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Azoramide PERK modulator

Cat.No.S8304

Azoramide is a small-molecule modulator of the unfolded protein response (UPR). It improves ER protein-folding ability and activates ER chaperone capacity to protect cells against ER stress.
Azoramide PERK modulator Chemical Structure

Chemical Structure

Molecular Weight: 308.83

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Quality Control

Batch: S830401 DMSO]61 mg/mL]false]Ethanol]61 mg/mL]false]Water]Insoluble]false Purity: 99.59%
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  • NMR
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99.59

Solubility

In vitro
Batch:

DMSO : 61 mg/mL (197.51 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 61 mg/mL

Water : 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 308.83 Formula

C15H17ClN2OS

 Storage (From the date of receipt)
CAS No. 932986-18-0 Download SDF Storage of Stock Solutions

Synonyms N/A Smiles CCCC(=O)NCCC1=CSC(=N1)C2=CC=C(C=C2)Cl

Mechanism of Action

Targets/IC50/Ki
UPR
In vitro
Azoramide may have the protective effects of enhancing chaperone expression and reducing protein synthesis without inducing cytotoxicity and apoptosis. This compound may require the presence of intact IRE1 and PERK branches of the UPR to fully increase chaperone capacity. It is found to be a kind of compound with the dual property of not only boosting ER folding acutely but also activating ER chaperone capacity chronically to promote ER homeostasis. Its treatment potently protects cells against chemically-induced ER stress conditions. This chemical preserves beta cell function and survival during metabolic ER stress. Its pretreatment does not impair ER function as part of its initial action. This treatment leads to increased SERCA expression, resulting in enhanced retention of Ca+2 within the ER. It interacts with UPR pathways to promote resolution of ER stress and improve ER function.
In vivo
Azoramide improves glucose homeostasis in mice with genetic obesity and diet-induced obesity. Remarkably, this compound treatment significantly improves insulin sensitivity and glucose tolerance and beta cell function in obese mice in multiple preclinical models.
References

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