Samiksha Jaiswal (Editor)

BOMT

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Routes of administration
  
Oral

CAS Number
  
24543-59-7

ChemSpider
  
140636

Route
  
Oral administration

ATC code
  
None

PubChem CID
  
159972

Molar mass
  
385.3358 g/mol

BOMT httpsuploadwikimediaorgwikipediacommonsthu

Synonyms
  
Ro 7-2340; 6α-bromo-4-oxa-17α-methyl-5α-dihydrotestosterone

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BOMT (developmental code name Ro 7-2340), also known as 6α-bromo-4-oxa-17α-methyl-5α-androstan-17β-ol-3-one, is a synthetic, steroidal, pure antiandrogen that was first developed in 1970 and was never marketed for clinical use. It is the 6α-brominated, 4-oxygenated, and 17α-methylated derivative of dihydrotestosterone (DHT). Along with benorterone, cyproterone (and its acetate ester, cyproterone acetate), and flutamide, BOMT was among the earliest antiandrogens to be developed and extensively studied, although it is less well-documented in comparison to the others. BOMT has been investigated clinically in the treatment of benign prostatic hyperplasia, though development for this use did not continue. There was also interest in BOMT for the potential applications of acne, androgenetic alopecia, and possibly prostate cancer, but it was not developed for these indications either.

Contents

BOMT is a selective competitive antagonist of the androgen receptor (AR), although it is described as an "only relatively weak competitor." The drug shows no androgenic, estrogenic, or progestogenic activity even at high doses, nor any inhibition of 5α-reductase, though it does show weak antigonadotropic effects. Due to its selectivity for and competitive inhibition of the AR, BOMT has been described as a "true" antiandrogen, similarly to benorterone, cyproterone, and flutamide. Like other steroidal antiandrogens, BOMT may actually be a weak partial agonist of the AR, as it appears to have the potential for weak androgenic effects in specific situations. On the basis of animal research, BOMT does not appear to act as an AR antagonist in central nervous system tissues, and in relation to this, does not disinhibit the hypothalamic-pituitary-gonadal axis or increase testosterone levels.

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References

BOMT Wikipedia