertainty about how large the wild population of Taxus brevifola was and what the eventual demand for taxol would be, it had been clear for many years that an alternative, sustainable source of supply would be needed. Initial attempts used needles from the tree, or material from other related Taxus species, including cultivated ones. But these attempts were bedevilled by the relatively low and often highly variable yields obtained. It was not until the early 1990s, at a time of increased sensitivity to the ecology of the forests of the Pacific Northwest, that taxol was successfully extracted on a clinically useful scale from these sources. From the late 1970s, chemists in the US and France had been interested in taxol. A number of US groups, including one led by Robert A. Holton, attempted a total synthesis of the molecule, starting from petrochemical-derived starting materials. This work was primarily motivated as a way of generating chemical knowledge, rather than with any expectation of developing a practical production technique. By contrast the French group of Pierre Potier at the CNRS quickly recognized the problem of yield. His laboratory was on a campus populated by the related yew Taxus baccata, so that needles were available locally in large quantity. By 1981 he had shown that it was feasible to isolate relatively large quantities of the compound 10-deacetylbaccatin, a plausible first step for a semi-synthetic production route to taxol. By 1988 he co-published such a semi-synthetic route from needles of Taxus baccata. The view of the NCI, however, was that even this route was not practical. By 1988, and particularly with Potier's publication, it was clear to Holton as well that a practical semi-synthetic production route would be important. By late 1989, Holton's group had developed a semi-synthetic route to paclitaxel with twice the yield of the Potier process. Florida State University, where Holton worked, signed a deal with Bristol-Myers Squibb to license this and future patents. In 1992, Holton patented an improved process with an 80% yield. BMS took the process in-house and started to manufacture paclitaxel in Ireland from 10-deacetylbaccatin isolated from the needles of the European yew. In early 1993, BMS were able to announce that they would cease reliance on Pacific yew bark by the end of 1995, effectively terminating the ecological controversy over its use. This announcement also made good their commitment to develop an alternative supply route, made to the NCI in their CRADA application of 1989. Currently, all paclitaxel production for BMS uses plant cell fermentation (PCF) technology developed by the biotechnology company Phyton Biotech, Inc and carried out at their plant in Germany. This starts from a specific taxus cell line propagated in aqueous medium in large fermentation tanks. Paclitaxel is then extracted directly, purified by chromatography and isolated by crystallization. Compared to the semi-synthesis, PCF eliminates the need for many hazardous chemicals and saves a considerable amount of energy. In 1993 it was discovered that taxol was coincidentally produced in a newly described fungus living in the yew tree.  It has since been found in a number of other endophytic fungi, including Nodulisporium sylviforme, opening the possibility of taxol production by culturing one of these fungal species. The initial motivation for synthetic approaches to paclitaxel included the opportunity to create closely related compounds. Indeed this approach led to the development of docetaxel.
TAXOL (paclitaxel) Injection is a clear, colorless to slightly yellow viscous solution. It is supplied as a nonaqueous solution intended for dilution with a suitable parenteral fluid prior to intravenous infusion. TAXOL is available in 30 mg (5 mL), 100 mg (16.7 mL), and 300 mg (50 mL) multidose vials. Each mL of sterile nonpyrogenic solution contains 6 mg paclitaxel, 527 mg of purified Cremophor® EL* (polyoxyethylated castor oil) and 49.7% (v/v) dehydrated alcohol, USP. Paclitaxel is a natural product with antitumor activity. TAXOL (paclitaxel) is obtained via a semi-synthetic process from Taxus baccata. The chemical name for paclitaxel is 5β,20-Epoxy-1,2α,4,7β,10β,13α-hexahydroxytax-11-en-9-one 4,10-diacetate 2-benzoate 13-ester with (2R,3S)-N-benzoyl-3-phenylisoserine.  Paclitaxel is a white to off-white crystalline powder with the empirical formula C47H51NO14 and a molecular weight of 853.9. It is highly lipophilic, insoluble in water, and melts at around 216-217° C.