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|Product Name:||Tamoxifen Citrate||CAS:||54965-24-1|
|Molecular Formula:||C32H37NO8||Molecular Weight:||563.64|
|Appearance:||White Crystalline Powder||Origin:||China|
Safe Oral / Injectable Tamoxifen Citrate/Nolvadex Anti Estrogen Steroids Without Side Effects
Product name: Tamoxifen citrate
CAS Registry Number: 54965-24-1
Molecular Formula: C32H37NO8
Molecular Weight: 563.64
Appearance: White crystalline powder
Use: Antitumor drugs raw material, suitable for breast cancer.
Usage: the goods to anti-estrogen fertility inducer, the objects in dysfunctional uterine bleeding, polycystic ovary, menstrual disorders and drug-induced amenorrhea and other gynecologic diseases;It is used as a first line defense against breast cancer.
Storage: Shading, confined preservation
The claim that Nolvadex reduces gains should not be taken too seriously. The fact is that any number of bodybuilders have made excellent gains while using Nolvadex. The belief that it reduces gains seems to stem from the fact that the scientific literature reports a slight reduction in IGF-1 (individuals using anabolic steroids were not studied though) from use of Nolvadex.
Tamoxifen slows or stops the growth of cancer cells that are already present in the body. It helps keep the original breast cancer from coming back and helps prevent new cancer in the opposite breast. It also reduces the risk of breast cancer in women who have a high risk for this disease.
Tamoxifen is highly effective in lowering the risk of breast cancer recurrence. In women who have already had breast cancer, tamoxifen also lowers the risk of breast cancer in the opposite breast (contralateral).
Tamoxifen is used to prevent and treat breast cancers that test positive for estrogen receptors (ER+). It blocks the effects that the hormone estrogen has on cancer cells and lowers the chance that breast cancer will grow. It is often called an "anti-estrogen."For postmenopausal women, a two-stage treatment using tamoxifen and then an aromatase inhibitor, such as anastrozole (Arimidex), exemestane (Aromasin), or letrozole (Femara) may work better than only taking tamoxifen.
Tamoxifen is an antagonist of the estrogen receptor in breast tissue via its active metabolite, 4-hydroxytamoxifen. In other tissues such as theendometrium, it behaves as an agonist, and thus may be characterized as a mixed agonist/antagonist. Tamoxifen is the usual endocrine(anti-estrogen) therapy for hormone receptor-positive breast cancer in pre-menopausal women, and is also a standard in post-menopausal women although aromatase inhibitors are also frequently used in that setting.
Some breast cancer cells require estrogen to grow. Estrogen binds to and activates the estrogen receptor in these cells. Tamoxifen is metabolized into compounds that also bind to the estrogen receptor but do not activate it. Because of this competitive antagonism, tamoxifen acts like a key broken off in the lock that prevents any other key from being inserted, preventing estrogen from binding to its receptor. Hence breast cancer cell growth is blocked.
Tamoxifen was discovered by pharmaceutical company Imperial Chemical Industries(now AstraZeneca) and is sold under the trade names Nolvadex,Istubal, and Valodex. However, the drug has been widely referred to by its generic name "tamoxifen", even before its patent expiration.
It is on the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system.
Tamoxifen is currently used for the treatment of both early and advanced ER+ (estrogen receptor positive) breast cancer in pre- and post-menopausalwomen. Additionally, it is the most common hormone treatment for male breast cancer. It is also approved by the FDA for the prevention of breast cancer in women at high risk of developing the disease. It has been further approved for the reduction of contralateral (in the opposite breast) cancer. The use of tamoxifen is recommended for 10 years.
In 2006, the large STAR clinical study concluded that raloxifene is equally effective in reducing the incidence of breast cancer, but after an average 4-year follow-up there were 36% fewer uterine cancers and 29% fewer blood clots in women taking raloxifene than in women taking tamoxifen, although the difference is not statistically significant.
In McCune-Albright syndrome (MAS) tamoxifen has been used to treat premature puberty and the consequences of premature puberty. Tamoxifen has been seen to decrease rapid bone maturation which is the result of excessive estrogen and alter predicted adult height (PAH). The same effects have also been seen in short pubertal boys.
However, one in vitro study in 2007 and later an in vivo study in 2008 have shown that tamoxifen induces apoptosis in growth plate chondrocytes, reduces serum IGF-I levels and causes persistent retardation of longitudinal and cortical radial bone growth in young male rats, leading the researches to express concern giving tamoxifen to growing individuals.
Tamoxifen is used to treat infertility in women with anovulatory disorders. A dose of 10-40 mg per day is administered in days 3-7 of a woman's cycle. In addition, a rare condition occasionally treated with tamoxifen is retroperitoneal fibrosis.
Tamoxifen is used to prevent estrogen-related gynecomastia, resulting from elevated estrogenic levels. It is taken as a preventative measure in small doses, or used at the onset of any symptoms such as nipple soreness or sensitivity. Other drugs are taken for similar purposes such as clomiphene citrate and the anti-aromatase drugs which are used in order to try to avoid the hormone related adverse effects. Tamoxifen is also sometimes used to treat or prevent gynecomastia in sex offenders undergoing temporary chemical castration.
Tamoxifen has been shown to be effective in the treatment of mania in patients with bipolar disorder by blocking protein kinase C (PKC), an enzyme that regulates neuron activity in thebrain. Researchers believe PKC is over-active during the mania in bipolar patients.
Angiogenesis and cancer
Tamoxifen is one of three drugs in an anti-angiogenetic protocol developed by Dr. Judah Folkman, a researcher at Children's Hospital at Harvard Medical School in Boston. Folkman discovered in the 1970s that angiogenesis - the growth of new blood vessels - plays a significant role in the development of cancer. Since his discovery, an entirely new field of cancer research has developed. Clinical trials on angiogenesis inhibitors have been underway since 1992 using myriad different drugs. The Harvard researchers developed a specific protocol for a golden retriever named Navy who was cancer-free after receiving the prescribed cocktail of celecoxib, doxycycline, and tamoxifen - the treatment subsequently became known as the Navy Protocol. Furthermore tamoxifen treatment alone has been shown to have anti-angiogenetic effects in animal models of cancer which appear to be, at least in part, independent of tamoxifen's estrogen receptor antagonist properties.
Control of gene expression
Tamoxifen is used as a research tool to trigger tissue-specific gene expression in many conditional expression constructs in genetically modified animals including a version of the Cre-Lox recombination technique.
Tamoxifen has been proposed as part of a treatment plan for Riedel's thyroiditis.
Mechanism of action
Crystallographic structure of 4-hydroxy-tamoxifen (carbon = white,oxygen = red, nitrogen = blue) complexed with ligand binding domainof estrogen receptor alpha (cyan ribbon).
Tamoxifen itself is a prodrug, having relatively little affinity for its target protein, the estrogen receptor. It is metabolized in the liver by thecytochrome P450 isoform CYP2D6 and CYP3A4 into active metabolites such as 4-hydroxytamoxifen (afimoxifene) and N-desmethyl-4-hydroxytamoxifen (endoxifen)which have 30-100 times more affinity with the estrogen receptor than tamoxifen itself. These active metabolites compete with estrogen in the body for binding to the estrogen receptor. In breast tissue, 4-hydroxytamoxifen acts as an estrogen receptor antagonist so that transcription of estrogen-responsive genes is inhibited.
4-hydroxytamoxifen binds to estrogen receptors (ER), the ER/tamoxifen complex recruits other proteins known as co-repressors and then binds to DNA to modulate gene expression. Some of these proteins include NCoR and SMRT. Tamoxifen function can be regulated by a number of different variables including growth factors. Tamoxifen needs to block growth factor proteins such as ErbB2/HER2 because high levels of ErbB2 have been shown to occur in tamoxifen resistant cancers. Tamoxifen seems to require a protein PAX2 for its full anticancer effect. In the presence of high PAX2 expression, the tamoxifen/estrogen receptor complex is able to suppress the expression of the pro-proliferative ERBB2 protein. In contrast, when AIB-1expression is higher than PAX2, tamoxifen/estrogen receptor complex upregulates the expression of ERBB2 resulting in stimulation of breast cancer growth.
4-Hydroxytamoxifen binds to estrogen receptors competitively (with respect to the endogenous agonist estrogen) in tumor cells and other tissue targets, producing a nuclear complex that decreases DNA synthesis and inhibits estrogen effects. It is a nonsteroidal agent with potent antiestrogenic properties which compete with estrogen for binding sites in breast and other tissues. Tamoxifen causes cells to remain in the G0 and G1 phases of the cell cycle. Because it prevents (pre)cancerous cells from dividing but does not cause cell death, tamoxifen is cytostatic rather than cytocidal.
The scientific literature is complex with respect to the activity of tamoxifen, and care should be taken to establish whether tamoxifen, or the 4-hydroxy metabolite was used, especially in in vitro assays.
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