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Idebenone ROS chemical

Cat.No.S2605

Idebenone (CV-2619) is a synthetic analog of coenzyme Q10 (CoQ10) and a brain stimulant. This compound is known for its neuroprotective properties and is often used in research related to mitochondrial diseases. It has also been studied for its potential benefits in treating cognitive decline.
Idebenone ROS chemical Chemical Structure

Chemical Structure

Molecular Weight: 338.44

Quality Control

Chemical Information, Storage & Stability

Molecular Weight 338.44 Formula

C19H30O5

Storage (From the date of receipt)
CAS No. 58186-27-9 Download SDF Storage of Stock Solutions

Synonyms CV-2619 Smiles CC1=C(C(=O)C(=C(C1=O)OC)OC)CCCCCCCCCCO

Solubility

In vitro
Batch:

DMSO : 68 mg/mL (200.92 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 68 mg/mL

Water : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
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In vivo Formulation Calculator (Clear solution)

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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Mechanism of Action

In vitro
Idebenone effectively protects from retinal cell injury after oxidative stress or hypoglycemia, whereas the protection afforded after postincubation of both antioxidants is decreased. This compound attenuates delayed retinal cell damage, mediated by chemical ischemia. [1] This chemical, a centrally active antioxidant used to treat multiinfarct dementia, protects cells from this form of glutamate-induced cytotoxicity in vitro. It provides significant protection against the neuronal degeneration induced by intrastriatal injection of kainic acid and quisqualic acid, but not the NMDA receptor agonist, quinolinic acid. [2]
In vivo
Idebenone prevents the behavioural deficits in Y-maze and water maze, but not passive avoidance, tasks in A beta-(1-42)-infused rats when they are repeatedly administered by mouth once a day from 3 days before the start of A beta infusion to the end of behavioural experiments. [3] This compound (100 and 300 mg/kg) is orally administered to rats for 3 days, it increases the state 3 respiration stimulated by ADP, slightly decreasez the state 4 respiration after the consumption of ADP and resultz in a significant increase of the respiratory control index (RCI) by 14-19% for glutamate oxidation and 10-17% for succinate oxidation, respectively. It significantly suppresses by about 10% the non-respiratory oxygen consumption, which closely associated with non-enzymatic reactions such as lipid peroxidation, membrane lysis and swelling of mitochondria. [4]
References

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01303406 Completed
Friedreich''s Ataxia
Santhera Pharmaceuticals
April 2011 Phase 3
NCT00758225 Completed
Duchenne Muscular Dystrophy
Santhera Pharmaceuticals
September 2008 Phase 2
NCT00747487 Completed
Leber''s Hereditary Optic Neuropathy
Santhera Pharmaceuticals
November 2007 Phase 2
NCT00229632 Completed
Friedreich Ataxia
National Institute of Neurological Disorders and Stroke (NINDS)|National Institutes of Health Clinical Center (CC)
September 27 2005 Phase 2

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