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Aminoguanidine hydrochloride NOS inhibitor

Cat.No.S4548

Aminoguanidine (Pimagedine, Guanyl hydrazine, Hydrazinecarboximidamide, Imino semicarbazide, Monoaminoguanidine) is a diamine oxidase and nitric oxide synthase inhibitor. It acts to reduce levels of advanced glycation end products (AGEs) through interacting with 3-deoxyglucosone.
Aminoguanidine hydrochloride NOS inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 110.55

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Quality Control

Batch: S454801 DMSO]22 mg/mL]false]Water]22 mg/mL]false]Ethanol]Insoluble]false Purity: 98.19%
98.19

Solubility

In vitro
Batch:

DMSO : 22 mg/mL (199.0 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : 22 mg/mL

Ethanol : Insoluble

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In vivo
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

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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Chemical Information, Storage & Stability

Molecular Weight 110.55 Formula

CH6N4.HCl

Storage (From the date of receipt)
CAS No. 1937-19-5 Download SDF Storage of Stock Solutions

Synonyms Pimagedine, Guanyl hydrazine, Hydrazinecarboximidamide, Imino semicarbazide, Monoaminoguanidine Smiles C(=NN)(N)N.Cl

Mechanism of Action

Targets/IC50/Ki
Diamine oxidase
NOS
advanced glycation end products (AGE)
In vivo
Aminoguanidine ameliorates neonatal hypoxic-ischemic brain damage and that temporal profiles of NO correlated with the neuroprotective effect of aminoguanidine. Neuroprotection by AG is attributable to suppression of NO produced by iNOS after the end of the hypoxic period, during the reoxygenation phase. The half-life of AG is estimated to be between 6 and 8 h in vivo and approximately 4.4 h in human with normal renal function.AG is also an inhibitor of the formation of advanced glycation end products. Systematically administered advanced glycation end product–modified BSA increases cerebral infarct size in an adult rat, which is attenuated by AG.
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