Ann: EMA DMD Scientific Advice and Regulatory Process Update, page-75

I have to say the more I re-read the MS trial results the more I think the future for ATL-1102 is going to be powerful, for patients and shareholders.

I think the Tysabri concerns can be alleviated greatly via clinical results as provided below.

Referring to ATL-1102 Pase 2 trial results.
'Scans were also reviewed by a board-certified neuroradiologist for progressive multifocal leukoencephalopathy (PML) independently of the team assessing the scans for efficacy.'
  
'Safety. The most common treatment-emergent adverse events (TEAEs) in the ATL1102 group were injection site erythema (25.0% patients), alanine aminotransferase (ALAT) increases (19.4%), MS relapses (16.7%), aspartate aminotransferase increases (11.1%), headache (11.1%), and thrombocytopenia (22.2%) (table e-1). MS relapse was the most frequent TEAE in the placebo group (19.5% patients). Injection site erythema, ALAT increases, and thrombocytopenia were more frequent in the ATL1102 group than in the placebo group (difference $5%). Serious TEAEs were MS relapses and one case of grade 2 thrombocytopenia in the ATL1102 group. No JC virus in the blood or PML was observed.'

'More analysis is required to characterize the pharmacologic and pharmacodynamic action of ATL1102. This also extends to ascertaining the profile of ATL1102 with respect to the risk of PML. Natalizumab increases the release of CD341 hematopoietic stem/progenitor cells and CD191 pre B cells and CD201 B cells into the blood, which carry latent low copy JC virus,30,31 including in individuals who are seronegative.31 Latent JC virus activation is theorized to involve B-cell differentiation, including B-cell DNA-binding protein Spi-B, which increases JCV transcription.30 Natalizumab has a long half-life in the blood (6 days), and a broad VLA-4 antagonist effect, and can impair JC virus immunosurveillance, leading to PML.4,30 Preliminary data have shown ATL1102 treatment increases CD341 RNA 50% at week 8 vs baseline, though its effects at the CD341 cell level need to be explored14 (appendix e-2). The reduction of CD191 (pre) B cells with ATL1102 treatment suggests that release of lymphoid precursors into the blood may be low or they do not survive, potentially reducing the pool of cells that may carry latent virus. ATL1102 does not bind cell surface VLA-4. Natalizumab binding to VLA-4 induces intracellular signaling–associated proinflammatory effects, leading to poor outcomes in patients with PML following treatment suspension.30,32 The short ATL1102 half-life in plasma of 4.8 hours14 potentially limits exposure of circulating leukocytes to drug, which may better preserve blood leukocyte VLA-4–mediated immunosurveillance and therefore be at less risk of causing PML. IFN-b1 treatment of RRMS reduces blood mononuclear cell CD49d RNA33 and VLA-4 expression on CD81 lymphocytes34 and CD41CD45RO1 primed memory T cells, while preserving other blood leukocyte VLA-4 function.35 IFN-b1 has not been associated with PML. ATL1102, which employs a unique antisense mechanism to reduce VLA-4 expression, has in this study substantially reduced disease activity in RRMS at doses that are generally well-tolerated. Longer-term trials are required to confirm its potential as a valuable additional therapeutic option in the treatment of RRMS.'

I am enthusiastic about the day we have the funding to recommence our MS activities.
And it is likely I believe that the previous p2 DMD trial and any of the upcoming EU/USA DMD trial results from data re CD94d/VLA-4 etc will be able to in part at least, and if not more, cross-correlate to the MS safety levels regarding the concerns and problems raised around Tysabri/ Natalizumab.