ATL1102 US Patent - very interesting, page-24

Hi @waynesworld ref your question

In short I ask the question:
Does the mechanism of action for ATL1102 include the protection of minute levels of dystrophin or a version of micro-dystrophin that become biologically active in exerting a functional outcome?

Have looked into this question Wayne and found a possible answer to that question

Ref this study
Could this be a possibility with reference to FAPS causing Cilia

see article below ( part off )

Like it or not, as we age, our muscle cells are slowly exchanged, one by one, for fat cells. This process quickens when we injure a muscle, and an extreme form of this process is also seen in muscle-wasting diseases such as Duchenne muscular dystrophy (DMD). Now, scientists at UC San Francisco have shown that cellular antennae called cilia, found on fat-forming cells interspersed in muscle, play a key role in this muscle-to-fat transformation.

The findings, revealed in experiments with mice, and published July 13, 2017 in Cell, suggest a previously unsuspected connection between cilia and tissue renewal. This fresh molecular understanding could open up new prospects for regenerative medicine, and one day enable researchers to improve muscle renewal during aging and disease.

Previous work has shown that when muscle is injured, fat-forming cells that live alongside muscle cells, called fibro/adipogenic progenitors (FAPs), divide and differentiate into fat cells. Kopinke found that, unlike muscle cells, these fat-forming FAPs are more likely to carry primary cilia, and that muscle injury further increased the abundance of FAPs with cilia. These observations suggested that cilia might be playing an important role in fat formation.

To test this hypothesis, the research team used two mouse models of muscle injury—an acute injury model created by injecting damaging agents into mouse muscles, and a chronic injury model with progressive loss of muscle fibers such as that seen in in DMD. When the scientists genetically blocked the ability of FAPs to form cilia, both injury models showed lower amounts of fat in muscle. What's more, the loss of cilia not only led to the loss of fat, but also aided muscle regeneration.
"That was unexpected," Kopinke said. "We converted muscle in a mouse model of DMD into muscle that was more like that of a normal mouse.


So Wayne could there be a remote possibility that ATL1102 targeting CD49d is halting the advancing inflammation and further muscle damage,

and in doing so stops the need for FAPS dividing and differentiating into fat cells and forming more primary Cilia and doing further damage,

Or is 1102 also just blocking the forming of Cilia as well as reducing the target CD49d

If this is the case it could well be aiding as described the regeneration of muscle

Which under MRI we have actually witnessed

Article

https://medicalxpress.com/news/2017-07-tiny-cellular-antennae-key-fat.html


See how we go