From today's announcement, ATL1102 modulation of (i) VCAM-1, a...

From today's announcement,

• ATL1102 modulation of (i) VCAM-1, a CD49d ligand, is supportive of ATL1102’s antisense mechanism of action in reducing CD49d and in reducing inflammation, (ii) CXCL16, a chemokine with a role in muscle regeneration, appears to align with the positive effects on muscle structure observed under MRI in DMD patients treated with ATL1102, and (iii) the two DMD disease genetic modifiers known to impact TGF beta and the rate of LoA in DMD patients, support ATL1102’s potential to reduce fibrosis in human disease.
• These together reflect the drugs reported positive effects in stabilizing muscle function and strength seen in non-ambulant patients treated with ATL1102
• Modulation of these plasma proteins has, to our knowledge not, previously been reported with the use of corticosteroid drugs in non-ambulant DMD patients
• ATL1102 stabilization of multiple muscle disease progression parameters together with these positive effects on the above proteins, positions ATL1102 as an exciting prospect for the treatment of both non ambulant and ambulant DMD patients.

and with the news from Solid Bio hopes a shred of positive DMD data will spark a much-needed rally after clinical hold drama:


"Another hurdle for all companies developing DMD treatments—and it’s a full pipeline—is that while early data have proven treatments can boost dystrophin, actual efficacy data have not materialized.This has been a challenge for leading DMD treatment maker Sarepta Therapeutics, which has plenty of biomarker data but not a lot on whether patients actually benefit from treatment. Sarepta has also been plagued by difficult side effects in clinical trials, but patients may be willing to accept certain adverse events given the challenging nature of the disease itself."


I believe most if not all DMD patients will now be looking for HOPE from ANP ATL1102!