MSB to dispute FDA finding in Type A meeting, page-37

Do you understand the inflammation pathway and what Rem-L does??

The treatment modulates the immune response and you see potency of that in terms of the biomarkers expressed and suppressed.

This is key in understanding how it works.



Lemme break it down for you.

1) TNFR1 get expressed - this binds to TNF-alpha (which is a pro-inflammatory cytokine)

2) This then leads to the phosphorylation of NF-kB (which is a protein complex that controls transcription of DNA, cytokine production and cell survival.)

3) As a result, CCL2 (a chemoattractant protein) gets produced which very importantly...

4) ... Polarizes the M1 Macrophage (which is an immune cell that promotes inflammation) into the M2 Macrophage state

5) This is important because the M2 Macrophage is involved in regulation of the resolution phase of inflammation and the repair of damaged tissues (think anti-inflammatory cytokines being produced, like IL-10)

Now, how they measure how potent the cell is, is seen in the assays where they see how much a principal inflammatory cytokine gets inhibited, while looking at how much TNFR1 gets expressed (remember that this the 'ignition' to the process)

So in the assay, they look at a) Inhibition of a principal inflammatory cytokine - in MSB's case, they look at how much IL-2R-alpha gets inhibited, and b) how much TNFR1 gets expressed.

This is the result of the assay using the optimized cells.



1) WAY more TNFR1 being expressed
2) WAY more IL-2Ra was inhibited



The quality has improved over time.

Tough to argue that the cells are not potent!