Avizafone
Avizafone (Pro-diazepam), a pro-drug of Diazepam, is an anticonvulsant agent. Avizafone can be used as an antidote of nerve agent poisoning. In vivo, Avizafone is rapidly hydrolyzed by aminopeptidase to produce lysine and diazepam. Avizafone has research areas including neurological disease, such as epilepsy.
For research use only. We do not sell to patients.
- CAS No.: 65617-86-9
- Formula: C22H27ClN4O3
- Molecular Weight:430.93
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Guinea pigs (300-350 g)[2]
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Dosage:3.5 mg/kg
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Administration:i.m.; single dose
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Result:Reduced clinical sign severity to score 1 vs. 3 in controls, achieved 0% 24-hour mortality, prevented seizures in 0/8 animals, reduced necrosis to 3/8 animals vs. 4/4 in controls, eliminated perivascular cuffs and edema, prevented seizures in 0/8 animals vs. 4/8 with diazepam, eliminated brain lesions, and showed no significant respiratory parameter modifications.
Chemical Information
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CAS No. 65617-86-9
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Molecular Weight 430.93
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Formula C22H27ClN4O3
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SMILES
O=C(CNC([C@H](CCCCN)N)=O)N(C1=CC=C(C=C1C(C2=CC=CC=C2)=O)Cl)C
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Synonyms
Pro-diazepam
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Neurological Diseases
PINK1/Parkin-mediated mitophagy pathway is a mitochondrial quality-control signaling axis in which mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, activates Parkin recruitment and E3 ubiquitin ligase activity, promotes ubiquitination of outer mitochondrial membrane proteins, recruits selective autophagy adaptors, and drives lysosomal degradation of damaged mitochondria. In neurological disease research, this pathway is experimentally important because neurons, especially dopaminergic neurons, are highly dependent on mitochondrial integrity, and defective mitochondrial turnover can lead to mitochondrial dysfunction, oxidative stress, impaired neuronal survival, α-synuclein accumulation, and neuroinflammatory damage-associated signals. The genetic disease link is strongest in Parkinson’s disease because mutations in PRKN/parkin cause autosomal recessive juvenile parkinsonism, mutations in PINK1 cause hereditary early-onset Parkinson’s disease, and Drosophila studie
Purity & Documentation
References
[1]. Clair P, et al. Stability study of a new antidote drug combination (Atropine-HI-6-Prodiazepam) for treatment of organophosphate poisoning. Eur J Pharm Sci. 2000 Jan;9(3):259-63. [Content Brief]
[2]. Lallement G, et al. Compared efficacy of diazepam or avizafone to prevent soman-induced electroencephalographic disturbances and neuropathology in primates: relationship to plasmatic benzodiazepine pharmacokinetics. Arch Toxicol. 2000 Oct;74(8):480-6. [Content Brief]
[3]. Taysse L, et al. Protection against soman-induced neuropathology and respiratory failure: a comparison of the efficacy of diazepam and avizafone in guinea pig. Toxicology. 2006;225(1):25-35. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)