Toremifene is an antineoplastic hormonal agent primarily used in the treatment of advanced breast cancer. Toremifene is a nonsteroidal agent that has demonstrated potent antiestrogenic properties in animal test systems. The antiestrogenic effects may be related to its ability to compete with estrogen for binding sites in target tissues such as breast. Toremifene inhibits the induction of rat mammary carcinoma induced by dimethylbenzanthracene (DMBA) and causes the regression of already established DMBA-induced tumors. In this rat model, Toremifene appears to exert its antitumor effects by binding the estrogen receptors. In cytosols derived from human breast adenocarcinomas, Toremifene competes with estradiol for estrogen receptor protein. Toremifene is a nonsteroidal triphenylethylene derivative. Toremifene binds to estrogen receptors and may exert estrogenic, antiestrogenic, or both activities, depending upon the duration of treatment, animal species, gender, target organ, or endpoint selected. The antitumor effect of toremifene in breast cancer is believed to be mainly due to its antiestrogenic effects, in other words, its ability to compete with estrogen for binding sites in the cancer, blocking the growth-stimulating effects of estrogen in the tumor. Toremifene may also inhibit tumor growth through other mechanisms, such as induction of apoptosis, regulation of oncogene expression, and growth factors. Toremifene is used for the treatment of metastatic breast cancer in postmenopausal women with estrogen receptor-positive or receptor-unknown tumors. Toremifene is currently under investigation as a preventative agent for prostate cancer in men with high-grade prostatic intraepithelial neoplasia and no evidence of prostate cancer. Toremifene is marketed in the United States under the brand name Fareston.

Daidzein, an isoflavonoid phytoestrogenic compound found in soybeans, possesses various biological properties. It may induce apoptosis of choriocarcinoma cells in a dose-dependent manner via the mitochondrial apoptotic pathway, in addition, it promotes proliferation and differentiation in osteoblastic OCT1 cells via activation of the BMP-2/Smads pathway. Daidzein exerts neuroprotective effects through the novel extranuclear GPR30 and the classical transcriptionally acting ERβ.

Droloxifene, a derivative of the triphenylethylene drug tamoxifen, is a novel selective estrogen receptor modulator (SERM). Droloxifene also exhibits more rapid pharmacokinetics, reaching peak concentrations and being eliminated much more rapidly than tamoxifen. Its higher affinity to the estrogen receptor, higher anti-estrogenic to estrogenic ratio, more effective inhibition of cell growth and division in estrogen receptor-positive cell lines, and lower toxicity give it theoretical advantages over tamoxifen in the treatment of human breast cancer. Short-term toxicity was generally mild, and similar to that seen with other antiestrogens. Droloxifene appears active and tolerable. It may have a particular role in situations in which rapid pharmacokinetics, or an increased antiestrogenic to estrogenic ratio, are required. Droloxifene may also be a potentially useful agent for the treatment of postmenopausal osteoporosis because it can prevent estrogen deficiency-induced bone loss without causing uterine hypertrophy. Droloxifene may have an effect on bone and breast tissue because it induces apoptosis. Droloxifene has an anti-implantation effect in rats, and the effect appears to be not completely due to its anti-estrogenic activity.

Formononetin, an isoflavone, derived from Astragalus membranaceus, possesses the potential to reduce obesity and associated metabolic disorders. Formononetin displays estrogenic properties and induces angiogenesis activities. It regulates adipocyte thermogenesis as a partial PPARγ agonist and produces proangiogenesis effects through estrogen receptor alpha (ERα)-enhanced ROCK-II signaling pathways, by direct binding to the ligand-binding domain (LBD) of ERα. Besides, was shown, that formononetin inhibits HMGB1 release by decreasing HMGB1 acetylation via upregulating SIRT1 in a PPARδ-dependent manner and the identification of this process may help to treat inflammation-related disorders.

Biochanin A, a natural organic compound derived from herbal plants such as peanuts, soy, and red clover, possesses various pharmacological properties including antioxidant and anti-inflammatory. In addition, the compound has anticancer activity, which was shown in the following cells: head and neck squamous cell carcinoma and in osteosarcoma. In both cases, biochanin A induced apoptotic signaling pathway. It has also been found biochanin-A was an inhibitor of fatty acid amide hydrolase.

Genistin is an 7-O-beta-D-glucosideform of genistein and is the predominant form of the isoflavone naturally occurring in a number of dietary plants like soy and kudzu. In vitro study have shown that both genistin and genistein are capable of enhancing bone metabolism in the femoral-metaphyseal tissues of elderly rats. The presence of genistein or genistin in the tissue culture caused a significant increase in alkaline phosphatase activity, deoxyribonucleic acid (DNA) and calcium contents. The effect of genistein was greater than that of genistin. It is also revealed that genistin has a strong bone loss preventive activity on experimental rats, and is especially enhanced by combination with fructooligosaccharides. The amount of new bone produced by grafting genistin in collagenmatrix was compared to the bone produced by collagen matrix alone in New Zealand White rabbits, and was observed that genistin caused significant increase in bone formation.

Toremifene is an antineoplastic hormonal agent primarily used in the treatment of advanced breast cancer. Toremifene is a nonsteroidal agent that has demonstrated potent antiestrogenic properties in animal test systems. The antiestrogenic effects may be related to its ability to compete with estrogen for binding sites in target tissues such as breast. Toremifene inhibits the induction of rat mammary carcinoma induced by dimethylbenzanthracene (DMBA) and causes the regression of already established DMBA-induced tumors. In this rat model, Toremifene appears to exert its antitumor effects by binding the estrogen receptors. In cytosols derived from human breast adenocarcinomas, Toremifene competes with estradiol for estrogen receptor protein. Toremifene is a nonsteroidal triphenylethylene derivative. Toremifene binds to estrogen receptors and may exert estrogenic, antiestrogenic, or both activities, depending upon the duration of treatment, animal species, gender, target organ, or endpoint selected. The antitumor effect of toremifene in breast cancer is believed to be mainly due to its antiestrogenic effects, in other words, its ability to compete with estrogen for binding sites in the cancer, blocking the growth-stimulating effects of estrogen in the tumor. Toremifene may also inhibit tumor growth through other mechanisms, such as induction of apoptosis, regulation of oncogene expression, and growth factors. Toremifene is used for the treatment of metastatic breast cancer in postmenopausal women with estrogen receptor-positive or receptor-unknown tumors. Toremifene is currently under investigation as a preventative agent for prostate cancer in men with high-grade prostatic intraepithelial neoplasia and no evidence of prostate cancer. Toremifene is marketed in the United States under the brand name Fareston.

Droloxifene, a derivative of the triphenylethylene drug tamoxifen, is a novel selective estrogen receptor modulator (SERM). Droloxifene also exhibits more rapid pharmacokinetics, reaching peak concentrations and being eliminated much more rapidly than tamoxifen. Its higher affinity to the estrogen receptor, higher anti-estrogenic to estrogenic ratio, more effective inhibition of cell growth and division in estrogen receptor-positive cell lines, and lower toxicity give it theoretical advantages over tamoxifen in the treatment of human breast cancer. Short-term toxicity was generally mild, and similar to that seen with other antiestrogens. Droloxifene appears active and tolerable. It may have a particular role in situations in which rapid pharmacokinetics, or an increased antiestrogenic to estrogenic ratio, are required. Droloxifene may also be a potentially useful agent for the treatment of postmenopausal osteoporosis because it can prevent estrogen deficiency-induced bone loss without causing uterine hypertrophy. Droloxifene may have an effect on bone and breast tissue because it induces apoptosis. Droloxifene has an anti-implantation effect in rats, and the effect appears to be not completely due to its anti-estrogenic activity.