Related Experiment Video
Updated: Aug 28, 2025

ALS - Motor Neuron Disease: Mechanism and Development of New Therapies
Published on: July 29, 2007
Pharmacotherapy for Amyotrophic Lateral Sclerosis: A Review of Approved and Upcoming Agents
Stephen A Johnson1, Ton Fang2, Fabiola De Marchi3,4
1Neurological Clinical Research Institute (NCRI), Healey & AMG Center for ALS, Massachusetts General Hospital, 165 Cambridge St, Suite 600, Boston, MA, 02114, USA.
Abstract:
Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative disorder involving loss of upper and lower motor neurons, with most cases ending in death within 3-5 years of onset. Several molecular and cellular pathways have been identified to cause ALS; however, treatments to stop or reverse disease progression are yet to be found. Riluzole, a neuroprotective agent offering only a modest survival benefit, has long been the sole disease-modifying therapy for ALS. Edaravone, which demonstrated statistically significant slowing of ALS disease progression, is gaining approval in an increasing number of countries since its first approval in 2015. Sodium phenylbutyrate and taurursodiol (PB-TURSO) was conditionally approved in Canada in 2022, having shown significant slowing of disease progression and prolonged survival. Most clinical trials have focused on testing small molecules affecting common cellular pathways in ALS: targeting glutamatergic, apoptotic, inflammatory, and oxidative stress mechanisms among others. More recently, clinical trials utilizing stem cell transplantation and other biologics have emerged. This rich and ever-growing pipeline of investigational products, along with innovative clinical trial designs, collaborative trial networks, and an engaged ALS community', provide renewed hope to finding a cure for ALS. This article reviews existing ALS therapies and the current clinical drug development pipeline.
Insights
Amyotrophic lateral sclerosis (ALS) treatments are advancing, with new therapies like edaravone and sodium phenylbutyrate/taurursodiol showing promise in slowing disease progression and improving survival for ALS patients.
Area of Science:
- Neurodegenerative disease research
- Drug development for neurological disorders
Background:
- Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with limited treatment options.
- Riluzole offers modest survival benefits, while edaravone and sodium phenylbutyrate/taurursodiol show recent promise in slowing ALS progression.
Purpose of the Study:
- To review current Amyotrophic lateral sclerosis (ALS) therapies.
- To examine the clinical drug development pipeline for ALS.
Main Methods:
- Review of existing ALS treatments, including riluzole, edaravone, and sodium phenylbutyrate/taurursodiol.
- Analysis of the current clinical trial landscape for investigational ALS products, including small molecules and biologics.
Main Results:
- Edaravone and sodium phenylbutyrate/taurursodiol have demonstrated significant slowing of ALS disease progression.
- A growing pipeline of investigational products, innovative trial designs, and collaborative networks offer hope for ALS treatment advancements.
Conclusions:
- While no cure exists, recent therapeutic advancements and a robust drug development pipeline provide renewed hope for effective Amyotrophic lateral sclerosis (ALS) treatments.
- Continued research and clinical trials are crucial for developing novel therapies to combat ALS.
More Related Videos
12:35Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis ALS
Published on: March 17, 2012
10:49Intraspinal Cell Transplantation for Targeting Cervical Ventral Horn in Amyotrophic Lateral Sclerosis and Traumatic Spinal Cord Injury
Published on: September 18, 2011
Related Concept Videos
Alzheimer's Disease: Treatment
Parkinson's Disease: Treatment
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of...
Parkinson's Disease: Overview
Drug Therapy
Antianxiety Medications
Indirect-Acting Cholinergic Agonists: Pharmacological Actions
At the neuromuscular junction, these agents work by inhibiting the breakdown of acetylcholine, allowing it to remain bound to the receptor and bind to nearby receptors. This process leads to repetitive firing of the endplate, causing muscle...
Myasthenia Gravis: Overview and Treatment
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which...