Replies to post #299242 on Innovation Pharmaceuticals Inc (IPIX)

[KMBJN]

Thanks for the thoughts on how brilacidin might work. Just so we are all speaking the same language:

which I referred the E -envelope that is a bilayer lipid membrane.

melts the bilayer membrane (known as Envelope Protein or E- protein)

My understanding is that E is short for an envelope protein sticking out of the viral lipid membrane, it is not the membrane itself.

https://virologydownunder.com/why-does-soap-work-so-well-on-sars-cov-2/



I think whether or not brilacidin can pierce the viral envelope depends on whether it has a net negative charge from the M and E proteins (negative like bacterial cell walls have, but human cells don't - why brilacidin is safe in human cells but kills bacteria).

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!

RNA replication happens inside the cell after the genetic material is released from the capsid. Punching a hole in viral envelope would not hinder RNA replication inside the cell. If brilacidin is a MPro main protease inhibitor of the virus, than it can keep the virus from assembling its progeny because it can't cut the main protein into the neeeded smaller fragments.

Apoptosis is programmed death of cells.

Not a top university virologist, but all the above should be common knowledge. I am looking forward to seeing the evidence that brilacidin works outside the cell as the company has stated. As far as I can discern, we have seen no evidence of brilacidin working outside the cell or preventing cell entry (via blocking S-ACE2 binding). It could be any of 3 or more mechanisms of action.

Wanted to also say that I am skeptical of your claim that brilacidin showing effectiveness to limit viral load in human kidney cells somehow means brilacidin can treat AKI. Unless your name is George then it would make sense.

[farrell90]

Thanks for posting. Any links which help you formulate your ideas would be appreciated.

Some points which may have been overlooked by many on the board. The ACE cell wall protein is present in many cells. In addition to renal cells it is present in pulmonary, GI and other cell walls.

https://pubmed.ncbi.nlm.nih.gov/15141377/

Since Brilacidin blocks Covid 19 binding to renal cells to prevent AKI it will also blocks Covid 19 through out the body and will fight the pulmonary, cardiac GI and other reported clinical effects of Covid19 including the main cause of death, pulmonary failure.

For the reason above the next RBL test for Brilacidin in Covid 19 infected pulmonary epithelial cells will also have a positive effect.

Brilacidin may also prevent viral replication through its effects on Covid19 M protease as suggesed by Cavasotto.

https://chemrxiv.org/articles/In_silico_Drug_Repurposing_for_COVID-19_Targeting_SARS-CoV-2_Proteins_through_Docking_and_Quantum_Mechanical_Scoring/1211019

IPIX is aware of the all the above and more. MR Ehrlich's statements IPIX is planning Brilacidin against Covid19 clinical trials are not idle boasts. They have enough clinical data to enter clinical trials. If you accept that premise then you also understand IPIX will need financial and technical help to plan and run the clinical trials. IMO we will be hearing those announcements soon.

All JMO

GLTA, Farrell