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Disease

Muscular Atrophy

Late-stage therapeutic developmentEmerging researchCooling momentum
7
Publications
20
Clinical trials
2025
Latest publication
Latest activity
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Recent clinical, regulatory, research and industry developments relating to this disease.

Effects of thyroid hormones in skeletal muscle protein turnover.

Research2024-07-01Journal of basic and clinical physiology and pharmacology

Sarcopenia - Molecular mechanisms and open questions.

Research2020-10-29Ageing research reviews

What's happening now

An analyst briefing on current research, clinical, regulatory and industry activity surrounding this disease.

Major developments
Important regulatory approvalHigh impact
Itvisma is indicated for the treatment of 5q spinal muscular atrophy (SMA) with a bi-allelic mutation in the SMN1 gene in patients 2 years of age and older.2026-06-30
Clinical Milestones8View
Regulatory Updates1View
  • 2026-06-30Approval — Onasemnogene abeparvovecItvisma is indicated for the treatment of 5q spinal muscular atrophy (SMA) with a bi-allelic mutation in the SMN1 gene in patients 2 years of age and older.
Activity timeline9

Therapeutic landscape

Therapies with a regulatory footing for this condition, alongside the wider set of agents co-studied with it in the literature.

Approved & established therapies

Approval — Itvisma is indicated for the treatment of 5q spinal muscular atrophy (SMA) with a bi-alle… (2026)

Risdiplamapproved

Accelerated approval — Evrysdi is indicated for the treatment of 5q spinal muscular atrophy (SMA) in patients wi… (2021)

Accelerated approval — Spinraza is indicated for the treatment of 5q Spinal Muscular Atrophy. (2017)

Clinical trials

10 sponsors · 3 new · 1 completed in the last 12 months (net +3)

The current development programme across all trial phases.

Clinical programme
20
All trials
6
Active
13
Late-stage
6
Completed
Late-stage studies
Recruiting
Recently completed

Regulatory timeline

Drug regulatory events matched to this condition by indication — EMA.

First approvals
2026emaApprovalOnasemnogene abeparvovec· Itvisma is indicated for the treatment of 5q spinal muscular atrophy (SMA) with a bi-allelic mutation in the SMN1 gene in patients 2 years of age and older. source ↗
2021emaAccelerated approvalRisdiplam· Evrysdi is indicated for the treatment of 5q spinal muscular atrophy (SMA) in patients with a clinical diagnosis of SMA Type 1, Type 2 or Type 3 or with one to four SMN2 copies.   source ↗
2020emaApprovalOnasemnogene abeparvovec· Zolgensma is indicated for the treatment of: patients with 5q spinal muscular atrophy (SMA) with a bi-allelic mutation in the SMN1 gene and a clinical diagnosis of SMA Type 1, or patients with 5q SMA with a bi-allelic mutation in the SMN1 gene and up to 3 copies of the SMN2 gene. source ↗
2017emaAccelerated approvalNusinersen sodium· Spinraza is indicated for the treatment of 5q Spinal Muscular Atrophy. source ↗
Other regulatory activity
2026emaCHMP positive opinionOnasemnogene abeparvovec· Treatment of 5q spinal muscular atrophy (SMA) source ↗

European Medicines Agency (CC BY 4.0). Events are matched to this condition by drug indication text — approvals/updates for drugs indicated for it, not disease-specific acts.

Research activity

7 papers

Key research shaping understanding of this disease, combining the latest publications with the most influential evidence.

Publications over time
20132025
Most influential
Recent publications
Major themes8
  • Muscle, Skeletal2
  • Muscular Atrophy2
  • Energy Metabolism1
  • Glucagon-Like Peptide-1 Receptor Agonists1
  • Health Behavior1
  • Hyperthyroidism1
  • Muscle Proteins1
  • Pandemics1
Leading journals6
  • Ageing research reviews1
  • Cells1
  • European journal of sport science1
  • International journal of molecular medicine1
  • Journal of basic and clinical physiology and pharmacology1
  • Scientific reports1
Leading researchers8
  • Bai X1
  • Baldassarre G1
  • Biolo G1
  • Blaauw B1
  • Cappello V1
  • Castro JP1
  • Cecchini M1
  • Ciciliot S1
Affiliations (unnormalised)6
  • Bispebjerg-Frederiksberg University Hospital1
  • Center for Nanotechnology1
  • CIR-MYO Myology Center1
  • Department of Clinical Medicine and Surgery1
  • German Institute of Human Nutrition Potsdam-Rehbrücke1
  • Heart and Vascular Institute1

Disease profile

A grounded synthesis of the condition — overview, causes, mechanism, risk factors and current standard of care.

Overview

Muscular atrophy is a reduction in the size and number of muscle fibers. It can occur with aging, reduced blood supply, immobilization, prolonged weightlessness, malnutrition, and especially denervation. The literature also treats it as a muscle-wasting state in which skeletal muscle mass and function decline.

Causes

The supplied grounding identifies aging, reduced blood supply, immobilization, prolonged weightlessness, malnutrition, and denervation as causes or triggers. Review material also links muscle wasting to thyroid dysfunction, sepsis-induced myopathy, and age-related sarcopenia as related clinical contexts. These sources support a multifactorial etiology rather than a single cause.

Pathophysiology

The central biological theme is an imbalance between muscle protein synthesis and protein degradation. Review abstracts describe involvement of IGF-1/Akt/mTOR signaling, FoxO-dependent ubiquitin-proteasome pathways, myostatin-Smad signaling, inflammatory pathways, and autophagy-related mechanisms. Changes in satellite cell activity, proteostasis, mitochondrial function, and neuromuscular drive are also described in the literature.

Risk factors

Aging is a major risk factor, and the grounding also supports immobilization, prolonged weightlessness, malnutrition, denervation, and reduced blood supply. Related literature additionally associates muscle wasting with thyroid dysfunction and sepsis. Sarcopenia is described as an age-related syndrome with higher risk of falls, fractures, metabolic disease, and mortality, but those are consequences rather than primary risk factors.

Current standard of care

The grounding does not support a single established standard treatment for muscular atrophy. The literature emphasizes prevention and modulation of underlying pathways, with drug-therapy discussions centered on anabolic or anti-catabolic signaling such as IGF-1-related pathways, myostatin inhibition, and GLP-1 receptor agonists in sepsis-induced muscle atrophy. At the modality level, strength exercise and contractile activity are described as stimuli that can promote muscle hypertrophy rather than atrophy.

AI-generated summary grounded in MeSH and 5 peer-reviewed sources. Informational only — not medical advice. Generated 2026-07-07.

Reference

Authoritative identity, definition & identifiers.

Defined in MeSH

Derangement in size and number of muscle fibers occurring with aging, reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation.

References & data sources
  • Disease identity & definition — NLM Medical Subject Headings (MeSH), public domain
  • Clinical trials — ClinicalTrials.gov (U.S. National Library of Medicine)
  • Research activity — Europe PMC (EMBL-EBI) + OpenAlex-derived paper links
  • Related entities are derived from literature co-mention (studied together) — associative, not causal.