Compound Information | SONAR Target prediction |
Name: | PACLITAXEL |
Unique Identifier: | SPE01503908 |
MolClass: | Checkout models in ver1.5 and ver1.0 |
Molecular Formula: | |
Molecular Weight: | 802.501 g/mol |
X log p: | 27.364 (online calculus) |
Lipinksi Failures | 3 |
TPSA | 148.57 |
Hydrogen Bond Donor Count: | 0 |
Hydrogen Bond Acceptors Count: | 15 |
Rotatable Bond Count: | 15 |
Canonical Smiles: | CC(=O)OC1C(=O)C2(C)C(O)CC3OCC3(OC(C)=O)C2C(OC(=O)c2ccccc2)C2(O)CC(OC(= O)C(O)C(NC(=O)c3ccccc3)c3ccccc3)C(C)=C1C2(C)C |
Class: | diterpene |
Source: | Taxus breviofolia |
Reference: | J Am Chem Soc 93: 2325 (1971) |
Therapeutics: | antineoplastic |
Generic_name: | Paclitaxel |
Chemical_iupac_name: | 5 beta,20-Epoxy-1,2a,4,7 beta,10 beta,13 alpha-hexahydroxytax-11-en-9-one 4,10-diacetate 2-benzoate 13-ester with (2 R,3S)-N-benzoyl-3-phenylisoserine |
Drug_type: | Approved Drug |
Pharmgkb_id: | PA450761 |
Kegg_compound_id: | C07394 |
Drugbank_id: | APRD00259 |
Melting_point: | 213-216 oC |
H2o_solubility: | Insoluble |
Logp: | 5.029 |
Cas_registry_number: | 33069-62-4 |
Drug_category: | Antineoplastic Agents; ATC:L01CD01 |
Indication: | Used in the treatment of Kaposi-s sarcoma and cancer of the lung, ovarian, and breast. |
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. |
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 paclitxel 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. |
Organisms_affected: | Humans and other mammals |