Below is a breakdown of the recently published paper that Biotron linked us to on their Letter to Shareholders. The paper,
Post-infection treatment with the E protein inhibitor BIT225 reduces disease severity and increases survival of K18-hACE2 transgenic mice infected with a lethal dose of SARS-CoV-2 has been based on their previous COV-SARS-2 studies, the second linked here
https://www.biotron.com.au/wp-content/uploads/2022/05/BIT225-Effective-Against-Established-SARS-CoV-2-in-Animals.pdf. They also made a presentation last Febuary at a US infectious disease conference:
SARS-CoV-2 E-PROTEIN VIROPORIN INHIBITOR BIT225 ACTIVE IN hACE2 TRANSGENIC MICE I've given a breakdown of the papers Abstract paragraph, which provides a basic overview of the paper, with some extra comments of my own.
In the title, the phrase, 'K18-hACE2 transgenetic mice,' means that the mice used were genetically modified to contain higher levels of the ACE2 cells that line many of our organ tissue, such in the lungs. These cells on the surface of tissues play a multifaceted role depending on the organ they're contained in, but generally help regulate blood pressure, oxygen and Co2 processes, and inflamation control. Unfortunaetly, the SARS2 virus Spike Protein (S) utilizes ACE2 receptors to attach to host cells, creating the beginning of the viral infection. As such, the genetically modified mice are more prone to infection and therefore well suited for experimenation.
SARS-CoV-2, the virus that causes COVID-19, has four structural proteins: S, M, N, E, of which E (Envelope) is a voroporin protein and the target of BIT225 (viroporin inhibitor). See image below.
E is the most conserved structural protein throughout the modern evolution of the SARS virus (2002/3), resulting in it being a meaningful drug target as it is less likely to mutate or adapt, making the drug less effective/obsolete, not withstanding the ability of viruses natural ability to adapt to its altered host, including from antiviral {mis}usage.
As much as the
conservation of E is an important factor for BIT225 potential, logically speaking, it is only coincidental, and not the determining factor in it being targeted. Rather, BIT225 is a viroporin inhibitor that interferes with the normal functions of E, resulting in reducing diseaese escalation. If succerssful in humans, then the fact that E remains much the same throughout new variants of SARS2, should result in BIT225 continually being useful. (Will there ever be more variants once BIT225 is released into the population?)
Viroporins are proteins that create gateways in cell membranes enabling virion release, and play important role in viral replication (not essentially or exclusively), putting it as simply as I can. Biotron was actually the first to identify back in the Garden of Eden that E of the initial SARS virus was in fact a viroporin. You can see some of that work here from one of my first posts taken from their research paper and initial patent.
https://hotcopper.com.au/posts/43808854/single with links to the original papers.
Sorry, gotta go. Writing this live rather than in Word, so better post it or lose it.
to be continued....
(20min delay)