Algernon Pharmaceuticals Inc (AGNPF)

[medchem]

Some more science:

Today Mark Williams said (im paraphrasing):

what could happen is that initial release of glutamate, there are NMDA receptor on neutrophils, increased CD11b, increase ICAM-1 excpression in the lung. Traffic neutrophils from lungs. Neutrophils could be releasing glutamate in the lungs and on T cells. NR2B subunit paper 2014 ifenprodil modulated t cell activity and reduced it. Its conceivable that (1) stop trafficking of neutrophils (2) decrease glutamate (3) decrease t cells (4) decrease the cytokine storm because this might be the biggest issue. Also high likelihood of anti-fibrotic effect.

ICAM-1..!

I've been preaching about this.

I hope he realizes that ICAM-1 is upregulated by TNF-alpha via matrix metalloproteinases (MMPs). More ICAM-1 means that the pulmonary capillary endothelium becomes leaky. Hence you get more acute respiratory distress syndrome (ARDS) from all the fluid and protein in the lungs. Hence why the patients can't breath. NMDA-antagonists like Ifenprodil = block the upregulation of ICAM-1 (likely mediated via TNF-alpha) and thus you get less fluid in the lungs. Less ARDS and quicker recovery.

But hey, i'm just out here doing my scientific DD and hope someones listening.