Herantis now has a very substantial dataset at its disposal regarding these biomarkers, and its more detailed analysis will take some time. What I personally paid attention to in that presentation was that the data also showed changes in blood samples (as I recall, this was related to mitochondrial DNA damage, which likely served as a proxy for oxidative stress). Based on the drug’s distribution, it is understandable that it also has effects outside the central nervous system, but now there is biological evidence for that as well.
The structure of HER-096 is based on the active domain of CDNF, which interacts with GRP78. The effect of CDNF itself might be more limited to, for example, neurons, meaning HER-096 could potentially have broader effects than CDNF would. What makes this interesting is that this active domain is conserved between CDNF and MANF. This raises the question: to what extent can HER-096 replicate the effects of MANF in the body? MANF is known to have a protective effect on pancreatic beta cells, meaning that in an optimal scenario, HER-096 could be useful in the treatment of diabetes, for example. But perhaps even more interesting (yet more speculative) is MANF’s link to parabiosis (parabiosis is, by the way, quite a “mad scientist” experimental setup…), which could point to an even broader potential for HER-096, provided that the GRP78 interaction is sufficient to replicate MANF’s effect. Anyway, these data will likely provide hints regarding these other potential effects of HER-096 once they can be analyzed in sufficient depth.