Thanks for referencing the article in Biopharmadive.com -- your comments are quality as usual. Dr. Traber correctly refers to
GR-MD-02 as "differentiated" from other drug candidates currently in clinical trials (eg. that of ICPT). Besides indicating GR-MD-02
may reverse Fibrosis no elaboration is offered. Here I have some brief comments. Exactly what functionally differentiates GALT's GR-MD-02 from ICPT's obeticholic acid? Could it be that in the complex sequence of causes ending in Fibrosis ICPT's drug acts upstream while GR-MD-02 intervenes downstream? Which is to say ICPT is distal while GR-MD-02 is proximal to Fibrosis generation. I claim that as my copyrightable conjecture, since nobody else seems to care. I note in a sequential flow of causes the most effective site of intervention isn't ipso facto the most proximal, especially in biological systems where there can be alternate pathways and regulatory adjustments. However in general distal interventions will be simpler (ounce of prevention) than proximal (liver transplant!). In that connection relatively small molecules such as ICPT's (a bile acid derivative) have a chance of escaping digestion in the GI tract, thus can be administered orally in pills.
However, just like statin drugs the pills will need to be taken daily...and perhaps forever since distal from Fibrosis activity. By contrast GR-MD-02, a large quasi-carbohydrate derivative is quite proximal to any anti-Fibrosis action (by blocking the Galectin-3 protein and thus a greater chance at Fibrosis reversal).
However as a carbohydrate derivative it risks digestion in the GI tract. Therefore intravenous infusion will most likely be mandatory. However its pedigree as proximal should prevail.
Note that Dr. Traber, being circumspect, mentions the eventual possibility of a drug combination being useful. In that case perhaps it would be our proximal intervention enhanced by an upstream helper.
