Home Metabolism Retinoid Receptor inhibitor AR7

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AR7 Retinoid Receptor inhibitor

Cat.No.S6605

AR7 is a retinoic acid receptor α (RARα) antagonist. This compound is a potent and selective inhibitor of RARα, demonstrating high affinity and specificity for this receptor subtype. It effectively blocks the binding of retinoic acid to RARα, thereby inhibiting downstream signaling pathways. In cellular assays, this chemical has been shown to suppress the proliferation of various cancer cell lines that are dependent on RARα signaling. Additionally, it induces apoptosis in these cells, highlighting its potential as a therapeutic agent. The pharmacological profile of this antagonist supports its use in studying RARα-mediated processes and in developing treatments for related diseases.
AR7 Retinoid Receptor inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 257.71

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Quality Control

Batch: S660501 DMSO]4 mg/mL]false]Water]Insoluble]false]Ethanol]Insoluble]false Purity: 99.87%
99.87

Solubility

In vitro
Batch:

DMSO : 4 mg/mL (15.52 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : Insoluble

Ethanol : Insoluble

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In vivo
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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 257.71 Formula

C15H12ClNO

 Storage (From the date of receipt) 3 years -20°C powder
CAS No. 80306-38-3 -- Storage of Stock Solutions

Synonyms N/A Smiles CC1=CC=C(C=C1)C2=NC3=C(C=C(C=C3)Cl)OC2

Mechanism of Action

In vitro

AR7 significantly activates CMA activity in mouse fibroblasts. A marked increase in CMA-activating potency is found when this compound and GR1 are combined, supporting their cooperative effect. Treatment with the transcriptional repressor Actinomycin D partially reduces the stimulatory effect of this chemical on CMA, consistent with transcriptional changes contributing to the upregulation of CMA.
In vivo

Reactivation of CMA by treatment with AR7 inhibits diclofenac-induced lipid accumulation and hepatotoxicity.

References

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