brryh, Chinese research teams are strong. Their business rules may be very different than ours. It is not a wonder if you get concerned. Somehow I trust in Masters and Florey Institute that they take care of these problems, despite Masters being not a business person but a top scientist.
Masters is an AD scientist and one of his interests has been amyloid and Zn. ATH gave up PBT2 and so PBT2 was left alone with nobody studying it. Finkelstein and Claassen are now the main scientists with 434.
IMO, Masters needs PBT2 to break the amyloid-Zn complex to load the amyloid on the monocytes to carry amyloid to the spinal fluid and back to circulation. I think that there is a gradually developing lack of energy in the monocytes to do this job. Perhaps some amyloids may not fit to be carried away by the monocytes. etc. A booster on the mitochondria of the monocyte is needed. Perhaps 434, an iron chelator, for that purpose works. These issues are far more complex but Masters may have it and IMO nobody else has at this time.
Sorry, just my simplistic thoughts. This monocyte story is strong, however. In AD diagnostics the sensitivity figure was very high and IMO it reflects also how important these monocytes are in eliminating amyloids from the brain. Earlier Masters thought that if you only break the amyloid-Zn connection by PBT2 the extra amyloid will leak away. Now he knows that it does not leak away, it needs to be carried out by the monocytes.
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