A subclass of antineoplastic drugs known as natural products in-cludes:
Â· vinca alkaloids
Vinca alkaloids are nitrogenous bases derived from the periwin-kle plant. These drugs are cell cycleâ€“specific for the M phase and include:
After I.V. administration, the vinca alkaloids are well distributed throughout the body.
Vinca alkaloids undergo moderate liver metabolism before being eliminated through different phases, primarily in stool with a small percentage eliminated in urine.
Vinca alkaloids may disrupt the normal function of the microtu-bules (structures within cells that are associated with the move-ment of DNA) by binding to the protein tubulin in the microtu-bules.
With the microtubules unable to separate chromosomes properly, the chromosomes are dispersed throughout the cytoplasm or arranged in unusual groupings. As a result, formation of the mitot-ic spindle is prevented, and the cells canâ€™t complete mitosis (cell division).
Cell division is arrested in metaphase, causing cell death. There-fore, vinca alkaloids are cell cycleâ€“specific for the M phase. Inter-ruption of the microtubule function may also impair some types of cellular movement, phagocytosis (engulfing and destroying micro-organisms and cellular debris), and CNS functions.
Vinca alkaloids are used in several therapeutic situations:
Â· Vinblastine is used to treat metastatic testicular cancer, lym-
Â· phomas, Kaposiâ€™s sarcoma (the most common acquired immuno-deficiency syndrome [AIDS]â€“related cancer), neuroblastoma (a highly malignant tumor originating in the sympathetic nervous system), breast cancer, and choriocarcinoma.
Â· Vincristine is used in combination therapy to treat Hodgkinâ€™s disease, non-Hodgkinâ€™s lymphoma, Wilmsâ€™ tumor, rhabdomyosar-coma, and acute lymphocytic leukemia.
Â· Vinorelbine is used to treat nonâ€“small-cell lung cancer. Itmay also be used in the treatment of metastatic breast cancer, cisplatin-resistant ovarian cancer, and Hodgkinâ€™s disease.
Vinca alkaloids can interact with other drugs.
Â§ Erythromycin may increase the toxicity of vinblastine.
Â§ Vinblastine decreases the plasma levels of phenytoin.
Â§ Vincristine reduces the effects of digoxin.
Â§ Asparaginase decreases liver metabolism of vincristine, increas-ing the risk of toxicity.
Â§ Calcium channel blockers enhance vincristine accumulation, in-creasing the tendency for toxicity. (See Adverse reactions to vin-ca alkaloids.)
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