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Namespace Prefixes

PrefixIRI
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Statements

Subject Item
n2:DB01248
rdf:type
n3:Drug
n3:description
Docetaxel is a clinically well established anti-mitotic chemotherapy medication used mainly for the treatment of breast, ovarian, and non-small cell lung cancer. Docetaxel binds to microtubules reversibly with high affinity and has a maximum stoichiometry of one mole docetaxel per mole tubulin in microtubules.
n3:dosage
n17:271B5EC0-363D-11E5-9242-09173F13E4C5 n17:271B5EC1-363D-11E5-9242-09173F13E4C5 n17:271B5EC2-363D-11E5-9242-09173F13E4C5 n17:271B5EC3-363D-11E5-9242-09173F13E4C5 n17:271B5EC9-363D-11E5-9242-09173F13E4C5 n17:271B5EBF-363D-11E5-9242-09173F13E4C5 n17:271B5EC5-363D-11E5-9242-09173F13E4C5 n17:271B5EC6-363D-11E5-9242-09173F13E4C5 n17:271B5EC7-363D-11E5-9242-09173F13E4C5 n17:271B5EC8-363D-11E5-9242-09173F13E4C5 n17:271B5EC4-363D-11E5-9242-09173F13E4C5
n3:generalReferences
# FDA label
n3:group
investigational approved
n3:halfLife
Dose-dependent. Doses of 70 mg per square meter of body surface area (mg/m 2 ) or higher produce a triphasic elimination profile. With lower doses, assay limitations precluded detection of the terminal elimination phase. The half-life of the alpha, beta, and gamma phase are 4 minutes, 36 minutes, and 11.1 hours, respectively.
n3:indication
For the treatment of patients with locally advanced or metastatic breast cancer after failure of prior chemotherapy. Also used as a single agent in the treatment of patients with locally advanced or metastatic non-small cell lung cancer after failure of prior platinum-based chemotherapy. It is also used in combination with prednisone, in the treatment of patients with androgen independent (hormone refractory) metastatic prostate cancer. Furthermore, docetaxel has uses in the treatment of gastric adenocarinoma and head and neck cancer.
owl:sameAs
n20:DB01248 n22:DB01248
dcterms:title
Docetaxel
adms:identifier
n6:D02165 n7:Docetaxel n21:130581 n23:DB01248 n24:4672 n25:0075-8001-80 n26:PA449383 n27:C11231 n28:148124 n29:46506766
n3:mechanismOfAction
Docetaxel interferes with the normal function of microtubule growth. Whereas drugs like colchicine cause the depolymerization of microtubules in vivo, docetaxel 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, docetaxel binds to the β-subunit of tubulin. Tubulin is the "building block" of mictotubules, and the binding of docetaxel locks these building blocks in place. The resulting microtubule/docetaxel 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 docetaxel 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.
n3:packager
n15:271B5EBD-363D-11E5-9242-09173F13E4C5
n3:patent
n12:5438072 n12:2149055 n12:2150576 n12:4814470
n3:routeOfElimination
Docetaxel was eliminated in both the urine and feces following oxidative metabolism of the tert-butyl ester group, but fecal excretion was the main elimination route. Within 7 days, urinary and fecal excretion accounted for approximately 6% and 75% of the administered radioactivity, respectively.
n3:synonym
Docetaxel anhydrous N-Debenzoyl-N-(tert-butoxycarbonyl)-10-deacetyltaxol N-Debenzoyl-N-(tert-butoxycarbonyl)-10-deacetylpaclitaxel TXL
n3:toxicity
Oral LD<sub>50</sub> in rat is >2000 mg/kg. Anticipated complications of overdosage include: bone marrow suppression, peripheral neurotoxicity, and mucositis. In two reports of overdose, one patient received 150 mg/m<sup>2</sup> and the other received 200 mg/m<sup>2</sup> as 1-hour infusions. Both patients experienced severe neutropenia, mild asthenia, cutaneous reactions, and mild paresthesia, and recovered without incident.
n3:volumeOfDistribution
The initial rapid decline represents distribution to the peripheral compartments and the late (terminal) phase is due, in part, to a relatively slow efflux of docetaxel from the peripheral compartment. * 113 L
n13:hasAHFSCode
n18:10-00-00
n3:proteinBinding
In vitro studies show that 94% protein bound, mainly to a1-acid glycoprotein, albumin, and lipoproteins. When measured in cancer patients, docetaxel is 97% bound to plasma protein. Dexamethasone does not affect the protein binding of docetaxel.
n3:synthesisReference
Nicholas J. Sisti, Charles S. Swindell, "Method for docetaxel synthesis." U.S. Patent US5688977, issued September, 1991.
n10:hasConcept
n11:M0184558
foaf:page
n9:docetaxel.htm n16:docetaxel.html
n3:IUPAC-Name
n4:271B5ECE-363D-11E5-9242-09173F13E4C5
n3:InChI
n4:271B5ED4-363D-11E5-9242-09173F13E4C5
n3:Molecular-Formula
n4:271B5ED3-363D-11E5-9242-09173F13E4C5
n3:Molecular-Weight
n4:271B5ED0-363D-11E5-9242-09173F13E4C5
n3:Monoisotopic-Weight
n4:271B5ED1-363D-11E5-9242-09173F13E4C5
n3:SMILES
n4:271B5ED2-363D-11E5-9242-09173F13E4C5
n3:Water-Solubility
n4:271B5ECC-363D-11E5-9242-09173F13E4C5 n4:271B5EE4-363D-11E5-9242-09173F13E4C5
n3:logP
n4:271B5ECD-363D-11E5-9242-09173F13E4C5 n4:271B5ECA-363D-11E5-9242-09173F13E4C5 n4:271B5EE6-363D-11E5-9242-09173F13E4C5
n3:logS
n4:271B5ECB-363D-11E5-9242-09173F13E4C5
n13:hasATCCode
n14:L01CD02
n3:H-Bond-Acceptor-Count
n4:271B5EDA-363D-11E5-9242-09173F13E4C5
n3:H-Bond-Donor-Count
n4:271B5EDB-363D-11E5-9242-09173F13E4C5
n3:InChIKey
n4:271B5ED5-363D-11E5-9242-09173F13E4C5
n3:Polar-Surface-Area--PSA-
n4:271B5ED6-363D-11E5-9242-09173F13E4C5
n3:Polarizability
n4:271B5ED8-363D-11E5-9242-09173F13E4C5
n3:Refractivity
n4:271B5ED7-363D-11E5-9242-09173F13E4C5
n3:Rotatable-Bond-Count
n4:271B5ED9-363D-11E5-9242-09173F13E4C5
n3:absorption
The pharmacokinetic profile is consistent with a three-compartment model. The area under the curve (AUC) was dose proportional following doses of 70 mg/m2 to 115 mg/m2 with infusion times of 1 to 2 hours.
n3:affectedOrganism
Humans and other mammals
n3:casRegistryNumber
114977-28-5
n3:category
n3:clearance
* 21 L/h/m2 [Total body clearance, cancer patients after IV administration of 20–115 mg/m2]
n3:containedIn
n30:271B5EBE-363D-11E5-9242-09173F13E4C5
n3:Bioavailability
n4:271B5EE0-363D-11E5-9242-09173F13E4C5
n3:Ghose-Filter
n4:271B5EE2-363D-11E5-9242-09173F13E4C5
n3:MDDR-Like-Rule
n4:271B5EE3-363D-11E5-9242-09173F13E4C5
n3:Melting-Point
n4:271B5EE5-363D-11E5-9242-09173F13E4C5
n3:Number-of-Rings
n4:271B5EDF-363D-11E5-9242-09173F13E4C5
n3:Physiological-Charge
n4:271B5EDE-363D-11E5-9242-09173F13E4C5
n3:Rule-of-Five
n4:271B5EE1-363D-11E5-9242-09173F13E4C5
n3:Traditional-IUPAC-Name
n4:271B5ECF-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-acidic-
n4:271B5EDC-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-basic-
n4:271B5EDD-363D-11E5-9242-09173F13E4C5