Why Aussie taxpayers?, page-13

kind of off topic but i see another soft bash used often that i get tired of seeing  is that PBT1 was toxic...  which is only true of a batch that was made for trials having higher impurity than desired/allowable  which meant remanufacture was required.   Which was pointless with PBT2 already in Phase I trials.

http://www.alzforum.org/news/resear...s-sideswipe-clioquinol-prevent-clinical-trial
Rudi Tanzi had this to say about it:
Prana's decision to cancel the phase II/III "PLACQUE" clinical trial of PBT1 is, of course, disappointing. PBT1 (clioquinol or "CQ") is an old drug that required redevelopment of its synthetic route to meet today's GMP standards. As was highlighted in Prana's press release, during large-scale synthesis, unacceptably high levels of a mutagenic impurity were found. The levels of this di-iodo derivative in the batch made for the PLACQUE trial exceeded new international impurity guidelines, and therefore this batch could not be used in the clinical trial. The trial thus could not proceed.
So why not try to purify or resynthesize CQ? While it may be theoretically possible after additional work to satisfactorily reduce or even eliminate the levels of the di-iodo impurity (either by new synthetic chemistry or by new purification techniques), this investment in time and money may not be the best option for several reasons, the first being that Prana has a pipeline of new, custom-designed drug candidates which have already passed testing in the same preclinical models for Alzheimer disease where CQ showed efficacy: The most advanced of these, PBT2, has already entered phase I clinical trials. In addition, the remanufacturing of PBT1 would require considerable time, quite possibly putting its testing behind PBT2, anyway. Finally, as Prana explained, the di-iodo contaminant cannot form with PBT2 because its structure does not contain any iodine.
Speaking on behalf of our research teams working on the metallochemistry of Aβ, we want to point out that the trial cancellation is neither because of problems with the underlying science, nor because of new concerns about the efficacy of the drug or its class (Metal Protein Attenuating Compounds, MPACs). We believe that the underlying science remains strong and can be used to screen for and test new drug candidates. Clioquinol established the principles that are involved in targeting abnormal metal-Aβ interactions to identify new orally bioavailable MPACs as drug candidates for Alzheimer disease.
In summary, being mindful that Prana has PBT2 and other candidate compounds in its development pipeline, it would seem prudent to shift emphasis to the testing of PBT2 and the newer drug candidates.
We hope this clarification is helpful.
Disclosure: Dr Ashley Bush and Dr Rudolph Tanzi disclose that they are shareholders and paid consultants for Prana.