Ann: Quarterly Activities/Appendix 4C Cash Flow Report, page-18

Well we can now see why we havnt had an Ann with ref to the dystrophyn side of things

Just imagine putting that sentence to market

An initial analysis of dystrophin levels was undertaken by MCRI. While dystrophin protein signals were observed in the muscle tissues of the treated mice, the results were inconclusive

So now we understand WHY and the delay

But in the initial Ann ref the mice showed a difference in muscle function against placebo

Yet drilling down we see inconclusive evidence at this moment in time of dystrophin restoration

NOW

i may well get shouted off this forum by some for suggesting this as a layman with no scientific background whatsoever, but with all that is going on with Sarepta and Gene Therapy and dystrophin restoration OR FAILURE TO RESTORE

and along with our recent findings in this Ann

IS everyone barking up the wrong tree so to speak

Look at our Ph2 results, results that had never been seen before,

Yet are we acyively seeking to restore Dytrophin

NO WE ARE NOT

OUR AIM
with Atl1102 is to seek to control Imflamation and in doing so we have actually seen results never heard of in the DMD field and that was to halt the progression of the disease over a 6 month period

Proffesior Voight made comment you could normally predict disease progression IE deterioration in these boys over the 6 month trial period This progression was not seen in our trial and some boys showed slight improvement

SO WHAT IS GOING ON

I believe somehow no scientist here so i am going to say somehow that our method of action in ATL1102 is following allong the lines of Satellos studies and theories

being the following


When it comes to Duchenne muscular dystrophy (DMD), Satellos’ scientists are the first to have discovered that faulty Dystrophin (missing or lacking protein in Duchenne) leads to impaired muscle regeneration in patients with DMD. Preclinical Satellos studies have shown that restoring the body’s natural ability to repair itself leads to significantly improved muscle quantity, quality, and function. Independent research has shown that functional muscle is possible despite not having Dystrophin, which makes our approach promising.



So upon reading the above do you not think that all the big boys may just have it wrong by trying to replace Dystrophin and little old ANPs ATL1102 is actually doing what Satellos are trying to achieve

AND  THAT IS

RESTORING THE BODIES OWN ABILITY TO REPAIR ITSELF
( we have a clinical trial actually showing this we just dont know why it is doing what it is doing )

Satellos go on to say

Independent research has shown that functional muscle is possible despite not having Dystrophin, which makes our approach promising.

The above statement is where i believe we are actually at Functional muscle is possible despite not having Dystrophin and i also believe that is what these mice results are showing

Improvement in muscle which has been Announced yet little to no sight of Dystrophin improvement

ARE ALL THESE $$$$$$BIL  being wasted chasing dystophin restoration when they should be looking elswhere

ATL1102 may just be that key to the restoration of muscle function despite not having Distrophin

Just imagine if we could get our drug into these boys with early onset

( I JUST  WONDER WHAT THAT OUTCOME WOULD BE  )