(NON-TRADING) COVID-19 ARDS DISCUSSION, page-13

@taylorstjames Thanks for your work on HC, setting up that resource directory was incredibly useful. There are many similarities between the cytokine storms seen in SR-aGVHD and Covid-19-ARDS, which means it’s likely to see similar MOA’s between the two diseases. One that is multimodal with many immunomodulatory properties. However, the beauty of MSC’s are that they have even more to give on top of modulating cytokine storms. To give a crack at summarising some of potential Rem-L’s mechanisms of action in C19-ARDS:

- Reduces pro-inflammatory factors such as CSG, MIG, Il-6, TNF-alpha and others. Seen both in aGHVD and C19-ARDS.
- Inhibition of T cell activity – Rem-L inhibits activated T cell proliferation which in turn reduces pro-inflammatory cytokine secretion by these cells. This pro-inflammatory sub-set of T cells (Th17) have been linked to severe immune injury in lungs.
- Promote proliferation and repair of alveolar epithelial cells (lung cells) and restore pulmonary lung function through the secretion of KGF, VEGF and HGF (growth factors).
- Mitochondrial transfer to injured alveolar epithelium cells and restore the ‘bioenergetic needs of damaged cells’. Everyone knows that the mitochondria is the ‘power house of the cell’, and there is increasing evidence that MSC’s can effectively bring lung cells back to life by mitochondrial transfer to damaged cells.

Bit tired of typing out abbreviations now but this is just some of the research out there supporting Rem-L in ARDS and lung injury in general.
It’s likely that timing this perfect won’t happen again in our lifetimes for a biotech nearing the commercialisation finish line to be handed a potential billion dollar label extension.