Regulation FD Disclosure (Form 8-K)

Item 7.01 Regulation FD Disclosure.

On March 11, 2026, Solid Biosciences Inc. (the "Company") made available an updated corporate presentation on its website.

The information provided under Item 7.01 of this Current Report on Form 8-K shall not be deemed "filed" for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the "Exchange Act"), or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference in any filing under the Securities Act of 1933, as amended, or the Exchange Act, except as expressly set forth by specific reference in such a filing.

Item 8.01 Other Events.

SGT-003

Interim Clinical Update for INSPIRE DUCHENNE

On March 11, 2026, the Company announced positive new interim data from its Phase 1/2 INSPIRE DUCHENNE clinical trial, a Phase 1/2 first-in-human, open-label, single-dose, multicenter trial designed to evaluate the safety, tolerability and efficacy of SGT-003 in pediatric participants with Duchenne muscular dystrophy ("Duchenne") at a dose level of 1E14vg/kg. SGT-003 is administered as a one-time intravenous infusion.

The interim clinical data reported is as of a February 23, 2026, data cutoff date. SGT-003 has been generally well tolerated in the 40 participants dosed as of March 11, 2026. The safety and tolerability profile observed in the INSPIRE DUCHENNE trial continued to be promising; SGT-003 is administered using a low-burden, steroid-only prophylactic immunomodulation regimen. The clinical trial is being conducted at 15 clinical sites across the United States, Canada, Italy and the United Kingdom and participant dosing remains ongoing.

Microdystrophin transduction and expression levels, beta-sarcoglycan localization and neuronal nitric oxide synthase ("nNOS") activity were evaluated by biopsy in 20 participants (ages 1-10 years) at Day 90 and in 3 participants at Day 360 (Table 1 below). Results demonstrated robust mean vector copies per nucleus and microdystrophin expression as well as properly localized and restored beta-sarcoglycan-positive fibers and nNOS activity-positive fibers. Beta-sarcoglycan and nNOS are critical components of the dystrophin-associated protein complex ("DAPC"). In Duchenne, the absence of dystrophin destabilizes the DAPC, triggering a cascade of structural, signaling and metabolic defects that impair muscle integrity. Reconstituting critical components of the DAPC, including beta-sarcoglycan and nNOS, could suggest biologic correlation of SGT-003's treatment effect. The Company's microdystrophin construct is the only microdystrophin gene therapy, approved or investigational, that contains the R16/R17 binding domain, which uniquely localizes nNOS to the muscle.

Table 1: 90- and 360-day biopsy results

Additionally, the Company has identified an extensive biomarker panel to comprehensively evaluate treatment effect on muscle integrity. Collectively, these observed biomarker improvements at Day 90 and Day 360 suggest improved muscle fiber health and stability, reduced ongoing muscle damage, and an interruption of the chronic degeneration/regeneration cycle that is characteristic of Duchenne.

In particular, embryonic myosin heavy chain ("eMHC") is an informative predictor of disease progression. eMHC is typically expressed during fetal development but is also expressed when muscle satellite cells differentiate into muscle fibers, which in Duchenne occurs in response to muscle fiber damage. In the absence of functional dystrophin, newly generated muscle fibers also fail, leading to continued but ultimately futile satellite cell activation. A mean 44% observed reduction in eMHC-positive fibers seen at Day 90 (n=20) suggests that SGT-003 treatment has potentially disrupted this chronic and futile degeneration-regeneration cycle, stabilizing muscle fibers and preserving the reservoir of satellite cells.

Table 2: Improvements in multiple biomarkers of muscle integrity observed at Day 90 and Day 360

While cardiac assessments were initially included as safety evaluations, stabilization-to-improvement in systolic function continues to be observed as of the data cutoff date, as measured by left ventricular ejection fraction ("LVEF"). Observed improvements were driven largely by participants with low-normal baseline LVEF (defined as ≤ 60%). Cardiomyopathy is a leading cause of death in Duchenne, with 25% of individuals displaying evidence of cardiomyopathy by six years of age, increasing to 59% by 10 years of age.

Regulatory Status

As announced on February 9, 2026, the Company has reached alignment with the U.S. Food and Drug Administration ("FDA") on the overall study design for the Company's randomized, double-blind, placebo-controlled Phase 3 clinical trial of SGT-003, IMPACT DUCHENNE. The FDA agreed that the trial design was reasonable including: the patient population of ambulant participants 7 to <12 years of age, the primary endpoint of change from baseline in Time to Rise ("TTR") velocity from supine position evaluated at 18 months and other key secondary endpoints. Participant screening is underway and the Company anticipates dosing the first participant in the IMPACT DUCHENNE trial in the first quarter of 2026.

The Company plans to have additional meetings with the FDA in the first half of 2026 to receive guidance on a potential accelerated approval pathway for SGT-003 and expects to provide additional regulatory and clinical updates mid-2026.