tamoxifen brands

Molecular formula: C26H29NO

Tamoxifen competitively inhibits estrogen binding to its receptor, which is critical for it's activity in breast cancer cells. Tamoxifen leads to a decrease in tumor growth factor α and insulin-like growth factor 1, and an increase in sex hormone binding globulin. The increase in sex hormon binding globulin limits the amount of freely available estradiol. These changes reduce levels of factors that stimulate tumor growth. Tamoxifen has also been shown to induce apoptosis in estrogen receptor positive cells. This action is thought to be the result of inhibition of protein kinase C, which prevents DNA synthesis. Alternate theories for the apoptotic effect of tamoxifen comes from the approximately 3 fold increase in intracellular and mitochondrial calcium ion levels after administration or the induction of tumor growth factor β. Tamoxifen is a nonsteroidal agent with potent antiestrogenic properties. The antiestrogen effects may be related to tamoxifen's ability to compete with estrogen for binding sites in target tissues such as breast. Tamoxifen competes with estradiol for estrogen receptor protein in cytosols derived from human breast adenocarcinomas. Tamoxifen has been shown to inhibit the induction of rat mammary carcinoma induced by dimethylbenzanthracene (DMBA) and causes the regression of already established DMBA-induced tumors. Tamoxifen appears to exert its antitumor effects by binding the estrogen receptors in this rat model. Tamoxifen may induce ovulation in anovulatory women, stimulating release of gonadotropin-releasing hormone from the hypothalamus, which in turn stimulates release of pituitary gonadotropins. In oligospermic males, tamoxifen increases serum concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estrogen. Tamoxifen is an antiestrogen frequently used in the treatment of breast cancer and is currently being assessed as a prophylactic for those at high risk of developing tumors. We have found that tamoxifen and its derivatives are high-affinity blockers of specific chloride channels. This blockade appears to be independent of the interaction of tamoxifen with the estrogen receptor and therefore reflects an alternative cellular target. One of the clinical side effects of tamoxifen is impaired vision and cataract. Chloride channels in the lens of the eye were shown to be essential for maintaining normal lens hydration and transmittance. These channels were blocked by tamoxifen and, in organ culture, tamoxifen led to lens opacity associated with cataracts at clinically relevant concentrations. These data suggest a molecular mechanism by which tamoxifen can cause cataract formation and have implications for the clinical use of tamoxifen and related antiestrogens.

Source: PubChem (NCBI) · compound 2733526