Paclitaxel Chemical formula
Synonyms: BMS-181339-01; NSC-125973; Paclitaxelum; Paklitakseeli; Paklitaksel; Paklitaxel; Taxol; Taxol A. (2S,5R,7S,10R,13S)-10,20-Bis(acetoxy)-2-benzoyloxy-1,7-dihydroxy-9-oxo-5,20-epoxytax-11-en13-yl (3S)-3-benzoylamino-3-phenyl
Cyrillic synonym: Паклитаксел.

💊 Chemical information

Chemical formula: C47H51NO14 = 853.9.
CAS — 33069-62-4.
ATC — L01CD01.
ATC Vet — QL01CD01.


In Eur. and US.

Ph. Eur. 6.2

(Paclitaxel). Isolated from natural sources or produced by fermentation or by a semisynthetic process. A white or almost white, crystalline powder. Practically insoluble in water; freely soluble in dichloromethane; soluble in methyl alcohol. Store in airtight containers. Protect from light.

USP 31

(Paclitaxel). A white to off-white powder. Insoluble in water; soluble in alcohol. Store in airtight containers at a temperature between 20° and 25°. Protect from light.


The vehicle for paclitaxel injection, which contains alcohol and polyoxl castor oil, was found to leach the plasticiser diethylhexyl phthalate from some plastic giving sets. 1,2 Consequently, licensed product information recommends the use of non-PVC containers and giving sets. Paclitaxel was found to be compatible with doxorubicin for at least 24 hours, but microcrystalline precipitation of paclitaxel occurred after 3 to 5 days. 3 For mention of the incompatibility of paclitaxel and cisplatin. 1. Trissel LA, et al. Compatibility of paclitaxel injection vehicle with intravenous administration and extension sets. Am J Hosp Pharm 1994; 51: 2804–10. 2. Mazzo DJ, et al. Compatibility of docetaxel and paclitaxel in intravenous solutions with polyvinyl chloride infusion materials. Am J Health-Syst Pharm 1997; 54: 566–9. 3. Trissel LA, et al. Compatibility and stability of paclitaxel combined with doxorubicin hydrochloride in infusion solutions. Ann Pharmacother 1998; 32: 1013–6.

💊 Adverse Effects, Treatment, and Precautions

Paclitaxel produces severe dose-limiting bone marrow depression, the nadir of the white cell count usually occurring after about 11 days, with recovery usually by day 15 to 21 after a dose. Myelosuppression may be less frequent and less severe when infusions are given over 3 rather than 24 hours. Peripheral neuropathy can also be severe, and occasionally dose-limiting. Hypersensitivity reactions, with flushing, rash, dyspnoea, hypotension, chest pain, and angioedema may occur, and all patients should be given initial premedication with corticosteroids, antihistamines, and histamine H 2 -antagonists. Other adverse effects include alopecia, arthralgia and myalgia, gastrointestinal disturbances, mucositis, bradycardia and ECG changes, nail dystrophies, and elevation of liver enzyme values. Infections are common, as are injection site reactions; extravasation may result in tissue damage. Rare adverse events include hypertension, severe thrombotic events, myocardial infarction, heart failure, severe cardiac conduction abnormalities, seizures, neuroencephalopathy, paralytic ileus, optic nerve disturbances, severe skin reactions, hepatic necrosis, and hepatic encephalopathy. There are rare reports of interstitial pneumonia and other lung disorders. Paclitaxel is not recommended in patients with severely impaired hepatic function. The drug is formulated in polyoxyl castor oil and should be avoided in patients hypersensitive to this substance. The formulation also contains alcohol, the CNS effects of which should be considered. Blood counts should be monitored frequently. Continuous cardiac monitoring is needed in patients who have had previous significant conduction abnormalities when given paclitaxel.

Alcohol intoxication.

Acute alcohol intoxication resulting from high-dose paclitaxel infusion has been reported;1 it was calculated that the dose used (348 mg/m2) supplied 50 mL of alcohol, or the equivalent of about 3 drinks (half a bottle of wine).
1. Wilson DB, et al. Paclitaxel formulation as a cause of ethanol intoxication. Ann Pharmacother 1997; 31: 873–5.

Effects on the eyes.

Optic neuritis has occurred with paclitaxel. There is a report of glaucoma possibly related to the use of docetaxel and paclitaxel in a patient also receiving corticosteroids.1
1. Fabre-Guillevin E, et al. Taxane-induced glaucoma. Lancet 1999; 354: 1181–2.

Effects on the heart.

Infusion of paclitaxel has been associated with sinus bradycardia, atrial arrhythmias, ventricular tachycardia, heart block, myocardial infarction, and sudden death.1,2Symptoms of heart failure have been reported.3 In another report sudden death 7 days after paclitaxel treatment raised the question of whether paclitaxel might have had a delayed effect.4 There is some evidence of cellular damage to the myocardium of a patient with paclitaxel-associated cardiac symptoms.3 Licensed product information notes that severe cardiovascular events have been seen more frequently after the use of paclitaxel in patients with non-small cell lung cancer than in those with breast or ovarian carcinoma.
1. Rowinsky EK, et al. Cardiac disturbances during the administration of taxol. J Clin Oncol 1991; 9: 1704–12
2. Arbuck SG, et al. A reassessment of cardiac toxicity associated with Taxol. J Natl Cancer Inst Monogr 1993; 15: 117–30
3. Jekunen A, et al. Paclitaxel-induced myocardial damage detected by electron microscopy. Lancet 1994; 343: 727–8
4. Alagaratnam TT. Sudden death 7 days after paclitaxel infusion for breast cancer. Lancet 1993; 342: 1232–3.

Effects on the musc

uloskeletal system. Gabapentin has been reported to be of benefit in the management of taxaneinduced arthralgia and myalgia.1,2
1. van Deventer H, Bernard S. Use of gabapentin to treat taxaneinduced myalgias. J Clin Oncol 1999; 17: 434–5
2. Nguyen VH, Lawrence HJ. Use of gabapentin in the prevention of taxane-induced arthralgias and myalgias. J Clin Oncol 2004; 22: 1767–9.

Effects on the respiratory system.

Acute bilateral interstitial pneumonitis has been reported rarely in patients receiving paclitaxel, despite premedication with corticosteroids and histamine antagonists.1 Symptoms resolved on treatment with parenteral corticosteroids.
1. Khan A, et al. Paclitaxel-induced acute bilateral pneumonitis. Ann Pharmacother 1997; 31: 1471–4.

Effects on the skin and nails.

Nail changes, noted as pigmentation or discoloration of the nail-bed, may occur with paclitaxel. Onycholysis (separation of the nail from the nail-bed) has also been reported.1 Discoloration and onycholysis can also occur after docetaxel use, and there are reports of subungual hyperkeratosis and haemorrhage.2-4 Localised oedema evolving into skin sclerosis, mimicking systemic sclerosis, has been reported after taxane use. In most patients, the sclerosis developed mainly on the extremities, and especially the lower extremities. Joint contracture may occur. The total cumulative dose of the taxane may contribute to the onset.5
1. Flory SM, et al. Onycholysis associated with weekly administration of paclitaxel. Ann Pharmacother 1999; 33: 584–5
2. Wasner G, et al. Clinical picture: nail changes secondary to docetaxel. Lancet 2001; 357: 910
3. Pavithran K, Doval DC. Nail changes due to docetaxel. Br J Dermatol 2002; 146: 709–10
4. Leonard GD, Zujewski JA. Docetaxel-related skin, nail, and vascular toxicity. Ann Pharmacother 2003; 37: 148
5. Itoh M, et al. Taxane-induced scleroderma. Br J Dermatol 2007; 156: 363–7.


Despite premedication with corticosteroids, antihistamines, and H2-antagonists, hypersensitivity reactions are common in patients given paclitaxel; up to about 40% of patients may have a mild reaction and about 2% a severe reaction. Fatalities have been reported. There are rare reports of delayed hypersensitivity reactions with paclitaxel; necrotic ulceration has occurred, without evidence of extravasation.1 Some consider the cause to be the polyoxyl castor oil diluent for paclitaxel, and docetaxel has been suggested as a suitable alternative.2 However, hypersensitivity reactions have also occurred with docetaxel and taxane cross-reactivity has been reported.3,4 Although the manufacturers of both drugs consider further use to be contra-indicated after a severe reaction, strategies for continuation of treatment and desensitisation have been described.5,6 Hypersensitivity reactions to paclitaxel-eluting stents have also been reported;7 however, the incidence is low, and some consider the polymer coating of the stent to be the likely cause.8
1. Beri R, et al. Severe dermatologic reactions at multiple sites after paclitaxel administration. Ann Pharmacother 2004; 38: 238–41
2. Bernstein BJ. Docetaxel as an alternative to paclitaxel after acute hypersensitivity reactions. Ann Pharmacother 2000; 34: 1332–5
3. Denman JP, et al. Hypersensitivity reaction (HSR) to docetaxel after a previous HSR to paclitaxel. J Clin Oncol 2002; 20: 2760–1
4. Karacan Ö, et al. Acute interstitial pneumopathy associated with docetaxel hypersensitivity. Onkologie 2004; 27: 563–5
5. Markman M, et al. Paclitaxel-associated hypersensitivity reactions: experience of the gynecologic oncology program of the Cleveland Clinic Cancer Center. J Clin Oncol 2000; 18: 102–5
6. Feldweg AM, et al. Rapid desensitization for hypersensitivity reactions to paclitaxel and docetaxel: a new standard protocol used in 77 successful treatments. Gynecol Oncol 2005; 96: 824–9
7. Nebeker JR, et al. Hypersensitivity cases associated with drugeluting coronary stents: a review of available cases from the Research on Adverse Drug Events and Reports (RADAR) project. J Am Coll Cardiol 2006; 47: 175–81
8. Azarbal B, Currier JW. Allergic reactions after the implantation of drug-eluting stents: is it the pill or the polymer? J Am Coll Cardiol 2006; 47: 182–3.


Paclitaxel has been shown to be fetotoxic in animal studies, but although the use of potentially teratogenic drugs would normally be avoided during pregnancy, the risk to the mother of inadequate treatment may outweigh whatever risks exist of abnormality in the fetus. Paclitaxel has been used in the treatment of a patient who presented at 27 weeks of gestation with ovarian cancer. She had cytoreductive surgery and then adjuvant chemotherapy consisting of 3 cycles of paclitaxel and cisplatin given every 3 weeks. A healthy child was delivered by caesarean section at 37 weeks, and showed normal growth and development at 30 months of age.1 Anhydramnios has been associated with the use of trastuzumab and paclitaxel, see Pregnancy, under Trastuzumab.
1. Sood AK, et al. Paclitaxel and platinum chemotherapy for ovarian carcinoma during pregnancy. Gynecol Oncol 2001; 83: 599–600.

💊 Interactions

For a general outline of antineoplastic drug interactions. Pretreatment with cisplatin may reduce the clearance of paclitaxel, resulting in increased toxicity, and when both drugs are given, paclitaxel should be given first.


For reference to enhanced cardiotoxicity when paclitaxel was given with doxorubicin. For the pharmacokinetic changes reported when paclitaxel was given with gemcitabine. Pretreatment with fluorouracil has been reported to inhibit paclitaxel’s cytotoxic action, possibly by preventing tumour cells from entering the G2-M phases of the cell cycle.1 The effect also occurred when the 2 drugs were given simultaneously, suggesting that combination therapy might not be appropriate. Valspodar inhibits P-glycoprotein, and a pharmacokinetic study2found that it decreased clearance of paclitaxel and prolonged the terminal half-life, increasing exposure to paclitaxel and myelosuppressive effects. The authors suggested that the dose of paclitaxel may need to be reduced by about 60%.
1. Johnson KR, et al. 5-Fluorouracil interferes with paclitaxel cytotoxicity against human solid tumor cells. Clin Cancer Res 1997; 3: 1739–45
2. Advani R, et al. A phase I trial of doxorubicin, paclitaxel, and valspodar (PSC 833), a modulator of multidrug resistance. Clin Cancer Res 2001; 7: 1221–9.


HIV-PROTEASE INHIBITORS. In a patient given various antiretrovirals during paclitaxel treatment for Kaposi’s sarcoma, pharmacokinetic parameters of paclitaxel were not significantly different when compared with historical controls.1 The first course of therapy combined paclitaxel with lamivudine, stavudine, and the HIV-protease inhibitors ritonavir and saquinavir. In subsequent courses, paclitaxel was given with nevirapine, and the final course consisted of paclitaxel given with ritonavir and indinavir. However, licensed product information for paclitaxel states that studies suggest that systemic clearance of paclitaxel was significantly lower in the presence of nelfinavir and ritonavir, but not indinavir, and that paclitaxel should be given with caution to patients taking HIV-protease inhibitors. HIV-protease inhibitors are metabolised by the cytochrome P450 isoenzyme CYP3A4, but are also reported to inhibit CYP3A activity. This may lead to increased adverse effects when given with taxanes; the combination of delavirdine and saquinavir has been reported to cause serious mucositis, severe myalgia, alopecia, and leucopenia when given with paclitaxel.2
1. Nannan Panday VR, et al. Paclitaxel in the treatment of human immunodeficiency virus 1-associated Kaposi’s sarcoma—drugdrug interactions with protease inhibitors and a nonnucleoside reverse transcriptase inhibitor: a case report study. Cancer Chemother Pharmacol 1999; 43: 516–19
2. Schwartz JD, et al. Potential interaction of antiretroviral therapy with paclitaxel in patients with AIDS-related Kaposi’s sarcoma. AIDS 1999; 13: 283–4.


Ciclosporin increased the oral absorption of paclitaxel, possibly by inhibiting the multidrug transporter P-glycoprotein in the gastrointestinal tract.1 For the effects of valspodar (an analogue of ciclosporin) on paclitaxel, see Antineoplastics, above.
1. Meerum Terwogt JM, et al. Co-administration of cyclosporin enables oral therapy with paclitaxel. Lancet 1998; 352: 285. Correction. ibid.; 824.

💊 Pharmacokinetics

Intravenous paclitaxel exhibits a biphasic decline in plasma concentrations, with a mean terminal half-life of anywhere between about 3 and 50 hours. The pharmacokinetics are non-linear. The steady-state volume of distribution is reported to range from 200 to 700 litres/m 2 , indicating extensive extravascular distribution, tissue binding, or both. Paclitaxel is 89% or more bound to plasma protein in vitro. The elimination of paclitaxel has not been fully elucidated; only about 1 to 12% of a dose is reported to be excreted in urine, as unchanged drug, indicating extensive non-renal clearance. Paclitaxel is metabolised in the liver, with the major metabolic pathway apparently mediated by the cytochrome P450 isoenzyme CYP2C8, although CYP3A4 may play a minor role. Metabolites are excreted in the faeces via the bile, the primary metabolite being 6 α-hydroxypaclitaxel.
1. Sonnichsen DS, Relling MV. Clinical pharmacokinetics of paclitaxel. Clin Pharmacokinet 1994; 27: 256–69
2. Walle T, et al. Taxol metabolism and disposition in cancer patients. Drug Metab Dispos 1995; 23: 506–12
3. Sonnichsen DS, et al. Variability in human cytochrome P450 paclitaxel metabolism. J Pharmacol Exp Ther 1995; 275: 566–75
4. Henningsson A, et al. Mechanism-based pharmacokinetic model for paclitaxel. J Clin Oncol 2001; 19: 4065–73.

💊 Uses and Administration

Paclitaxel is a taxane originally derived from the bark of the Pacific yew tree Taxus brevifolia (Taxaceae), and now obtained semisynthetically from a taxane precursor derived from the needles of the European yew, Tax us baccata. Paclitaxel’s antineoplastic action arises from induction of microtubule formation and stabilisation of microtubules, thereby disrupting normal cell division in the G 2 and M phases of the cell cycle. Paclitaxel is used for the primary treatment of advanced ovarian cancer with cisplatin or carboplatin, and for secondary treatment. In the treatment of node-positive breast cancer, paclitaxel is used for primary adjuvant therapy after anthracycline-containing chemotherapy. In locally advanced or metastatic breast cancer, it is used first-line with an anthracycline, or as a second-line single-agent, usually after failure of anthracycline-based therapy. In patients with metastatic disease who overexpress HER2 (human epidermal growth receptor 2) it may be used with trastuzumab as initial therapy. Paclitaxel is used with cisplatin or carboplatin, for the primary treatment of advanced non-small cell lung cancer. It may be used for the second-line treatment of AIDS-related Kaposi’s sarcoma, and has been tried in other neoplasms including cancers of the head and neck, and relapsed germ-cell tumours. The recommended dose for the primary treatment of ovarian cancer is 135 mg/m 2 infused over 24 hours, followed by cisplatin, and repeated at 3-week intervals. Alternatively 175 mg/m 2 may be infused over 3 hours, followed by cisplatin, every 3 weeks. For the secondary treatment of ovarian cancer, the suggested dose as a single agent is 135 or 175 mg/m 2 infused over 3 hours once every 3 weeks. For breast cancer, a dose of paclitaxel 175 mg/m 2 infused over 3 hours once every 3 weeks is recommended for adjuvant treatment (for 4 courses), for secondline monotherapy, and for first-line treatment with trastuzumab; paclitaxel is given the day after the first dose of trastuzumab, or immediately after subsequent doses if well-tolerated. When used first-line with doxorubicin, paclitaxel 220 mg/m 2 is infused over 3 hours once every 3 weeks; the dose is given 24 hours after doxorubicin. In non-small cell lung cancer, the recommended dose is 135 mg/m 2 over 24 hours or 175 mg/m 2 over 3 hours, followed by cisplatin, and repeated at 3-week intervals. A dose of 135 mg/m 2 over 3 hours once every 3 weeks has been suggested for AIDS-related Kaposi’s sarcoma. Alternatively, 100 mg/m 2 over 3 hours every 2 weeks may be given, especially in patients with poor performance status. Regular blood counts should be performed, and dosage should not be repeated until the neutrophil and platelet counts are at acceptable levels; the neutrophil count should be above 1000 cells/mm 3 in patients with AIDS. The dose should be reduced by 20% in subsequent courses in patients who have severe neutropenia or peripheral neuropathy. Patients should be pretreated with corticosteroids, antihistamines, and histamine H 2 -antagonists. The dose of paclitaxel may need to be reduced in patients with hepatic impairment (see below). Various formulations have been developed to avoid the use of polyoxyl castor oil and improve the efficacy and safety of paclitaxel. An injectable suspension of albumin-bound paclitaxel nanoparticles (Abraxane; Abraxis, USA; ABI-007) is available for the treatment of refractory or relapsed breast cancer. The dose is 260 mg/m 2 given intravenously over 30 minutes every 3 weeks. Other formulations in development include paclitaxel linked to docosahexaenoic acid or biodegradable polymers (such as paclitaxel poliglumex), micellar and liposomal formulations, and an oral dosage form. An injectable vitamin E-based emulsion of paclitaxel has been investigated for the treatment of urothelial cancer and metastatic breast cancer. Paclitaxel-releasing stents may be used to reduce restenosis after coronary artery stent placement.
1. Gelmon K. The taxoids: paclitaxel and docetaxel. Lancet 1994; 344: 1267–72
2. Long HJ. Paclitaxel (Taxol): a novel anticancer chemotherapeutic drug. Mayo Clin Proc 1994: 69: 341–5
3. Spencer CM, Faulds D. Paclitaxel: a review of its pharmacodynamic and pharmacokinetic properties and therapeutic potential in the treatment of cancer. Drugs 1994; 48: 794–847
4. Rowinsky EK, Donehower RC. Paclitaxel (Taxol). N Engl J Med 1995; 332: 1004–14. Correction. ibid.; 333: 75
5. Anonymous. Paclitaxel and docetaxel in breast and ovarian cancer. Drug Ther Bull 1997; 35: 43–6
6. Eisenhauer EA, Vermorken JB. The taxoids: comparative clinical pharmacology and therapeutic potential. Drugs 1998; 55: 5–30
7. Crown J, O’Leary M. The taxanes: an update. Lancet 2000; 355: 1176–8
8. Michaud LB, et al. Risks and benefits of taxanes in breast and ovarian cancer. Drug Safety 2000; 23: 401–28
9. Simpson D, Plosker GL. Paclitaxel: as adjuvant or neoadjuvant therapy in early breast cancer. Drugs 2004; 64: 1839–47
10. Anonymous. Albumin-bound paclitaxel (Abraxane) for advanced breast cancer. Med Lett Drugs Ther 2005; 47: 39–40
11. Harries M, et al. Nanoparticle albumin-bound paclitaxel for metastatic breast cancer. J Clin Oncol 2005; 23: 7768–71
12. Robinson DM, Keating GM. Albumin-bound paclitaxel: in metastatic breast cancer. Drugs 2006; 66: 941–8
13. Hayes DF, et al. Cancer and Leukemia Group B (CALGB) Investigators. HER2 and response to paclitaxel in node-positive breast cancer. N Engl J Med 2007; 357: 1496–1506
14. Seidman AD, et al. Randomized phase III trial of weekly compared with every-3-weeks paclitaxel for metastatic breast cancer, with trastuzumab for all HER-2 overexpressors and random assignment to trastuzumab or not in HER-2 nonoverexpressors: final results of Cancer and Leukemia Group B protocol 9840. J Clin Oncol 2008; 26: 1642–9.


Although many of the original studies of paclitaxel employed a 24-hour infusion regimen, the use of 3-hour infusions has subsequently become widespread. A systematic review1 noted that although it was difficult to compare efficacy in studies of unlike malignancies there was no conclusive evidence of a difference in effectiveness with differing length of infusion; however, there were differences in the adverse effect profile, neutropenia being much less marked with the shorter infusion, although neurotoxic effects were reduced with 24-hour administration. There has also been considerable interest in evaluating the use of paclitaxel in reduced-dose weekly schedules.2-12 Various dosage regimens have been tried: most have found that doses of between 50 and about 100 mg/m2 weekly, usually by infusion over 1 hour rather than a conventional 3-hour infusion, can be given with relatively modest toxicity. Although higher doses have been tried, neurotoxicity and myelosuppression become problematic and tend to limit dose intensity. A number of studies have addressed the combination of weekly paclitaxel with other antineoplastics, for example with trastuzumab in breast cancer, estramustine in prostate cancer, and with platinum compounds or gemcitabine in other solid tumours such as those of the ovary or lung. Weekly paclitaxel is also under investigation in combination with radiotherapy in the management of lung cancer and glioblastoma multiforme.
1. Williams C, et al. Short versus long duration infusions of paclitaxel for any advanced adenocarcinoma. Available in The Cochrane Database of Systematic Reviews; Issu
3. Chichester: John Wiley; 2002 (accessed 12/05/05)
2. Seidman AD, et al. Dose-dense therapy with weekly 1-hour paclitaxel infusions in the treatment of metastatic breast cancer. J Clin Oncol 1998; 16: 3353–61
3. Fountzilas G, et al. Radiation and concomitant weekly administration of paclitaxel in patients with glioblastoma multiforme: a phase II study. J Neurooncol 1999; 45: 159–65
4. Markman M. Weekly paclitaxel in the management of ovarian cancer. Semin Oncol 2000; 27 (suppl 7): 37–40
5. De Pas T, et al. Phase I and pharmacologic study of weekly gemcitabine and paclitaxel in chemo-naive patients with advanced non-small-cell lung cancer. Ann Oncol 2000; 11: 821–7
6. Langer CJ, et al. Paclitaxel by 1-h infusion in combination with carboplatin in advanced non-small cell lung carcinoma (NSCLC). Eur J Cancer 2000; 36: 183–93
7. Akerley W. Recent developments in weekly paclitaxel therapy in lung cancer. Curr Oncol Rep 2001; 3: 165–9
8. Haas N, et al. Phase I trial of weekly paclitaxel plus oral estramustine phosphate in patients with hormone-refractory prostate cancer. Urology 2001; 58: 59–64
9. Seidman AD, et al. Weekly trastuzumab and paclitaxel therapy for metastatic breast cancer with analysis of efficacy by HER2 immunophenotype and gene amplification. J Clin Oncol 2001; 19: 2587–95
10. Kouroussis C, et al. A dose-finding study of the weekly administration of paclitaxel in patients with advanced solid tumors. Am J Clin Oncol 2001; 24: 404–7
11. Brambilla L, et al. Weekly paclitaxel for advanced aggressive classic Kaposi sarcoma: experience in 17 cases. Br J Dermatol 2008; 158: 1339–44
12. Sparano JA, et al. Weekly paclitaxel in the adjuvant treatment of breast cancer. N Engl J Med 2008; 358: 1663–71. Correction. ibid.; 359: 106.

Administration in hepatic impairment.

The US licensed product information makes recommendations for initial dosage adjustment of some paclitaxel regimens in patients with hepatic impairment, according to transaminase and bilirubin concentrations. They suggest paclitaxel should not be given if transaminase values are more than 10 times normal upper limits, or if bilirubin is more than 75 micrograms/mL or 5 times the normal upper limit.

Reperfusion and revascularisation procedures.

Restenosis is a particular problem after percutaneous coronary revascularisation procedures and various drugs have been tried for its prevention. Coronary stents that elute paclitaxel effectively reduce restenosis and have been widely used, although there is some suggestion that sirolimus-eluting stents may be superior to paclitaxel-eluting stents in terms of clinical outcome and rates of restenosis.1-3 In a study compared with bare metal stents, paclitaxel-releasing stents reduced the risk of restenosis and the need for repeat revascularisation procedures, although the follow-up rates of death from cardiac causes or myocardial infarction were not significantly reduced at 9 months4 and 1 year.5 However, between 9 months and 1 year, major cardiac adverse events were significantly reduced in the paclitaxel-releasing stent group compared to controls.5 A review6 of various stent designs concluded that safety of paclitaxel-releasing stents was independent of design, dose-density, or presence or absence of a polymer carrier system; however, those without a polymer carrier were unable to show a positive effect on clinical outcome in patients with de novo coronary lesions. However, in a paclitaxel-releasing stent system, failure of the stent-delivery balloon to deflate has been associated with serious injuries and 1 fatality.7 The risk of late stent thrombosis may also be increased with drug eluting stents,8 although the evidence is controversial,9 and their role in complex interventions is not yet established.10,11 Positive effects on restenosis have also been reported12 with use of a paclitaxel-coated angioplasty balloon.
1. Windecker S, et al. Sirolimus-eluting and paclitaxel-eluting stents for coronary revascularization. N Engl J Med 2005; 353: 653–62
2. Dibra A, et al. Paclitaxel-eluting or sirolimus-eluting stents to prevent restenosis in diabetic patients. N Engl J Med 2005; 353: 663–70
3. Hofma SH, et al. One year clinical follow up of paclitaxel eluting stents for acute myocardial infarction compared with sirolimus eluting stents. Heart 2005; 91: 1176–80
4. Stone GW, et al. A polymer-based, paclitaxel-eluting stent in patients with coronary artery disease. N Engl J Med 2004; 350: 221–31
5. Stone GW, et al. One-year clinical results with the slow-release, polymer-based, paclitaxel-eluting TAXUS stent: the TAXUSIV trial. Circulation 2004; 109: 1942–7
6. Silber S. Paclitaxel-eluting stents: are they all equal? An analysis of six randomized controlled trials in de novo lesions of 3,319 patients. J Interv Cardiol 2003; 16: 485–90
7. Muni NI, Gross TP. Problems with drug-eluting coronary stents—the FDA perspective. N Engl J Med 2004; 351: 1593–5
8. Stone GW, et al. Safety and efficacy of sirolimus- and paclitaxel-eluting coronary stents. N Engl J Med 2007; 356: 998–1008
9. Mauri L, et al. Stent thrombosis in randomized clinical trials of drug-eluting stents. N Engl J Med 2007; 356: 1020–9
10. Beohar N, et al. Outcomes and complications associated with off-label and untested use of drug-eluting stents. JAMA 2007; 297: 1992–2000
11. Win HK, et al. Clinical outcomes and stent thrombosis following off-label use of drug-eluting stents. JAMA 2007; 297: 2001–9
12. Scheller B, et al. Treatment of coronary in-stent restenosis with a paclitaxel-coated balloon catheter. N Engl J Med 2006; 355: 2113–24.

💊 Preparations

USP 31: Paclitaxel Injection.

Proprietary Preparations

Arg.: Asotax; Clitaxel; Dalys; Drifen; Erioxal; Paclikebir; Pacliteva; Paklitaxfil; Panataxel; Tarvexol; Taxocris; Taxol; Taycovit; Austral.: Anzatax; Taxol; Austria: Ebetaxel; Taxol; Belg.: Paclitaxin; Paxene; Taxol; Braz.: Biopaxel; Onxel; Paclitax; Parexel; Paxel†; Taclipaxol†; Taclix†; Tarvexol; Taxilan; Taxol; Canad.: Ta x o l ; Chile: Britaxol; Oncoplaxel; Praxel; Taxodiol; Cz.: Anzatax; OncoTax; Onxol; Paclimedac; Pacline; Paxene; Taxol; Denm.: Ta x o l ; Fin.: Ta x o l ; Fr.: Paxene; Taxol; Ger.: NeoTaxan; Ribotax; Taxol; Gr.: Biotaxel; Ovapac; Paclit; Paclitaxin; Paclitol; Paclixel; Pataxel; Paxene; Ribotal; Taxogen; Tax o l ; Ta x o pr o l ; Hong Kong: Anzatax; Taxol; Hung.: Genexol; Intaxel; Magytax; Paxene; Taxol; India: Intaxel; Paclitax; Petaxel; Indon.: Anzatax; Paxus; Taxol; Irl.: Paxene; Taxol; Israel: Biotax; Ebetaxel; Medixel; Taxol†; Ital.: Anzatax; Paxene; Taxol; Jpn: Ta x o l ; Malaysia: Anzatax; Formoxol; Mitotax; Taxol; Mex.: Asotax; BrisTaxol; Cryoxet; Daburex; Ifaxol; Paclisan; Praxel; Neth.: Paclitaxin; Paxene; Taxol; Norw.: Ta x o l ; NZ: Ta x o l ; Philipp.: Intaxel; Taxol; Unitaxel; Pol.: Poltaxel; Sindaxel; Taxol; Port.: Paxene; Taxobine; Taxol; Rus.: Abitaxel (Абитаксел)†; Mitotax (Митотакс); Paxene (Паксен); Taxol (Таксол); S.Afr.: Anzatax; Biolyse; Taxol; Singapore: Anzatax; Genexol; Taxol; Spain: Paxene; Taxol; Swed.: Paxene; Taxol; Switz.: Ta x o l ; Thai.: Anzatax; Intaxel; Oncotaxel; Praxel; Taxol; Turk.: Anzatax; Ta x o l ; UK: Paxene; Taxol; USA: Abraxane; Onxol; Taxol; Venez.: Clitaxel; Intaxel; Paclitax.
Published February 01, 2019.