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it was found that these mice experienced a reduction of 36% and 41% in total cholesterol and LDL cholesterol upon activation of the Rev-erb.
showed significant reduction in total cholesterol (36%), LDL-C (41%) and triglycerides (40%) in response to SR9009 treatment. HDL-C levels were not affected by SR9009
SR9009 treatment of bone marrow-derived mouse macrophages (BMDM) reduced the polarization of BMDMs to pro-inflammatory M1 macrophage while increasing the polarization of BMDMs to anti-inflammatory M2 macrophages
SR9009 prevents cardiomyocyte hypertrophy, reduces fibrosis, and halts heart failure progression in mice
In mice with pressure-induced cardiac hypertrophy caused by transverse aortic constriction, SR9009 lowered protein kinase B (AKT) expression and reduced cardiac hypertrophy
REV-ERBα activation by SR9009 inhibits transcription of inflammatory factors IL-1β, IL-6, MMP-9, and Ccl2 in astrocytes. SR9009 significantly attenuates hepatic damage and inflammatory responses, it is effective in suppressing clinical markers of liver damage, circulating lipids, hepatic fibrosis, and markers of inflammation
REV-ERBα overexpression partially or totally blunted dexamethasone-mediated induction of the catabolic (Atrogin, Murf1, Foxo1 and Foxo3a) and anti-anabolic (Klf15, Redd1 and Bcat2) genes
REV-ERBs are potently anticarcinogenic.
decreased REV-ERBα expression was associated with poor prognosis
The treatment with the small-molecule agonists of REV-ERBs SR9011 and SR9009 led to a reduction in the GSC proliferation rate