Galectin Therapeutics Inc. (GALT)

[Darwinian]

Thanks for your informed reply.

After the interim report from cohort 3, I looked into the A2M levels, and what you say seems to be correct about A2M correlating with liver function. But what I really found interesting, from the perspective of judging efficacy and progress of our trial, is that according to the abstract that I'll paste below, A2M levels are increased in a predictable way with increased levels of fibrosis. I may be making a leap here but it stands to reason that significantly reduced levels of A2M would indicate lessening fibrosis and the result of the reduced fibrosis being improved liver function. It's a small distinction but I think it's important.

The liver is an incredible organ. It has so many functions in the body. I think retail investors, especially non-science minded people, won't take the time to look into and try to understand the drug and it's MOA. It's easier to take the word of an accepted social media figure who deems himself adequately informed to declare pass or fail—something that most Dr's aren't qualified to do at this point. I think you are right about this being a winner. I waver sometimes but going back and looking over PR's and other research brings me back to the need for patience.

Following is an excerpt from this abstract: http://www.jbiomedsci.com/content/17/1/58
There are many other similar supporting links on Google.

Background
The gold standard of assessing liver fibrosis is liver biopsy, which is invasive and not without risk. Therefore, searching for noninvasive serologic biomarkers for liver fibrosis is an importantly clinical issue.

Methods
A total of 16 healthy volunteers and 45 patients with chronic hepatitis C virus (HCV) were enrolled (F0: n = 16, F1: n = 7, F2: n = 17, F3: n = 8 and F4: n = 13, according to the METAVIR classification). Three serum samples of each fibrotic stage were analyzed by two-dimension difference gel electrophoresis (2D-DIGE). The differential proteins were identified by the cooperation of MALDI-TOF/TOF and MASCOT; then western blotting and Bio-Plex Suspension Array were used to quantify the protein levels.

Results
Three prominent candidate biomarkers were identified: alpha 2 macroglobulin (A2M) is up regulated; vitamin D binding protein (VDBP) and apolipoprotein AI (ApoAI) are down regulated. The serum concentration of A2M was significantly different among normal, mild (F1/F2) and advanced fibrosis (F3/F4) (p < 0.01). The protein levels of VDBP and ApoAI were significantly higher in normal/mild fibrosis, when compared to those in advanced fibrosis (both p < 0.01).

Conclusions
This study not only reveals three putative biomarkers of liver fibrosis (A2M, VDBP and ApoAI) but also proves the differential expressions of those markers in different stages of fibrosis. We expect that combination of these novel biomarkers could be applied clinically to predict the stage of liver fibrosis without the need of liver biopsy.