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Science, muscle regeneration (muscular dystrophy), music, chess, big data, ...

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@AlexDelarge6553 Rheostatics / King Cobb Steelie / Max Webster / Jeff Healey Band / Blue Rodeo / Cowboy Junkies

[Chess Feed @chess_feed]

Best Checkmate Combination Ever

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@Biotech2k1 $MSLE Satellos - “MSLE remains the biggest sleeper binary this year. I think they will hit.”

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@rbrobbi @RUSH_Roadtrips Different Strings with an extended jam outro / Neurotica / We Hold On

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@Mikehomeseller @vivien2112 Angine de Poitrine -

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@TheBio_Hunter $MSLE Muscle regeneration for muscular dystrophies and other muscle disorders

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@sciencegirl Paul Kelly - Petrichor https://t.co/wv16qqN3AR

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https://t.co/AEnXdcccoI Dr. Michael Rudnicki from Satellos $MSLE #NGBi

[Elijah Stacy @Elijahjstacy]

UNPRECEDENTED DATA: Satellos recently presented MRI data, an objective measure, showing a 3.7% mean decrease in fat fraction in the bicep of all 4 adult DMD patients compared to their baseline. Fat fraction looks at how much fat there is compared to mainly how much lean muscle there is, and this measure isn’t effort dependent or up for debate.

These results haven’t been seen before in a clinical setting. Other studies may use the word “reduction” in fat fraction, but that is different as that is comparing to natural history (how a disease progresses without treatment) or a control group (group of patients followed without treatment). Satellos is comparing from where these patients started to where they are now on drug.

Since Duchenne is a muscle wasting disease, muscle degenerates and is replaced with fat/fibrosis, which is why DMD leads to an increase in fat fraction every year. In other words, you lose muscle, never gain it.

This is why seeing a decrease in fat fraction is unprecedented, and in combination with strength measures like TE99C (think smart watch patients wear at home) increasing 34% on average over 6 months, suggests, in my opinion, muscle is regenerating as well as function is returning.

DISCLAIMER: I am a shareholder and former consultant for Satellos. $MSLE

[Defeat Duchenne Canada @defeatduchenne]

Satellos has shared six months of new trial data from the TRAILHEAD study. The data offers very encouraging news for the #Duchenne community: https://t.co/bAaEDkln59

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$MSLE #dmd https://t.co/1evWXp6msW

[Massimo @Rainmaker1973]

What shuffling a deck of cards actually means

[🎞️ lisarqrsedb / vsauce]
https://t.co/TVpAtesvl5

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FSHD P2 trial starting H2 2026 - Insightful primer on SAT-3247 with Satellos CMO Dr. Wildon Farwell - #Duchenne #FSHD $msclf is now $MSLE on NASDAQ $mscl https://t.co/3sVwclxiMi

[Satellos Bioscience @SatellosBio]

In a recent @CheckRare feature, Satellos CMO Dr. Wildon Farwell discusses the science behind SAT-3247 and how restoring the #muscleregeneration process could offer a new therapeutic approach for people living with #Duchenne muscular dystrophy. Watch the interview: https://t.co/SNNNy7AlJG

$MSCL $MSCLF

[Daniel Rensch @DanielRensch]

Huge congrats to Judit Polgár on the release of Queen of Chess on Netflix today! So proud to celebrate her story and the generations of women she’s inspired, a true legend!

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Insightful primer on SAT-3247 with Satellos CMO Dr. Wildon Farwell - #Duchenne #FSHD $msclf $mscl https://t.co/4mEBYYOo8r

[Satellos Bioscience @SatellosBio]

In a recent @CheckRare feature, Satellos CMO Dr. Wildon Farwell discusses the science behind SAT-3247 and how restoring the #muscleregeneration process could offer a new therapeutic approach for people living with #Duchenne muscular dystrophy. Watch the interview: https://t.co/SNNNy7AlJG

$MSCL $MSCLF

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@yaireinhorn $MSCLF Satellos - it would be good to read your analysis

[Chess Feed @chess_feed]

White to move, mate in 2!

[Chess.com @chesscom]

Happy 35th birthday to the strongest-ever chess player, and 18x world champion, Magnus Carlsen 🐐

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@mvcinvesting Satellos $MSCLF $MSCL is a top hidden-gem pick / muscular dystrophy / muscle regeneration - https://t.co/SagGL5IuUf

[Fidelis Aurelius @FidelisAurelius]

A pretty crazy paper on DMD just dropped.

- DMD pathology starts in fetal secondary myogenesis (aka in the womb), not from postnatal wear and tear.

- It starts even before any mechanical stress, necrosis, or inflammation, when dystrophin-null muscle stem cells mis-handle Numb/Notch polarity and under-produce progenitor cells.

- In mdx mice, deleting AAK1 fixes this, restoring polarity, progenitor output, and largely normal fetal muscle architecture.

What does this imply for $MSCL's AAK1 inhibitor....?!

https://t.co/alntQcQEP8