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Edaravone | CAS No: 89-25-8 | GMP-certified suppliers
A medication that provides neuroprotective benefits by slowing progression of amyotrophic lateral sclerosis and treating acute ischemic stroke through antioxidant activity.
Therapeutic categories
AntioxidantsCentral Nervous System AgentsCompounds used in a research, industrial, or household settingFree Radical ScavengersMiscellaneous Central Nervous System AgentsNervous System
Generic name
Edaravone
Molecule type
small molecule
CAS number
89-25-8
DrugBank ID
DB12243
Approval status
Approved drug, Investigational drug
ATC code
N07XX14
Primary indications
- Edaravone is indicated for the treatment of amyotrophic lateral sclerosis (ALS) in the US and Canada
- It is also indicated to treat acute ischemic stroke in Japan
Product Snapshot
- Edaravone is available primarily as injectable formulations including solutions, suspensions, and kits, suitable for intravenous administration
- It is utilized mainly for treating amyotrophic lateral sclerosis (ALS) and acute ischemic stroke
- The product holds regulatory approvals in the US, Canada, and Japan, with both approved and investigational statuses
Clinical Overview
Edaravone (CAS Number 89-25-8) is a neuroprotective agent primarily indicated for the treatment of amyotrophic lateral sclerosis (ALS) in the United States and Canada, and for acute ischemic stroke in Japan. It belongs to the chemical class of pyrazolones, characterized by a pyrazole ring bearing a ketone group. The compound exhibits three tautomeric forms and functions as a free radical scavenger with potent antioxidant properties.
Pharmacodynamically, edaravone delays disease progression in neurological disorders such as ALS and ischemic stroke by mitigating neuronal damage and cell death. Its mechanism of action involves scavenging reactive oxygen species (ROS), particularly hydroxyl radicals and peroxynitrite radicals, which contribute to oxidative stress implicated in these conditions. By inhibiting lipid peroxidation and preventing endothelial and neuronal cell membrane damage induced by ROS, edaravone offers neuroprotective effects. Additionally, preclinical evidence suggests possible anti-inflammatory activity through suppression of neutrophil activation and downregulation of inducible and neuronal nitric oxide synthases, thereby reducing inflammatory oxidative stress following cerebral ischemia. Notably, edaravone does not inhibit superoxide production.
Regarding absorption, distribution, metabolism, and excretion (ADME), edaravone is known to be a substrate for various UDP-glucuronosyltransferase (UGT) enzymes, including UGT1A1, UGT1A6, UGT1A9, UGT2B7, and UGT2B17, as well as organic anion transporters OAT1 and OAT3. These pathways contribute to its metabolism and clearance, although detailed pharmacokinetic parameters vary by formulation and indication.
Safety considerations include the necessity for monitoring potential side effects and long-term efficacy, which led to regulatory scrutiny in Europe. The marketing authorization application was withdrawn by the manufacturer in 2019 following requests for additional long-term safety data. Edaravone has been investigated in other neurological conditions such as Alzheimer’s disease and neuropathic pain but is primarily utilized for ALS and ischemic stroke treatment.
Edaravone is marketed under various formulations, including intravenous and oral suspension forms, with approvals differing by region. Procurement of high-quality edaravone API requires attention to tautomeric stability, purity standards, and compliance with regulatory guidelines. API sources should provide thorough documentation on manufacturing processes and ensure consistency to support clinical and pharmaceutical development programs.
Pharmacodynamically, edaravone delays disease progression in neurological disorders such as ALS and ischemic stroke by mitigating neuronal damage and cell death. Its mechanism of action involves scavenging reactive oxygen species (ROS), particularly hydroxyl radicals and peroxynitrite radicals, which contribute to oxidative stress implicated in these conditions. By inhibiting lipid peroxidation and preventing endothelial and neuronal cell membrane damage induced by ROS, edaravone offers neuroprotective effects. Additionally, preclinical evidence suggests possible anti-inflammatory activity through suppression of neutrophil activation and downregulation of inducible and neuronal nitric oxide synthases, thereby reducing inflammatory oxidative stress following cerebral ischemia. Notably, edaravone does not inhibit superoxide production.
Regarding absorption, distribution, metabolism, and excretion (ADME), edaravone is known to be a substrate for various UDP-glucuronosyltransferase (UGT) enzymes, including UGT1A1, UGT1A6, UGT1A9, UGT2B7, and UGT2B17, as well as organic anion transporters OAT1 and OAT3. These pathways contribute to its metabolism and clearance, although detailed pharmacokinetic parameters vary by formulation and indication.
Safety considerations include the necessity for monitoring potential side effects and long-term efficacy, which led to regulatory scrutiny in Europe. The marketing authorization application was withdrawn by the manufacturer in 2019 following requests for additional long-term safety data. Edaravone has been investigated in other neurological conditions such as Alzheimer’s disease and neuropathic pain but is primarily utilized for ALS and ischemic stroke treatment.
Edaravone is marketed under various formulations, including intravenous and oral suspension forms, with approvals differing by region. Procurement of high-quality edaravone API requires attention to tautomeric stability, purity standards, and compliance with regulatory guidelines. API sources should provide thorough documentation on manufacturing processes and ensure consistency to support clinical and pharmaceutical development programs.
Identification & chemistry
| Generic name | Edaravone |
|---|---|
| Molecule type | Small molecule |
| CAS | 89-25-8 |
| UNII | S798V6YJRP |
| DrugBank ID | DB12243 |
Pharmacology
| Summary | Edaravone acts as a free radical scavenger targeting hydroxyl and peroxynitrite radicals, thereby reducing oxidative stress implicated in neurological disorders such as amyotrophic lateral sclerosis (ALS) and ischemic stroke. Its antioxidant activity limits lipid peroxidation and endothelial cell damage, contributing to neuroprotection. Additionally, edaravone may modulate inflammatory pathways by inhibiting neutrophil activation and nitric oxide synthase expression. |
|---|---|
| Mechanism of action | Oxidative stress and reactive oxygen species (ROS) production have been implicated in various neurological disorders, such as amyotrophic lateral sclerosis (ALS) and cerebral ischemia. Oxidative stress caused by excess ROS damages endothelial cells in the cerebral vasculature as well as neuronal cell membranes, leading to neuronal cell death. Edaravone is a free radical scavenger that scavenges and suppresses the generation of hydroxyl radicals and peroxynitrite radicals. The exact mechanism of action of edaravone in ALS has not been fully elucidated; however, edaravone is thought to mediate therapeutic effects via its antioxidant properties. Since oxidative stress has been implicated in the pathophysiology of ALS and cerebral ischemia, inhibiting lipid peroxidation, suppressing endothelial cell damage induced by lipid peroxides, and scavenging free radicals may lead to neuroprotective effects. Edaravone has no effect on superoxide production. It is suggested that edaravone may also possess anti-inflammatory properties, as it inhibited neutrophil activation and suppressed inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS) expression in animal models. It was also shown to ameliorate ROS-induced inflammatory oxidative stress after ischemic brain reperfusion. |
| Pharmacodynamics | Edaravone works to delay the disease progression of neurological disorders such as ischemic stroke and ALS by limiting the extent of neuronal damage or death. |
ADME / PK
| Absorption | One study investigated the absorption of edaravone in healthy adults, who either received a single oral (105 mg/mL) or intravenous (60 mg/60 min) dose. The mean C<sub>max</sub> (CV%) and T<sub>max</sub> were 1656 (44.3) ng/mL and 0.5 hours, respectively, following oral administration. The absolute oral bioavailability is about 57% because of first-pass metabolism. The mean C<sub>max</sub> (CV%) and T<sub>max</sub> were 1253 (18.3) ng/mL and one hour, respectively, following intravenous administration. When intravenously administered, the maximum plasma concentration (C<sub>max</sub>) of edaravone was reached by the end of infusion. The C<sub>max</sub> and area under the concentration-time curve (AUC) of edaravone increases more than dose-proportional over the dose range of 30 to 300 mg. Edaravone does not accumulate in plasma with once-daily or multiple-dose administration. The C<sub>max</sub> and AUC decreased when the oral suspension formulation of edaravone was administered with a high-fat meal. |
|---|---|
| Half-life | The mean terminal elimination half-life of edaravone is approximately 4.5 to nine hours. The half-lives of its metabolites range from three to six hours. |
| Protein binding | Edaravone is 92% bound to human serum proteins, mainly to albumin, with no concentration dependence in the range of 0.1 to 50 micromol/L. |
| Metabolism | The metabolites of edaravone have not been fully characterized. Edaravone is metabolized to a sulfate conjugate and a glucuronide conjugate, which are not pharmacologically active. The glucuronide conjugation of edaravone involves multiple uridine diphosphate glucuronosyltransferase (UGT) isoforms (UGT1A1, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT1A10, UGT2B7, and UGT2B17). In human plasma, edaravone is mainly detected as the sulfate conjugate, which is presumed to be formed by sulfotransferases. Oral edaravone results in 1.3- and 1.7-fold higher exposures for both sulfate and glucuronide metabolites, respectively, when compared to intravenously-administered edaravone because of first-pass metabolism. |
| Route of elimination | In Japanese and Caucasian healthy volunteer studies, edaravone was excreted mainly in the urine as its glucuronide conjugate (60-80% of the dose up to 48 hours). Approximately 6-8% of the dose was recovered in the urine as the sulfate conjugate, and <1% of the dose was recovered in the urine as the unchanged drug. _In vitro_ studies suggest that the sulfate conjugate of edaravone is hydrolyzed back to edaravone, which is then converted to the glucuronide conjugate in the kidney before excretion into the urine. |
| Volume of distribution | After intravenous administration, edaravone has a mean volume of distribution of 63.1 L, suggesting substantial tissue distribution. Edaravone has an apparent volume of distribution of 164 L following oral administration. Edaravone readily crosses the blood-brain barrier. |
| Clearance | Following intravenous administration, the total clearance of edaravone is estimated to be 35.9 L/h. The apparent total clearance of edaravone is estimated to be 67.9L/h following oral administration. |
Formulation & handling
- Edaravone is available in both intravenous injectable and oral suspension forms, necessitating formulation considerations for solubility and stability in each route. Being a small molecule pyrazolone, it does not require peptide-specific handling but requires attention to its moderate water solubility for dissolution and formulation. Oral administration requires fasting due to food sensitivity, with dosing recommended on an empty stomach and avoidance of food for at least one hour post-dose.
Regulatory status
| Lifecycle | The API is marketed in the US and Canada, with initial patents expiring in 2020 and additional patents extending protection through 2039 in the United States, indicating a mature market with ongoing patent coverage. |
|---|
| Markets | US, Canada |
|---|
Supply Chain
| Supply chain summary | Edaravone is primarily supplied by originator companies with branded products marketed mainly in the US and Canada. Multiple US patents extending through 2039 indicate ongoing patent protection, suggesting limited generic competition in these markets at present. The supply landscape is thus characterized by a controlled number of originators maintaining exclusive rights within North America. |
|---|
Safety
| Toxicity | Oral and intravenous LD<sub>50</sub> in rats are 1915 mg/kg and 631 mg/kg, respectively. There is limited information on the acute toxicity of edaravone. |
|---|
High Level Warnings:
- Edaravone exhibits moderate acute toxicity with rat LD50 values of 1915 mg/kg (oral) and 631 mg/kg (intravenous)
- Limited data are available regarding the compound’s full toxicity profile, necessitating cautious handling
- Appropriate protective measures should be employed to minimize occupational exposure due to potential toxicity
Aminodihexylquat API manufacturers & distributors
Compare qualified Aminodihexylquat API suppliers worldwide. We currently have 1 companies offering Aminodihexylquat API, with manufacturing taking place in 1 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| LGM Pharma | Distributor | United States | World | BSE/TSE, CEP, CoA, GMP, MSDS, USDMF | 441 products |
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