Replies to post #361571 on Innovation Pharmaceuticals Inc (IPIX)

[joseytheoutlawwales]

I’ll have to look at that, as nowhere else in trial published literature or even in current clinical practice, has Remdesivir shown anything like 99%.

[Focusakker]

Could you please provide the quote that Remdesivir was 99% on a stand alone basis?

Here's what I read: "In contrast, combination of brilacidin with remdesivir at 10 and 2.5 µM concentrations, respectively, reduced the viral infectious titer by >99%, thus providing a highly effective inhibition profile (Figure 5B) and achieving greater inhibition than with either compound alone. This synergistic inhibition continued to remain higher than 99% when the concentrations of both compounds were equal (2.5 µM each)".

The combination was 99%. In fact, when Remdesivir was reduced by 75%, he reduction remained at 99%.

I could have missed the Remdesivir alone, so please p;rovide.

Thanks, Paul

[MaskedCat]

But,

Adverse effects are common with remdesivir, but few studies exist that focus on remdesivir and its effects on the cardiovascular system [1,2,9,10,12,13]. Out of a study of 53 patients receiving remdesivir, 32 patients (60%) experienced adverse events during follow-up [5].Oct 24, 2020

[Stockman886]

Lol if that was the case and Remdesivir was that effective it’s use wouldn’t have been criticized as it also wouldn’t have been dropped by other countries after they have used it

[jav0033]

This kills the 426 vs 129.87 SI if Remdesivir reduces higher viral load

[farrell90]

Remdesivirs in vitro studies were one of the reasons it was quickly studied for Covid 19. Unfotunately further studies showed it lack efficay against Covid 19. Why?

Redesivir's poor clinical showing in spite of relative good in vitro studies is due to its hepatic toxicity which limits higher dosing and its relatively complicated conversion to its active metabolite requires an intracellular conversion.

https://www.statnews.com/2020/05/14/gilead-should-ditch-remdesivir-and-focus-on-its-simpler-safer-ancestor/

"Remdesivir’s lackluster results in patients with advanced Covid-19 in the NIAID-sponsored trial and the finding that it provided no statistically significant benefit in a clinical trial conducted in China among patients with severe Covid-19 symptoms are likely due to the suboptimal level of active GS-441524 triphosphate in the lungs. Patients with advanced or severe Covid-19 generally have a high viral load in their lungs and would need a high concentration of GS-441524 triphosphate to combat it. The benefit of using GS-441524 over remdesivir is that GS-441524 can almost certainly be given at much higher doses due to its lower toxicity. This would result in more conversion to the active compound, GS-441524 triphosphate, in the lungs."

Remdesivir IC 50 in vitro is .77um, but it has to enter the host cells to prevent intracellular viral reproduction. Remdesivir is a prodrug and is converted inside the cell to its active metabolite which is estimated to have an IC 50 of 38um to 231um or 7.7um in other studies, well below that of Brilacidin's IC 50 of .565um.

Its pharmacology explains Remdesivir's poor clinical performance in spite of a relatively good in vitro IC 50.

In addition Remdesivir's hepatotoxicity limits higher dosing.

"Assuming similar distribution and accumulation ratios of remdesivir and Nuc-TP in the lung between humans and monkeys, an optimistic estimation of Nuc-TP in the human lung tissues is 2 to 3-fold higher at a steady state than that observed in the monkey lung tissues [1]. This suggests that an IV dose of 200 mg remdesivir in a human may only achieve a suboptimal concentration of active form of Nuc-TP of <?2–5 µM in the human lung tissues (TableIII). Given that the intracellular volume (0.54 l) is 46% of the total volume of the lung (1.17 l) [17], the intracellular concentration of Nuc-TP in the human lung may be only at 4–10 µM (TableIII), which may be below the estimated intracellular IC50 and IC90 of Nuc-TP. Unfortunately, systemic adverse effects such as hepatotoxicity preclude escalation of the remdesivir dose to more than 200 mg/day."

The following article demonstrates these findings in great detail.

https://link.springer.com/article/10.1208/s12248-020-00459-8

GLTA,Farrell

[Lemoncat]

Bleach reduces viral titer by 99% too in vitro.

Prurisol reduced lesions by 97% in mice.

Things don't always work the same when they go into the clinic.

Remdesivir is a prodrug which clearly did not match in vitro results when brought into the clinic. It really never has succeeded at treating any virus or other malady.

Brilacidin has a much simpler MOA. What is infused is what treats...there is no transformation required. It has proven itself a very effective anti-infective against Staph (the number one cause of Pneumonia). It has shown anti-inflammatory traits in the OM and UP trials. On top of that it showed good a good anti-viral effect in vitro.

There is much reason to believe that Brilacidin may outperform Remdesivir in the clinic.

Go IPIX!