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Stanozolol (Winstrol Tablets)

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by Bill Roberts - Winstrol is a potent anabolic, but also binds to the progesterone receptor and to LAGS in the liver. In muscle tissue, it has been found to stimulate immediate-early gene expression by a means independent of the AR. Stanozolol can stimulate the production of prostaglandin E2 and the matrix metalloproteases collegenase and stromelysin in skin fibroblasts. It has been found to inhibit growth factor stimulated DNA synthesis and fibroblasts. The drug has substantial fibrinolytic properties, and has been effective in the treatment of urticaria, Raynaud's phenomenon, cryptofibrinogenemia, and lipodermatosclerosis. It has also effected cures of osteonecrosis in cases resistant to all other therapy. Stanozolol has been used successfully in treatment of AIDS wasting syndrome.

This drug is also useful in treatment of hereditary angioedema. It is somewhat hepatotoxic, but less so than many other oral anabolic steroids. It influences some immunological processes. Stanozolol has been found to increase lymphocyte count and CD8+ cell numbers, but to decrease CD4+ and CD3+ in postmenopausal women using it for osteoporosis. This effect would plausibly be useful for treatment of autoimmune disorders.

Stanozolol also lowers lipoprotein (a).

Stanozolol is the chemical name of active ingredient in Winstrol. Winstrol is a registered trademark of Sanofi-Synthelabo Inc. in the United States and/or other countries. Sanofi has licensed rights of Wnstrol to Ovation Pharmaceuticals.

Winstrol Tablet Resources

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Winstrol (Stanozolol) Pictures and Photographs

Stanozolol (Winstrol) Chemical Structure

Substance name Stanozolol [USAN]
Chemical name 2'H-Androst-2-eno(3,2-c)pyrazol-17-ol, 17-methyl-, (5alpha,17beta)-
Systematic name N/A
CAS number 10418-03-8
Merck Index Number Merck 11, 8754
Chemical formula C21-H32-N2O
Molecular weight 328.497 g/mol
Bioavailability
Metabolism Hepatic
Elimination half-life
Excretion Renal: 84%
Pregnancy category X
Legal status Prescription only (US); DEA Schedule III (US)
Routes of administration Intramuscular

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Publication Date: March 1, 1999