One of my biggest questions is whether the "inactive" enantiomer is actually inactive. There were differences in the off-target binding screen and it appears that LNS8801 is >2x as active as G-1 in multiple settings.

This preprint provides key insights:
-GPER is essential for LNS8801's activity, validated in 3 independent systems.
-LNS8801 is orally bioavailable, effective at low doses (and exposures).
-A hypofunctional germline GPER variation attenuates activation by LNS8801.

During our work translating GPER agonists, we discovered that G-1, the widely studied "selective GPER agonist," is actually a mixture. By isolating its individual molecules, we identified LNS8801 as the active component, which is now advancing through clinical trials.

I'd blindly follow Bede anywhere except Boston.