In a previous post (#2175) I cited four rigorous scientific publications on the significance of the Galectin-3 protein (Gal-3)in fibrosis generation. I now conclude with some brief comments on those publications.
Publication 1: describes Gal-3 as a "pleiotropic" molecule -- which is to say Gal-3 is multifunctional. A rough (very) analogy is a football quarterback. In biological systems there are networks of signals (causes and effects) which can intersect ("crosstalk"). The signals can include opposing ones (agonists/antagonists)(checks and balances). With many moving parts, comprehensive delineation is a major challenge in cell biology/chemistry. Resultantly, it's common for Pharma to throw various molecular monkey wrenches at diseases to see if some hunch or another works. As I see it, targeting Gal-3 in fibrosis is a superior choice. So far, GR-MD-02 has measured up.
Publication 2: reinforces the multifunctional nature of Gal-3, and reviews its relevance to fibrotic diseases in general (Liver,Renal, Cardiac, Pulmonary). The authors assert: "The enigmatic role of Gal-3 in fibrotic diseases and the antifibrotic effect of Gal-3 inhibition of fibrogenesis raises the possibility that Gal-3 inhibition may be a novel therapeutic strategy for treating tissue fibrosis". The text points out the need for delineation of Gal-3's multifunctionality.
Publication 3: is a review which merits reading. But in the paper's abstract, regarding clinical efficacy, the authors advise: "fibrosis reversibility is less likely to be achieved in humans than in animal models". That's more or less OK as a pro forma disclaimer. But it is an established fact (unmentioned by the authors) that the mouse genome has a great deal in common with the human genome. Consequently it's not a surprise that mice can (upon induction) develop fibrosis. Furthermore mice show a capacity for reversal. Doesn't that suggest ditto for humans?
Publication 4: provides an up-to-date perspective on Gal-3. It reports that Gal-3 is regulatory of liver progenitor cells. These cells occur in a "niche" comprising other additional cells and structures that function in differentiation and regeneration. This finding marks an incremental advance towards delineation of a complex train of causes and effects. That GALT's GR-MD-02 targets a regulator within the said niche is compatible with possible modulatory participation in pathways that include tissue regeneration.
It's ironic that GALT's shares are situated where they are -- down in the bargain basement. Yes, a sound technical approach to fibrosis (a Plan A) isn't a guarantee and could collapse into a mere heap of spent words. Duh. But the company has a Plan B and a Plan C (Psoriasis and Cancer). Actually both of these are already in motion on their own respective merits (are not merely contingencies), so financing for continuation may be tractable. Bargain basement for sure, but financier Czirr, having played football at Michigan, isn't likely to go down easily.
