Pharmacological Management of Amyotrophic Lateral Sclerosis
Sahab Uddin, Rashid Mamunur in Advances in Neuropharmacology, 2020
Secondly, edaravone is a free radical scavenger used intravenously which gets rid of lipid peroxide and hydroxyl radicals and might accordingly be categorized as an anti-oxidative agent. As mentioned earlier, the action of ROS is believed to add to pathology of ALS. Therapeutic properties of edaravone were established in a wobbler mice bearing signs and symptoms similar to ALS, previous to the beginning of clinical upgrading (Kimura and Yoshino, 2006). The first two trails had been unsuccessful. On the premise of the outcomes of the most effective phase three trial, edaravone acquired advertising and marketing authorization solely in Japan in 2015.
Spinal Cord Disease
Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw in Hankey's Clinical Neurology, 2020
Edaravone is a free radical scavenger that has been shown to have a benefit in patients with ALS. In trials, it was shown to slow the decline of the ALS functional rating scale (ALSFRS-R). Edaravone is given intravenously and necessitates frequent infusions. It is given for 14 days consecutively followed by a 14-day holiday. Subsequent cycles are given for 10 of 14 days, followed by 14 days off. The most common side effect reported is easy bruising.
Micronutrients in Improvement of the Standard Therapy in Traumatic Brain Injury
Kedar N. Prasad in Micronutrients in Health and Disease, 2019
Edaravone, an FDA-approved drug, reduced oxidative damage by neutralizing free radicals after TBI in humans.168 No significant studies on single or multiple antioxidants in human TBI have been performed.
Edaravone prevents high glucose-induced injury in retinal Müller cells through thioredoxin1 and the PGC-1α/NRF1/TFAM pathway
Published in Pharmaceutical Biology, 2021
Edaravone is a neuroprotective drug that was first approved by Japan for the treatment of acute cerebral ischaemia and infarction disease. It is a powerful antioxidant that has a strong free radical scavenging ability and can protect tissues from oxidative stress (Yoshida et al. 2006). Several studies have shown that edaravone can protect retinal ganglion cells in rat models of retinal detachment and mouse models of light-induced damage by scavenging ROS (Hironaka et al. 2011; Shimazaki et al. 2011; Xu et al. 2017). However, there are no studies on the protective effect of edaravone on animal models of DR. Thioredoxin (TRX) was first identified by Laurent et al. (1964) as an enzyme necessary for DNA synthesis. It was later confirmed to be widely distributed in mammalian tissues. TRX plays an important role in numerous biological processes, including antioxidation, anti-apoptosis, immune response and virus infection (Lu and Holmgren 2014). TRX, TRX reductase (TRXR) and NADPH form the TRX system (Lu and Holmgren 2014), which works with glutathione (GSH), peroxiredoxin and other molecules to maintain the redox balance in the cell, protecting cells from oxidative stress (Förstermann 2008). It can also regulate the expression of a variety of genes and induce the production of multiple enzymes with biological activity (Dunn et al. 2010). However, the association between edaravone and TRX in high-glucose induced cell injury has not been studied yet.
Early post-marketing experience with edaravone in an unselected group of patients with ALS
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2019
Alon Abraham, Beatrice Nefussy, Yaara Fainmesser, Yoram Ebrahimi, Arnon Karni, Vivian E. Drory
Edaravone is a neuroprotective drug with free radical scavenger properties, which has been approved for the treatment of ALS in Japan and Korea in 2015, and for all ALS patients by the United States Food and Drug Administration (FDA) in May 2017. Treatment with edaravone has shown a slower rate of progression of ALS in a phase III trial in a subgroup of patients, showing a lower rate of decline of the ALS Functional rating scale (ALSFRS-R) score by approximately 33% (1). Study inclusion criteria were based on a post hoc analysis of a previous study (2), and were restricted to independent ALS patients with a disease duration of less than 2 years, score for each item of ALSFRS-R ≥ 2 points, and forced vital capacity (FVC) ≥80%. However, it has been estimated that less than 7% of ALS patients seen in ALS clinics fulfill these stringent criteria (3). Following the FDA approval, many ALS patients worldwide chose to be treated with edaravone, irrespective of their fulfilling of the original clinical trial criteria. In the current study, we aimed to explore retrospectively the efficacy of edaravone in unselected ALS patients treated at our clinic, without restriction for these stringent criteria.
Edaravone for the treatment of amyotrophic lateral sclerosis
Published in Expert Review of Neurotherapeutics, 2019
Free radicals are involved in the pathology of ALS.The free radical scavenger edaravone reduces the level of 3-nitrotyrosine, a marker of free radical peroxynitrate reactions, in the cerebrospinal fluid of ALS patients.Edaravone is the first drug for which inhibition of motor function deterioration in ALS patients has been demonstrated.The success of the second phase 3 trial (MCI186-19 study) was determined based on post hoc analyses of the first phase 3 study (MCI186-16 study) and an extended double-blind study (MCI186-17 study).An early initiation of edaravone treatment is recommended as soon as ALS is diagnosed.Further study is necessary to determine whether edaravone can extend the lifespan of ALS patients.Although edaravone is considered to be a safe drug, respiratory symptoms should be monitored when breathing capacity begins to decrease.
Related Knowledge Centers
- Glucuronide
- Oxidative Stress
- Medication
- Als
- Intravenous Therapy
- Oral Administration
- First-In-Class Medication