RE:RE:Couple of studies After phase 2 flop, Novo Nordisk says its NASH work is 'still very much on track'
After phase 2 flop, Novo Nordisk says its NASH work is 'still very much on track'
“A golden opportunity awaits for whoever can conquer NASH. The market opportunity has been estimated to be as high as $35 billion.”
Interesting how NN clarified their NASH program.
The other interesting thing is the market opportunities $35 Billion and growing.
The patent Tesamorelin has and pending applications below might be more I am
not an expert so no comments but the indications are crystal clear.
https://patents.google.com/patent/US10946073B2/en
qwerty22 wrote:
Because it was EASL a week or two ago there's been quite a bit of news around NASH. Novo Nordisk clarified their approach. While looking into what they had I ended up on their pipeline. They have a GH secretalogue which they are developing for GHD diagnosis but which essentially does the same thing as Egrifta. It works on a different receptor but still stimulates endogenous GH production. It got me thinking that maybe the weakness in THTX IP might be the presence of these other GH stimulators (including oral drugs) which could do the same job as Egrifta. The THTX patent makes a couple of general references to GH secretalogues but the bulk is specifically around the GHRH sequence and variants of it. I've started to wonder whether this is the weakness in the NASH program.
scarlet1967 wrote:
GH/IGF-1 axis is associated with intrahepatic lipid content and hepatocellular damage in overweight/obesity
“Higher peak-stimulated GH was also associated with lower ALT. Higher IGF-1 was associated with lower risk of liver fibrosis by Fibrosis-4 scores.
Individuals with NAFLD have lower peak-stimulated GH but similar IGF-1 levels versus controls. Higher peak-stimulated GH is associated with lower IHL and less hepatocellular damage. Higher IGF-1 is associated with more favorable fibrosis risk scores. These data implicate GH and IGF-1 as potential disease modifiers in the development and progression of NAFLD.”
So there are concluding higher IGF-1 levels will result in lower fibrosis by fibrosis-4 score.
https://academic.oup.com/cid/advance-article-abstract/doi/10.1093/cid/ciac337/6577095?redirectedFrom=PDF
The FibroScan–aspartate aminotransferase (FAST) score was developed to identify patients who have histologic NASH with high nonalcoholic fatty liver disease activity score (NAS ≥4) and significant liver fibrosis (≥F2), which has been associated with higher risk of end-stage liver disease.
“On multivariable analysis, HIV infection was associated with 3.7-fold higher odds of elevated FAST score (P = .002), and greater waist circumference (per 10cm) was associated with 1.7-fold higher odds (P < .001).
Our findings suggest that HIV is an independent risk factor for NASH with significant activity and fibrosis.”
Again HIV seems to increase not only NAS score but also the fibrosis and we know Tesamorelin was only tried in PLWH.
I have sent both studies to Christian. I don’t have access to the full articles!