Very good find, although I am not completely sure how to interpret these results (or actually I am, I think the results are incomplete the way they are presented here). Of course, we have the binding affinities on the left, indicating good selectivity of WAY-2000070 for ER-beta. On the right, we have the transactivation of the receptor, however, it is not specified to what extent the receptors are activated. For example, the compound 7-alpha-hydroxy-DHEA (7-HD) only has an EC50 of 20 uM, but is able to activate ER-beta with 60-70% potency of E2*. So, we see that the EC50 for transactivation of WAY-2000070 for ER-beta is 31nM, but it does not specify the transcriptional activity of the receptor at that concentration. This is a really important difference, since you might end up with a compound that can only activate a small part of ER-beta associated genes.
As a side note, the more I read about estrogens and their relation to hair growth, the more I am starting to doubt E2's real global efficacy (and the more I realise estrogens are very poorly understood, with many pathways other than ligand-binding that influence tissue genetic expression). In my previous post I mentioned that E2 lengthens anagen in frontotemporal male follicles (FMF), but induces catagen in the same female follicles (FFF)**. The authors of the associated paper conclude that E2 may have vastly different local effects depending on the scalp region. To complicate things even further, E2 is also known to strongly decrease AR density***, which may or may not account for some if not all of its positive effects on FMFs. If we were to replace E2 with a selective ER-beta ligand, we might not get any positive effects or maybe even induce catagen, like in the FFFs. To me, it is not clear enough whether ER-beta truly is the holy grail for hair growth. There has been only one study to my knowledge on these positive effects, and that one was executed on mice****. Since male and female human follicles already behave differently, these results are absolutely not transferable to human (male) follicles.
Personally, I think that E2 can definitely be useful. However, based on the current knowledge it should preferably be used locally, only on the frontotemporal region (for males, that is). Whether the positive effects are coming from direct estrogen-related gene transcription or AR supression is still unknown, unfortunately (at least to me). Also, anyone wanting to experiment with E2 (or any hormone for that matter) should be aware of all its direct and downstream effects, some of which are especially detrimental to males. Of course I am always open for discussion on this topic, as we can all learn from each other.
Source list (again, no hyperlinks, still restricted on my account):
*Estrogen Receptor b Ligands: Recent Advances and Biomedical Applications
**Estrogens and the hair follicle
***The hair follicle as estrogen target and source (really nice, complete article with tons of information)
****Hair cycle control by estrogens: catagen induction via estrogen receptor (ER)-alpha is checked by ER beta signaling