Withintraperitoneal injection to mice, deoxygedunin crosses theblood-brain-barrier into thecentral 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 bindingaffinity for TrkB (Kd = 1.4 μM).[1][2] However, it is more potent than 7,8-DHFin vivo withintraperitoneal injection in multiple assays.[1] Deoxygedunin has also been found to beorally andtopically active.[1][4] The compound, in contrast to 7,8-DHF, has poorwater solubility,[1] and hence itsbioavailability, 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 simplerchemical structure and that theflavonoids were easier to modify for improved biological effects than thegedunins.[1]
Similarly togedunin, a closely structurally related compound also found inAzadirachta indica, deoxygedunin has additionally been found to activateHSF1 and induceHsp70, and was observed to possessneuroprotective effects in a model ofHuntington'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.
