#Leronlimab is an antibody that blocks a cell receptor called CCR5. The #CCR5 receptor just happens to be a key doorway HIV uses to get inside a cell so that’s why we developed it as an HIV treatment. But the actual function of CCR5 inside our body is to direct cell movement and
Function. Breast, prostate, and a few other cancers co-opt the immune system to support their growth by using the CCR5 receptor to control cell movement and function. We were targeting that role of CCR5 to support cancer cell growth when COVID-19 hit. Our early signals of success
in breast cancer led us to believe we could impact the inflammation, or #cytokinestorm, that is killing patients with Covid-19 since it is the same cell movement and function controlled by CCR5 that is involved. And, as incredible as it sounds, I believe we got very lucky and
that Leronlimab will be shown to work better than anyone could ever have imagined.
How did you first know this drug would work on COVID-19?
It’s a peculiar situation where the drug demonstrated its efficacy before we ever got to randomized, placebo-controlled, clinical
How did you first know this drug would work on COVID-19?
It’s a peculiar situation where the drug demonstrated its efficacy before we ever got to randomized, placebo-controlled, clinical
studies. Leronlimab has been given on an emergency basis to over 60 individuals in the US who were in dire condition due to COVID-19. What we saw in a group of those patients at day three after a single dose is reversal of severe immune exhaustion, calming of the cytokine storm
and even decreases in viral load. There is nothing subtle or ambiguous about these amazing results and we’ve seen this in every patient we’ve treated and evaluated. We were also fortunate to identify the cytokine that appears to be driving the whole inflammatory mess. It’s called
