I return to the poster of Dr. Pall ( Friedreich's ataxia ) and...

I return to the poster of Dr. Pall ( Friedreich's ataxia ) and his conclusions:

"The unique iron binding properties of ATH434 suggests
this drug could be suited to assist in intracellular iron
targeting and delivery. These novel properties include:
• Low micromolar binding affinity for intracellular Fe2+
,similar to endogenous iron chaperones including
FXN and PCBP [1-3]
• Sub-micromolar affinity for Fe3+
, significantly weaker
than that of traditional chelators DFX and DFP [5-6],
allowing for selective targeting of pathogenic Fe2+
• 1:1 Fe2+ stoichiometry, a coordination architecture
that would allow for the recognition and drug-protein
exchange of Fe2+ bound ATH434".

This study is important to us, who are waiting for the results of the open ATH434 study in MSA in one month. ATH434 is similar to normal iron chaperones as FXN and PCBP. FXN and PCBP do not harm the tissues, they are normal iron chaperones of our tissues. So we can expect that that is the case also with ATH434. But this was not so with DFP. It failed when tested in the PD population.

This same conclusion was made in the Kosman paper almost 3 y ago, (What did Prof. Kosman tell almost 3 y ago?)