So I have been called out? Why and what for? Such nonsense. I stand firm. Su, T. and his colleagues came to this conclusion:
"Notably, in comparison to the reference compound clioquinol, it inhibited metal-induced Aβ1-42 aggregation more effectively and promoted greater disassembly of the highly structured Aβ fibrils generated through Cu(2+)-induced Aβ aggregation. "
IMO the poster who copied the article did not comprehend the fact that the Chinese researchers with their PDE9 inhibitor surpassed PBT2 and its clioquinol heritage. It is moot since the multitude of clinical trials of various genomic work, biologicals and small molecules now approaching and in Phase 3 will leave the clioquinol derivatives and PDE9 inhibitors far behind IMO.
The abstract authors may not consider themselves in competition with Prana whom they may not know, but Prana should certainly consider the Chinese scientists to be competitors since they have pointed out PDE9's superiority to clioquinol which is the basis for ALL of Prana's research leading to the PBT's which have not been proven successful in almost two decades of watching and waiting.
The abstract copy did nothing good for Prana's cause IMHO. To anyone interested, it called attention to the above quote from the abstract. Prana used clioquinol in the PBT1 for AD trial which was abandoned many years ago. PBT2 quickly became a direct clioquinol descendant known as an 8-hydroxyquinol. All MPAC PBT's spring from the same clioquinol heritage. Clioquinol was once used as an antimicrobial, anti-fungal and antiamoebal compound. The FDA still awaits safety evidence from Prana following issuance of the Partial Clinical Hold last year.
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