Share Price, page-4767

Cant remember where I saw someone ask about mouse models of NNZ 2566 Vs 2591? My reading of the data is that the mouse model results were more impressive in 2591 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2644158/ is an article for 2566, whereas 2591 results generally equaled the wild-type mice).
The mechanism of action is quite different between the 2, but both end up effecting levels of bioavailable IGF-1. 2566 does seem like a bit of a stab in the dark creation, regarding possible efficacy, as it is not a full blown analog of IGF-1, just an analog of a terminal peptide of IGF-1. I think it was developed and trialed with the hope it would have IGF-1 properties in vivo.
2591 is a full analog of Cyclic glycine-proline, which regulates IGF-1 homeostasis by altering the binding of IGFBP-3 to IGF-1. Once 2591 knocks IGFBP-3 off binding to IGF-1, more IGF-1 becomes bioavailable to do its positive stuff in the brain. Its much more of a "clean" way of increasing IGF-1 bioavailable, and is also more stable, orally bioavailable and more readily crosses the blood-brain barrier, compared to 2566.
This is why John sees 2591 as the "Jewel in the Crown", and why there may be so many more indications for it to come. Its why his eyes light up when talking about it.
I dont think the market has much understanding of the science, and thus it is IMO hugely undervalued even at this point in its development.
Hope that helps!
Cheers