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Chemical Compound Review

Agovirin     [(8S,9S,10R,13S,14S,17S)- 10,13-dimethyl-3...

Synonyms: Androlon, Masenate, Synerone, Testodet, Testogen, ...
 
 
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Disease relevance of Agovirin

 

Psychiatry related information on Agovirin

 

High impact information on Agovirin

 

Chemical compound and disease context of Agovirin

 

Biological context of Agovirin

  • The term "partial androgen insensitivity syndrome" describes this condition more accurately than a term based on clinical phenotype [19].
  • The low amount of androgen receptor and the combination of high serum gonadotropins and plasma testosterone production rates suggest that the defective spermatogenesis in these infertile men was the consequence of androgen insensitivity [20].
  • Our results suggest that AR amplification emerges during androgen deprivation therapy by facilitating tumour cell growth in low androgen concentrations [21].
  • The 5' LTR of this element corresponds to the previously characterized hormone-responsive enhancer associated with Slp regulation, leading to the conclusion that the provirus has conferred androgen response on the adjacent Slp gene [22].
  • Vasomotor hot flashes are a common symptom in women during menopause and in men who have undergone androgen-deprivation therapy for prostate cancer [23].
 

Anatomical context of Agovirin

  • One mutation was in the same codon as the mutation found previously in the androgen-independent prostate-cancer cell line [24].
  • Dihydrotestosterone binding studies in skin fibroblasts demonstrated two genetic variants similar to those reported in complete androgen insensitivity syndrome [19].
  • Dependent cells form tumors preferentially in male animals and dependent cell cytosols contain significant amounts (approximately 300 femtomoles per mg protein) of a specific androgen-binding macromolecule [3].
  • BACKGROUND: Men with benign prostatic hyperplasia can be treated with alpha 1-adrenergic-antagonist drugs that relax prostatic smooth muscle or with drugs that inhibit 5 alpha-reductase and therefore reduce tissue androgen concentrations [25].
  • The source of the excess androgen may be either the ovaries or the adrenal glands, and distinguishing between these sources may be difficult [26].
 

Associations of Agovirin with other chemical compounds

 

Gene context of Agovirin

 

Analytical, diagnostic and therapeutic context of Agovirin

References

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