BNN-27

Source: Wikipedia, the free encyclopedia.
BNN-27
Clinical data
Other namesBNN27; (20R)-3β,21-Dihydroxy-17α,20-epoxypregn-5-ene; 17α,20R-Epoxypregn-5-ene-3β,21-diol
Identifiers
  • (3S,8R,9S,10R,13S,14S,17R)-3'-(Hydroxymethyl)-10,13-dimethylspiro[1,2,3,4,7,8,9,11,12,14,15,16-dodecahydrocyclopenta[a]phenanthrene-17,2'-oxirane]-3-ol
JSmol)
  • C[C@]12CC[C@@H](CC1=CC[C@@H]3[C@@H]2CC[C@]4([C@H]3CC[C@]45C(O5)CO)C)O
  • InChI=1S/C21H32O3/c1-19-8-5-14(23)11-13(19)3-4-15-16(19)6-9-20(2)17(15)7-10-21(20)18(12-22)24-21/h3,14-18,22-23H,4-12H2,1-2H3/t14-,15+,16-,17-,18?,19-,20-,21-/m0/s1
  • Key:FMOHTQBFGJULLE-HNFJNZPISA-N

BNN-27, also known as 17α,20R-epoxypregn-5-ene-3β,21-diol, is a

brain trauma.[2][3]

In 2011, the surprising discovery was made that DHEA, as well as DHEA-S, directly bind to and activate the TrkA and p75NTR with high affinity.

neurotrophic factors.[5] These findings may explain the positive association between decreased circulating DHEA levels with age and age-related neurodegenerative diseases.[5]

Subsequently, a series of

hormonal actions.[2][3] Also, it was found to lack the problematic hyperalgesic actions of NGF.[2][3] As such, BNN-27 has been described as an NGF mimetic and was proposed as a potential novel treatment for neurodegenerative diseases and brain trauma.[2][3]

See also

References


This page is based on the copyrighted Wikipedia article: BNN-27. Articles is available under the CC BY-SA 3.0 license; additional terms may apply.Privacy Policy