With
intraperitoneal injection to mice, deoxygedunin crosses the
blood-brain-barrier into the
central nervous system and possesses a long duration of action, with onset of action at 2 hours post-administration and peaking between 4–8 hours.[1] Relative to 7,8-DHF, deoxygedunin has weaker binding
affinity for TrkB (Kd = 1.4 μM).[1][2] However, it is more potent than 7,8-DHF in vivo with
intraperitoneal injection in multiple assays.[1] Deoxygedunin has also been found to be
orally and
topically active.[1][4] The compound, in contrast to 7,8-DHF, has poor
water solubility,[1] and hence its
bioavailability, especially oral, may be suboptimal.[6] The researchers who discovered deoxygedunin expressed that they were attempting to find analogues with improved water solubility that retained the biological activity of deoxygedunin, but, as of 2016, there appear to have been no subsequent reports on this effort since the original paper (2010) was published.[1] They also stated in the paper that 7,8-DHF has a simpler
chemical structure and that the
flavonoids were easier to modify for improved biological effects than the
gedunins.[1]
Similarly to
gedunin, a closely structurally related compound also found in Azadirachta indica, deoxygedunin has additionally been found to activate
HSF1 and induce
Hsp70, and was observed to possess
neuroprotective effects in a model of
Huntington's disease.[7]
^Zhang JC, Yao W, Dong C, Yang C, Ren Q, Ma M, et al. (December 2015). "Comparison of ketamine, 7,8-dihydroxyflavone, and ANA-12 antidepressant effects in the social defeat stress model of depression". Psychopharmacology. 232 (23): 4325–4335.
doi:
10.1007/s00213-015-4062-3.
PMID26337614.
S2CID15076700.