rev-erbβ

SR10067 is a potent, selective, and brain-penetrant agonist of Rev-Erbβ (IC50 = 160 nM) and Rev-Erbα (IC50 = 170 nM) with anxiolytic activity.

SR9011 is a REV-ERB agonist (IC50: 790 nM, REV-ERBα; IC50: 560 nM, REV-ERBβ).

SR9011 hydrochloride is a REV-ERBα/β agonist, exhibiting IC50 values of 790 nM for REV-ERBα and 560 nM for REV-ERBβ.

SR12418 is a specific synthetic ligand for REV-ERB, demonstrating binding affinity for both REV-ERBα (IC50 = 68 nM) and REV-ERBβ (IC50 = 119 nM) in TR-FRET assays. SR12418 inhibits IL-17A expression in EL4 cells and suppresses TH17 cell differentiation, making it suitable for studies on experimental autoimmune encephalomyelitis (EAE) and colitis.

BE2012 is an orally active metabolic regulator and potential anti-diabetic candidate. It effectively lowers blood glucose levels in pharmacological models of insulin resistance and type 2 diabetes by enhancing peripheral glucose uptake and significantly suppressing hepatic gluconeogenesis.

GSK1362 is a selective inverse agonist of REV-ERB. It disrupts the interaction between REV-ERBα and corepressors (NCoR1, SMRT2, RIP140). By enhancing the transcription of BMAL1, GSK1362 acts as an inverse agonist, counteracting endogenous REV-ERB ligands that inhibit BMAL1. GSK1362 suppresses the expression of inflammation factors induced by LPS and inhibits IL-1β-induced Cxcl5 transcription in cells. It is utilized in the study of inflammatory diseases.

GSK4112 (SR6452) is a Rev-erbα agonist with an EC50 of 0.4 μM and serves as a small molecule chemical probe for studying the cell biology of the nuclear heme receptor Rev-erbα.

SR 1001 is an inverse agonist for RORα/RORγ (Kis: 172/111 nM).

STL1267 is a REV-ERB agonist that can cross the blood-brain barrier and inhibits BMAL1 gene expression. It can be used to study chronic diseases and inflammatory pain.

SR8278 is an REV-ERBα antagonist(EC50 = 0.47 µM), blocking activation of the receptor by the synthetic agonist GSK 4112

SR9009 (Stenabolic), a REV-ERB agonist, increases the constitutive repression of genes regulated by REV-ERBα/ERBβ (IC50: 670/800 nM). Through activation of REV-ERB, SR9009 can decrease circadian locomotor activity during the dark phase and alter the expression pattern of core clock genes in the hypothalami of mice. The circadian pattern of expression of an array of metabolic genes in the liver, skeletal muscle, and adipose tissue was also altered in mice exposed to SR9009, resulting in increased energy expenditure. In Diet-induced obese mice, SR9009 (100 mg/kg, i.p., b.i.d., for 30 days) could decrease fat mass and markedly improve dyslipidemia and hyperglycemia.

Autophagy/REV-ERB-IN-1 is a dual inhibitor of autophagy and REV-ERB. It exhibits antitumor activity, with a CC50 value of 2.3 μM in BTB-474 cells.

Autophagy/REV-ERB-IN-1 hydrochloride (Compound 24) is a dual inhibitor of autophagy and REV-ERB with anticancer properties. It enhances the efficacy of autophagy blockade and increases cytotoxicity against cancer cells. Autophagy/REV-ERB-IN-1 (hydrochloride) is applicable in melanoma research.

ARN5187 is a lysosomal compound, REV-ERB β Ligand. ARN5187 inhibits REV-ERB-mediated transcriptional regulation and autophagy. ARN5187 shows lysosomal efficacy and cytotoxicity, and can induce apoptosis.

ARN5187 trihydrochloride is a lysosomal REV-ERBβ ligand that inhibits REV-ERB-mediated transcriptional regulation and autophagy. ARN5187 trihydrochloride has lysosomal potency and cytotoxicity and induces apoptosis.