Lambert-Eaton Myasthenic Syndrome
Recent clinical, regulatory, research and industry developments relating to this disease.
Anti-CD19 CAR-T cells are effective in severe idiopathic Lambert-Eaton myasthenic syndrome.
Approval: Firdapse (previously Zenas) (EMA)
What's happening now
An analyst briefing on current research, clinical, regulatory and industry activity surrounding this disease.
Therapeutic landscape
Therapies with a regulatory footing for this condition, alongside the wider set of agents co-studied with it in the literature.
Approval — Symptomatic treatment of Lambert-Eaton myasthenic syndrome (LEMS) in adults. (2009)
Clinical trials
The current development programme across all trial phases.
Regulatory timeline
Drug regulatory events matched to this condition by indication — EMA.
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
Key research shaping understanding of this disease, combining the latest publications with the most influential evidence.
Major themes3
- Antigens, CD191
- Immunotherapy, Adoptive1
- Lambert-Eaton Myasthenic Syndrome1
Leading journals1
- Cell reports. Medicine1
Leading researchers8
- Borie D1
- Dudziak D1
- Geis C1
- Heger L1
- Hochhaus A1
- Rinke J1
- Sayer-Klink A1
- Schnetzke U1
Affiliations (unnormalised)4
- Comprehensive Cancer Center Central Germany1
- Institute for Transfusion Medicine1
- Jena University Hospital1
- Laboratory of Dendritic Cell Biology1
Reference
Authoritative identity, definition & identifiers.
An autoimmune disease characterized by weakness and fatigability of proximal muscles, particularly of the pelvic girdle, lower extremities, trunk, and shoulder girdle. There is relative sparing of extraocular and bulbar muscles. CARCINOMA, SMALL CELL of the lung is a frequently associated condition, although other malignancies and autoimmune diseases may be associated. Muscular weakness results from impaired impulse transmission at the NEUROMUSCULAR JUNCTION. Presynaptic calcium channel dysfunction leads to a reduced amount of acetylcholine being released in response to stimulation of the nerve. (From Adams et al., Principles of Neurology, 6th ed, pp 1471)
- 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.