Proteome Sciences. AGM Statement.

kistakat - TC-1734 is a nicotinic acetylcholine receptor modulator and has no direct action on tau phosphorylation - which is PRM's proposed mode of action.

Whilst not necessarily the case, AD drugs currently in Phase III have not proven to be particularly effective and it is not expected that this will change significantly with release of more trial results. In Phase II, there is again nothing to be excited about really - largely down to the way the drugs work. Things get more interesting in Phase I and pre-clinical stages. Of note are the beta-amyloid immunotherapies and the gamma-secretase modulators IMO.

It is still unclear whether these approaches will work. Here I am referring in all cases to an aim of preventing progression of the disease as this is the holy grail (and cognitive & functional enhancers simply cannot bring significant long term benefits in the face of the relentless neuronal degradation).

It is possible, that if targetted early enough, then techniques aimed at reducing beta-amyloid levels may slow or stop the disease (other treatments for those stuck at a more advanced stage will still be needed to provide cognitive and functional enhancement).

PRM's target goes a step further in that it may still prevent disease progression if beta-amyloid modulators dont work. If the biomarkers are to be believed, then PRM's target could represent the earliest stages of the disease and so, possibly the root cause. Also being highly specific, side effects possible with other therapies, may be avoided.

Richard - yes, very true. It is quite possible that we wouldnt know until well into Phase III as the FDA dont have to release that sort of info! But, I just dont think it likely that it is in fact yet in any more advanced stages than discovery/ early pre-clinical (??)