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MSLE: SAT-3247 Fast Tracked; BASECAMP Readout During 4Q26

Published: 2026-06-29Institution: Guggenheim Securities LLCCompany / ticker: MSCL.TOPages: 5Original language: 英语Evidence page: 1

Research evidence excerpt

MSLE: SAT-3247 Fast Tracked; BASECAMP Readout During 4Q26

FLASH NOTE

June 29, 2026

Debjit Chattopadhyay, Ph.D. debjit.chattopadhyay@guggenheimpartners.com MSLE: SAT-3247 Fast Tracked; BASECAMP

212 823 6584 Readout During 4Q26

Moritz Reiterer, Ph.D.

moritz.reiterer@guggenheimpartners.com

212 372 6368 Key Message: SAT-3247, an oral, pan-exon, QD treatment for DMD now has Fast Track

designation. Lack of dystrophin in DMD impairs asymmetric muscle stem (MuSC) cell Hannah Wei

hannah.wei@guggenheimpartners.com divisions, which are essential for muscle regeneration. SAT-3247 restores asymmetric

212 518 5896 MuSC divisions via dystrophin-independent mechanism and restores regenerative

capacity. Pediatric BASECAMP study readout in Q426 will be the first proof-of-concept

and MoA study for -3247 in patients who are likely to benefit from the therapy (ambulatory,

preserved muscle mass). Recall, the BASECAMP study is a placebo-controlled clinical

trial in ambulatory DMD patients aged 7-10, with mgmt suggesting that dynamometryMSLE will be the key secondary and functional readout. On July 8, 2026, at the ICNMD, we Satellos Bioscience Inc.

Sector: Biotechnology anticipate six-month follow-up data from adult participants who completed the Ph 1b trial

and are enrolled in the TRAILHEAD study.

Company Update

Figure 1 - SAT-3247 has a unique mechanism, which we see as complementary to Share Price $7.08

exon-skipping and microdystrophin gene therapies.

Asymmetric muscle stem cell division, which is essential for muscle regeneration, are dysfunctional in DMD.

SAT-3247 inhibits a positive regulator of Notch signaling AAK1 to restore NUMB polarity via a dystrophin-

Market Data independent mechanism, which restore assymmetric cell divisions.

52-Week Range $4.56 - $13.39

Shares Out (M) 20.8

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