NDB is a selective human FXRα (hFXRα) antagonist that is effective in modulating transcription of FXRα downstream genes. NDB can be used in anti-diabetes research[1].
NDB induces rearrangements of helix 11 (H11) and helix 12 (H12, AF-2) by forming a homodimer of hFXRα-LBD, totally different from the active conformation in monomer state[1].
NDB (25 μM) effectively antagonizes the GW4064-stimulated FXR/RXR interaction and FXRα target gene expression in primary mouse hepatocytes, including the small heterodimer partner (SHP) and bile-salt export pump (BSEP)[1].
NDB (24 mg/kg; intraperitoneal injection; once a day; for 4 weeks) efficiently decreases the gene expressions of phosphoenolpyruvate carboxykinase (PEPCK), glucose 6-phosphatase (G6-pase), small heterodimer partner, and BSEP in db/db mice[1].
| Animal Model: | Male C57BL/6J db/db mice (8 weeks of age)[1] |
| Dosage: | 24 mg/kg |
| Administration: | Intraperitoneal injection; once a day; for 4 weeks |
| Result: | Decreased the gene expressions of PEPCK, G6-pase, small heterodimer partner, and BSEP. |
[1]. Xing Xu, et al. Structural Basis for Small Molecule NDB (N-Benzyl-N-(3-(tert-butyl)-4-droxyphenyl)-2,6-dichloro-4-(dimetlamino) Benzamide) as a Selective Antagonist of Farnesoid X Receptor α (FXRα) in Stabilizing the Homodimerization of the Receptor.