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Spinal Cord Disease
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, 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.
Pharmacological Management of Amyotrophic Lateral Sclerosis
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Shalini Mani, Chahat Kubba, Tanya Sharma, Manisha Singh
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.
Micronutrients in Improvement of the Standard Therapy in Traumatic Brain Injury
Published in Kedar N. Prasad, 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.
Isolated pulmonary recovery in a veteran with late stage bulbar ALS following edaravone treatment and cessation
Published in The Journal of Spinal Cord Medicine, 2022
Susama Verma, Jungjae Lim, Teaghen Buscemi-Kimmins, Steven W. Brose
As he was interested in edaravone, a newly FDA approved treatment for ALS at the time, neurology consult was obtained and infusions were initiated three months following admission to the center. He was the first veteran at the SCI/D center to be started on this medication to slow the advancement of ALS. His initial forced vital capacity (FVC) was 1.77 L. The veteran was provided with aggressive noninvasive pulmonary management including incentive spirometry, a vibratory expiratory device for secretion clearance (acapella), assisted quad cough, a high frequency chest wall oscillation device (VEST), as well as positive and negative pressure noninvasive ventilation (cough assist). Despite these measures, which were continued throughout the admission, the veteran suffered pulmonary and multisystem decline, as detailed in Table 1. He completed four full cycles of edaravone until he was no longer considered a candidate to continue the medication due to functional decline. Each edaravone cycle consisted of 60 mg administered intravenously daily within 14 days, and was followed by a 14-day drug-free period.
Pharmacological management of cerebral ischemia in the elderly
Published in Expert Opinion on Pharmacotherapy, 2021
Adithya Kannan, Mychael Delgardo, William Pennington-FitzGerald, Enoch X. Jiang, Brandon R. Christophe, E Sander Connolly
Edaravone is a synthetic antioxidant compound that was approved in 2001 as an option for the treatment of AIS in Japan, but is currently not approved for use in the US. Edaravone freely crosses the blood brain barrier and is thought to function primarily by scavenging free radicals, thereby inhibiting the inflammatory responses of endothelial cells and neurons in the wake of ischemia [48]. Edaravone may also function by reducing long term inflammation, vascular endothelial cell damage, and preventing neuronal cell death [49]. In a randomized clinical trial that enrolled 250 patients, a 14-day course of edaravone administered within 72 hours of stroke onset was associated with a significant improvement in mRS scores compared to placebo [48]. This effect persisted through a 12-month follow-up period. The study suffered from a relatively small sample size and a wide window in which treatment could be administered, but subsequent small trials of edaravone have replicated these results.
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.