I thought about this recently too - what happened to the inflammation in HIV patients study when it appeared last year at one point and late the year before that this would be our first trial after the Hold?

Well, we know that fatty Liver is seen more prevalent in HIV patients than in non HIV patients. The trial was set to look at changes in inflammatory biomarkers (CRP etc.) but then there was also mouse model trials in MASH looking at fibrosis (steatosis) and fat deposits in the liver. One of these trials set out to, and appeared to prove that LL can reverse fibrosis (and I’m assuming reduce fat deposits in the liver) regardless of etiology.

So maybe the company wanted to make sure they could prove that LL worked in reversing steatosis regardless of etiology to build a stronger case for not not only studying the impact LL has on inflammation in HIV patients but also on fatty liver disease in these HIV patients who have a higher risk for said disease.

I don’t know but I feel like there is a connection here.