Sanofi and Regeneron's Kevzera showed no therapeutic benefit in CV19 patients. I am not shocked. At all. So that leaves two big pharma with no therapeutic drug to address CV19. Arthritic drugs will not work in my opinion.
Amgen is repurposing its Otesla drug to address respiratory illness as preventative therapy. Just like Bril, Ostela shares somewhat similar anti-inflammatory properties in inhibit PDE4. But Bril has more with its 3-in-1 action.
It's looking like Bril is an i-o platform with potentially treating AKI as well. This is a blockbuster drug in the making once we get results back and phase II gets going, IMO.
Two pathways so far: cAMP + IFnB. Lastly, my previous tweet a few weeks back to postulate how Bril exhibits its antiviral effects(2) was posted here as well and the recent pr confirmed it. We have a great science here in Bril!
My hypothesis is slightly different from Spike protein and SARsCoV2's cell membrane, which I referred the E -envelope that is a bilayer lipid membrane. In my previous contributions, I mentioned that Bril inhibits viral replications by ENTRY AND REPLICATION; and the MOA of actions will not only involve the virus wall membrane that most think here but it will also include the S-protein. The spike protein of SARScoV2 has always been the mediator of how the virus enters, infect, and induce the pathogenesis into the host cells. So S-protein structure consists of S1 AND S2, for receptor binding and for fusion, respectively, that interfaces with the human ACE2 protein receptor. This S-spike matches up well with Bril since both contain hydrophilic and hydrophobic regions. Bril amphipathic regions simply bind to S-protein. Like-to-like binding affinity molecules between Hydrophobic and hydrophilic. This is remarkable!
What happens next is your positive curvature (convex) change in the physicochemical properties of S-protein binding to Bril. So this distortion of the shape hinders S-protein ability to bind to ACE2 receptor into the host cells. That's your inhibition of antiviral via entry. The last one is inhibition by replication. This the portion where Bril's antimicrobial peptide degenerates, compromises, or melts the bilayer membrane (known as Envelope Protein or E- protein), to make the wall porous and creating a negative curvature that it ultimately inhibits RNA replication. Apoptosis happens!
But we shall see what UNIVERSITY top virologists say!
