What does Tocilizumab's COVID-19 trial failure mean for Biotron?

On July 31st, Roche reported that its phase III trial for its first in class IL-6 receptor drug, Tocilizumab, failed both its primary and a key secondary end point in its trial against ARDS in COVID-19 patients.

This is a significant anti-milestone in the pursuit of C19 treatment because the IL-6 receptor has been shown to be well expressed in C-19 critical cases. IL-6 is one protein responsible for the severe lung inflammation that leads to ARDS. Interestingly, 'tocilizumab effectively reversed the cytokine storm in acute lymphocytic anaemia' (Schoeman and Fielding, June 2020).

For those who have closely read the above mentioned research paper will know that the authors are focused on the E protein of coronaviruses and have contributed significant research in this field. In their latest work they explored the relationship between E and ARDS, the latter mostly form what was learnt from SARS and the ARDS illness that developed that is identical now in C19 cases. In their work they also showed how E is related to the inflammazone pathway in ARDS cases and what part E plays in it. More specifically, they linked E directly, more or less, to the proteins responsible, specifically the IL-6, and actually refer to tocilizumab as being a potential treatment.

Now that this drug has failed so far in treating C19, where does this leave the potential for E to be part of any other cure?

Fortunately, in my view, the answer is very positive. The IL-6 receptor may be one human protein responsible for severe lung inflammation in C19 cases, but what triggers these cytokine proteins to become active at all? The activation of IL-6 and other cytokine proteins are a response to a cause, and that cause is the SARS-CoV-2 virus.

Stop the cause, and the response fails. Stopping the virus from replicating, and the cause of the cytokine proteins are also proportionally stopped.

This bodes well for Biotron's viroporin technology that has been shown to prevent ion channelling activity in E in two other strains of CoV, one being SARS, and as we know, E in SARS and SARS-CoV-2 are well preserved.

The conclusion that follows is still valid.