Lixumistat (IM156) AMPK activator

Cat.No.S9604

Lixumistat (IM156) is a potent activator of AMPK that increases AMPK phosphorylation. It blocks oxidative phosphorylation (OXPHOS) through the inhibition of complex I and increases apoptosis. This compound ameliorates various types of fibrosis and inhibits tumors.
Lixumistat (IM156) AMPK activator Chemical Structure

Chemical Structure

Molecular Weight: 315.29

Quality Control

Batch: S960401 DMSO]63 mg/mL]false]Ethanol]20 mg/mL]false]Water]Insoluble]false Purity: 99.93%
99.93

Chemical Information, Storage & Stability

Molecular Weight 315.29 Formula

C13H16F3N5O

Storage (From the date of receipt) 3 years -20°C powder
CAS No. 1422365-93-2 -- Storage of Stock Solutions

Synonyms HL156A Smiles FC(F)(F)OC1=CC=C(NC(=N)NC(=N)N2CCCC2)C=C1

Solubility

In vitro
Batch:

DMSO : 63 mg/mL (199.81 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 20 mg/mL

Water : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

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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Mechanism of Action

Targets/IC50/Ki
AMPK [1]
OXPHOS [2]
In vitro

Lixumistat (IM156) treatment of RPMCs inhibits HG-induced myofibroblast transdifferentiation and markers of epithelial-mesenchymal transition (EMT). Moreover, this compound ameliorates HG-induced transforming growth factor-β1, Smad3, Snail, and fibronectin expression in the RPMCs via AMPK upregulation.[3] It also decreases complex I-dependent NADH oxidation in a significant, dose-dependent manner.[2]

In vivo

Treatment with Lixumistat (IM156) in vivo exacerbated the memory differentiation of virus-specific CD8+ T cells, resulting in an increase in short-lived effector cells but a decrease in memory precursor effector cells. Thus, this compound impairs the function of virus-specific memory CD8+ T cells, indicating that excessive AMPK activation weakens memory T cell differentiation, thereby suppressing recall immune responses.[1]

References

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