European Fair Park 2 trial progress., page-2

Here we come again to the same discussion we have had several times: Supplement Fig 8 in the paper by Tardiff et al ( included Lindquist) in Feb 2012 telling that metal chelation did not alone explain the positive effect of PBT2. Now we have PBT434, not a hydroxyquinoline but a

8-hydroxyquinazolin-4(3H)-one​

, designed to help Parkinson's patient and to have affinity to iron. It is a molecule chemically very close to mitochondrion division inhibitor-1 ( also an quinazolinone ). There are many different quinazolinones. Mdivi-1 has the best quality to prevent mitochondrial division ( see Cassidy-Stone et al 2008 ). However there is some info that mdivi-1 ( and perhaps also other quinazolinones ) does not work in an environment where is a lot of iron (?). In the animal models of Parkinson's disease PBT434 and mdivi-1 work in very similar way.
So IMO PBT434 could have these two qualities: (1) iron chelator and (2) mitochondrion division inhibitor. We know that it is an iron chelator but we do not know if it has any efficacy it self to inhibit mitochondrion division. My strong guess is that PBT434 has both of these qualities and that is why the results in MSA were robust. Now when it looks like iron accumulation activates mitochondrion fission ( Huang XT, Oct 31 2018) so it could be that iron chelation itself could also activate mitochondrion fusion. To me it is self clear or even a must that Prana will soon study how PBT434 helps the energy supply of the nerves and how it does that will be also important when comparing it to the other iron chelators.