Knowde Enhanced TDS
Identification & Functionality
- Chemical Name
- Pharma & Nutraceuticals Functions
- CAS No.
- 89-25-8
- EC No.
- 201-891-0
- Technologies
- Product Families
- Chemical Structure
Applications & Uses
- Markets
- Function of Edaravone in the Treatment of Amyotrophic Lateral Sclerosis
Introduction of Amyotrophic Lateral Sclerosis:
Amyotrophic lateral sclerosis (ALS) is a group of rare neurological diseases. ALS belongs to a wider group of disorders known as motor neuron diseases, which are caused by gradual deterioration (degeneration) and death of motor neurons. Motor neurons are nerve cells that extend from the brain to the spinal cord and to muscles throughout the body. These motor neurons initiate and provide vital communication links between the brain and the voluntary muscles. The disease is progressive, meaning the symptoms get worse over time.
Treatments can't reverse the damage of amyotrophic lateral sclerosis, but they can slow the progression of symptoms, prevent complications, and make you more comfortable and independent.
Edaravone was approved in Japan in 2015, and in the U.S. in 2017, based primarily on positive results of a single clinical trial in early-stage ALS patients conducted in Japan.
Edaravone has been available in Japan since 2003 for the treatment of acute stroke, but also showed promise in mouse models for ALS. An initial randomized controlled trial in patients with ALS did not show benefit for all patients, although a subgroup of patients in the earliest disease phase did benefit. A subsequent trial compared edaravone plus riluzole versus riluzole alone in patients with early-stage ALS who were free of substantial respiratory muscle weakness and who had progressed over a 3-month observation period. This study showed a 33% slowing in the rate of disease progression over a 6-month treatment period.
Mechanism of Action:
Nootropic and neuroprotective effects are mediated through inhibiting lipid peroxidation and scavenging free radicals. Free radicals are byproducts of normal cellular processes that produce energy. Normally, the body quickly removes them. If they remain in the body, they can cause oxidative stress, leading to damage and cell death.
Researchers think that oxidative stress due to free radicals is one of the causes of nerve cell death in ALS.
Edaravone acts to increase prostacyclin production, decrease lipoxygenase metabolism of arachidonic acid by trapping hydroxyl radicals, and inhibit alloxan-induced lipid peroxidation and quench active oxygen species. It targets various kinds of cells, including neurons, endothelial cells and myocardial cells.
Properties
- Soluble in
- Ethanol, Methanol, Acetic acid
- Slightly Soluble In
- Water or Diethyl ether
Safety & Health
- Side Effects
In U.S. clinical trials and in post-marketing data from outside the U.S., the most serious adverse effects reported with edaravone treatment included hypersensitivity and sulfite allergic reactions, including anaphylactic symptoms. Bruising or contusions, gait disturbance, headache, dermatitis, and eczema were the most common adverse reactions observed in 10% or greater of edaravone-treated patients during the studies. The adverse reactions that occurred in 2% or more of edaravone-treated patients and at least 2% more frequently than in the placebo group appear in Table below.
Adverse Event Edaravone (n = 184) % Placebo (n = 184) % Contusion 15 9 Gait disturbance 13 9 Headache 10 6 Dermatitis 8 5 Eczema 7 4 Respiratory failure,
respiratory disorder, hypoxia6 4 Glycosuria 4 2 Tinea infection 4 2 Alfa Chemistry offers high quality of edaravone which meets the CP.