There are several ways to consider the liklihood of a successful...

There are several ways to consider the liklihood of a successful human trial to treat C19, best of all would be reviewing the trial results, which of course some fortunate mango farmers have had the pleasure of, whereas us mere pickers have to wait our turn. But we're not left completely alone under a bare tree. There has been other trials worth considering.

Did you know that the antivirals used throughout the pandemic such as Remdesivir, Molnupiravir, Nirmatrelvir and the 3CL protease inhibitor GC376, all performed mice trials just as Biotron did in 2023. But that is where the commonality stops. The results cannot be compared for the BIT225 treatment group had oustanding results in all outcomes, whereas the others performed quite poorly. Biotron considered that the comparison was worthy of printing in their second round of mice studies:

The high efficacy of BIT225 treatment even when treatment was delayed for 24 or 48 hours after infection is notable, as monoclonal antibodies and other direct-acting antiviral agents have previously shown significant losses of efficacy when treatment initiation was delayed in lethal SARS-CoV mouse models. Treatment of SARS-CoV infection in the MA15 mouse model with GS-5734 (Remdesivir) showed outcomes similar to vehicle control when treatment started on Day 2 after infection [41]. Early treatment start was required for differentiation from vehicle, but even that could not fully protect mice from weight loss during treatment [41]. Similarly, treatment with EIDD-2801 (Molnupiravir) in this mouse model showed a significant loss of efficacy when treatment was delayed by 24 or 48 hours after infection [42]. When mice implanted with human lung tissue and infected with SARS-CoV-2 were treated with Molnupiravir, the treatment efficacy measured as a reduction of lung virus titres was lower when treatment was started at 48 hours after infection, as compared to earlier treatment starts [43]. Reports on treatment of hACE2 transgenic K18 mice infected with SARS-CoV-2 with Remdesivir, Molnupiravir, Nirmatrelvir or the 3CL protease inhibitor GC376 demonstrate the difficulty of protecting SARS-Cov-2 infected K18 mice from weight loss in this challenging mouse model of severe virus-induced pathogenicity. A 5-day treatment starting 6 hours after infection with Remdesivir, Molnupiravir or Nirmatrelvir protected < 50% of mice from death and could not protect mice from weight loss during treatment. A combination of Molnupiravir and Nirmatrelvir could achieve 80% survival [44]. A 10-day treatment with a deuterated analog of GC-573 starting 24 hours after infection of K18 mice with SARS-CoV-2 could protect all mice from death, but mice still showed significant weight loss during treatment [45]. 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

These results alone cannot be underestimated for the probability to treat humans with the same efficacy, and a key to appreciating this lies in the comparison to the other abovementioned drugs. There is a striking parallel between the other antiviral drugs poor performance in treating mice and their similiar ability to treat humans with C19. You see where this is going?

That relationship between those drugs poor performance, especially in post-infection treatment, and their similiary poor performance in treating humans bodes very well for BIT225. It's ability to treat mice was exceptional, and its likelihood for treating humans will therefore be the same.

This is not the case solely because the inductive reasoning is sound, but because the facts, even though we are not privy to them, will be successful, and the reasoning reflects this like an unshakeable shadow.

But we can go beyond this mere forward looking reasoning and consider another angle.

How is it that BIT225 has succeeded in protecting mice from C19 when other antiviral drugs have failed? Obviously, it is BIT225's unique mode of action. BIT225 is the only viroporin inhibitor amoung these drugs under question, and it speaks for itself in its efficacy, not only for treating Covid, which is yet to be proclaimed, but also HIV, which is also about to be further verified.