GSK1362 

GSK1362 is a selective inverse agonist of REV-ERB. GSK1362disrupts the interaction of REV-ERBα with repressive co-modulators (NCoR1, SMRT2, RIP140). GSK1362 exerts an inverse agonist effect by increasing the transcription of BMAL1 to relieve BMAL1 repression by endogenous REV-ERB ligands. GSK1362 suppresses LPS (HY-D1056)-induced inflammatory cytokine expression, inhibits IL-1β-induced Cxcl5 transcription in cells. GSK1362 can be used for the study of inflammatory diseases^[1].

GSK1362 (24 h) increases transcription in a concentration-dependent manner in HEK293 cells cotransfected with HA-Rev-Erbα and Bmal1-Luc reporter, exerting an inverse agonist effect to relieve BMAL1 repression by endogenous REV-ERB ligands like heme^[1].
GSK1362 (10 μM, 4 h) inhibits LPS (HY-D1056)-induced production of several inflammatory cytokines in alveolar macrophages collected at ZT8^[1].
GSK1362 (10 μM, 16 h) inhibits the induction of Cxcl5 transcription in serum shock-synchronized mouse LA-4 cells^[1].
GSK1362 (10 μM, 4 h) significantly increases REV-ERBα protein abundance in serum shock-synchronized human primary bronchial epithelial (NHBE) cells^[1].
GSK1362 (10 μM, pretreated for 15 min) stabilizes REV-ERBα protein and counteracts IL-1β-induced REV-ERBα protein degradation in serum shock-synchronized NHBE cells^[1].
GSK1362 (10 μM, 4 h) blocks IL-1β or TNF-α-induced ubiquitination of REV-ERBα in HEK293T cells transfected with HA-Rev-Erbα, His-Ub and SENP-1 plasmids^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

396.87

C₂₁H₂₁ClN₄O₂

2986733-57-5

N#CC1=C(NCCOC)OC(C2=CC=C(N(CC3=CC=C(C=C3)Cl)C)C=C2)=N1

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• [1]. Pariollaud M, et al. Circadian clock component REV-ERBα controls homeostatic regulation of pulmonary inflammation. J Clin Invest. 2018 Jun 1;128(6):2281-2296.