Chemistry:GSK-4112
From HandWiki
Short description: Chemical compound
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| Formula | C18H21ClN2O4S |
| Molar mass | 396.89 g·mol−1 |
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GSK-4112 is an experimental drug that was developed by GlaxoSmithKline as an agonist of Rev-ErbAα.[1] It is used for studying regulation of the circadian rhythm and its influence on diverse processes such as adipogenesis,[2][3] regulation of bone density,[4] and inflammation.[5][6][7][8]
See also
References
- ↑ "GSK4112, a small molecule chemical probe for the cell biology of the nuclear heme receptor Rev-erbα". ACS Chemical Biology 5 (10): 925–32. October 2010. doi:10.1021/cb100141y. PMID 20677822.
- ↑ "A role for rev-erbα ligands in regulation of adipogenesis". Current Pharmaceutical Design 17 (4): 320–4. 2011. doi:10.2174/138161211795164211. PMID 21375499.
- ↑ "Rev-erbα Inhibits Proliferation and Promotes Apoptosis of Preadipocytes through the Agonist GSK4112". International Journal of Molecular Sciences 20 (18): 4524. September 2019. doi:10.3390/ijms20184524. PMID 31547330.
- ↑ "Rev-erbα Negatively Regulates Osteoclast and Osteoblast Differentiation through p38 MAPK Signaling Pathway". Molecules and Cells 43 (1): 34–47. January 2020. doi:10.14348/molcells.2019.0232. PMID 31896234.
- ↑ "A circadian clock gene, Rev-erbα, modulates the inflammatory function of macrophages through the negative regulation of Ccl2 expression". Journal of Immunology 192 (1): 407–17. January 2014. doi:10.4049/jimmunol.1301982. PMID 24307731.
- ↑ "The nuclear receptor and clock gene REV-ERBα regulates cigarette smoke-induced lung inflammation". Biochemical and Biophysical Research Communications 493 (4): 1390–1395. December 2017. doi:10.1016/j.bbrc.2017.09.157. PMID 28974420.
- ↑ "Pharmacological activation of REV-ERBα represses LPS-induced microglial activation through the NF-κB pathway". Acta Pharmacologica Sinica 40 (1): 26–34. January 2019. doi:10.1038/s41401-018-0064-0. PMID 29950615.
- ↑ "Stimulation of nuclear receptor REV-ERBs suppresses production of pronociceptive molecules in cultured spinal astrocytes and ameliorates mechanical hypersensitivity of inflammatory and neuropathic pain of mice". Brain, Behavior, and Immunity 78: 116–130. May 2019. doi:10.1016/j.bbi.2019.01.014. PMID 30682503. http://ir.lib.hiroshima-u.ac.jp/files/public/4/48640/20200219135443391439/BrainBehavImmun_78_116.pdf.
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