GSK4112

• Catalog No.: G0673
• M. F.: C18H21ClN2O4S
• M. W.: 396.88834
• Purity: ≥98% (HPLC)

SYNONYMS

• IUPAC name: tert-butyl 2-{[(4-chlorophenyl)methyl][(5-nitrothiophen-2-yl)methyl]amino}acetate
• IUPAC Traditional name: tert-butyl 2-{[(4-chlorophenyl)methyl][(5-nitrothiophen-2-yl)methyl]amino}acetate
• Synonyms: 1,1-Dimethylethyl N-[(4-chlorophenyl)methyl]-N-[(5-nitro-2-thienyl)methyl])glycinate; SR6452

DATABASE IDS

• MDL Number: MFCD12912412

PROPERTIES

• Empirical Formula (Hill Notation): C18H21ClN2O4S
• Purity: ≥98% (HPLC)
• Apperance: off-white to tan powder
• Solubility: DMSO: >20 mg/mL
• GHS Signal Word: Danger
• GHS Hazard statements: H318-H334
• European Hazard Symbols: Irritant (Xi)
• GHS Precautionary statements: P261-P280-P305 + P351 + P338-P342 + P311
• Risk Statements: 41-43
• Safety Statements: 26-36/37/39
• Storage Temperature: 2-8°C
• German water hazard class: 1

DETAILS

Description (English)

Biochem/physiol Actions
GSK4112 is a rev-erbα, (orphan nuclear receptor NR1D1) agonist, the first agent able to reset the circadian clock in a phase-dependent manner. Rev-erbα impacts the precision of the circadian clock by repressing target gene activities with the help of a nuclear receptor co-repressor complex (NCoR) and HDAC3. GSK4112 competes with heme (rev-erb′s natural ligand) and enhances co-repressor complex recruitment and thus, repression of transcription. suggests that pharmacological modulation through Rev-erb may provide new routes to treat metabolic diseases, especially disorders of adipogenesis regulated by rev-erba.1

Description (简体中文)

Biochem/physiol Actions
GSK4112 is a rev-erbα, (orphan nuclear receptor NR1D1) agonist, the first agent able to reset the circadian clock in a phase-dependent manner. Rev-erbα impacts the precision of the circadian clock by repressing target gene activities with the help of a nuclear receptor co-repressor complex (NCoR) and HDAC3. GSK4112 competes with heme (rev-erb′s natural ligand) and enhances co-repressor complex recruitment and thus, repression of transcription. suggests that pharmacological modulation through Rev-erb may provide new routes to treat metabolic diseases, especially disorders of adipogenesis regulated by rev-erba.1