In a nutshell, I don't think the exact mechanism of action of...

In a nutshell, I don't think the exact mechanism of action of ATH434 is not known. And I think a lot of the companies think tank is trying to figure out how the drug shows clinical improvement.

1) We have shown clinical improvement
2) We have shown safety and efficacy.

From the companies website



The MRI scans have not shown any statistical significance of iron reduction although it continues to increase in the placebo group. Question is what is happening here with the Iron chaperone/chelating? apart from the Substantia Niagra and globes Pallidus, they haven't looked at any other basal ganglia regions at least from what what published.

So there is reduction/redistribution of excess iron, but from where?
They have mentioned in the conclusions: Results require further exploration of the role of excess labile iron in neurodegeneration.

Both the alpha synuclein SAA and nfl are biomarkers in parkinsonian disorders. Personally I am waiting for a really positive note if they can pinpoint a SAA for MSA given they were no differences in the CSF nfl levels in all groups.
And I can't see anything where it has shown to reduce alpha synuclein. Happy to be corrected

If there was no change in the NFL levels in all groups, neuronal damage is ongoing. This is somewhat mind boggling as there is evidence to show reduced cerebral atrophy with ATH434 (which possibly means less neuronal damage?), this on the setting of observable improvement whilst staying on the drug.

DYOR