Fig. 1: Pharmacological profiling of niacin, acipimox, and MMF on GPR109A.
a Diagrammatic illustration of GPR109A activation and downstream signaling outcomes (created with BioRender.com). b Chemical structures of niacin, acipimox, and MMF. c, d NanoBiT-based heterotrimeric GoA/GoB dissociation assay in response to acipimox and MMF with niacin as a reference ligand, (mean ± SEM; n = 3–4 independent experiments, i.e., for GoA dissociation with acipimox: n = 4, for GoA dissociation with MMF: n = 3, for GoB dissociation in response to acipimox and MMF: n = 4; fold normalized with the minimum concentration for each ligand as 1). e Acipimox and MMF stimulated decrease in forskolin-induced cAMP level measured by GloSensor assay (mean ± SEM; n = 3–4 independent experiments, i.e, for acipimox induced response: n = 3 and for MMF induced response: n = 4; % normalized with the minimum concentration for each ligand as 100). f, g NanoBiT-based βarr1/2 recruitment in response to acipimox and MMF (mean ± SEM; n = 4–5 independent experiments, i.e., for βarr1 recruitment: n = 4, for βarr2 recruitment in response to acipimox: n = 5 and in response to MMF: n = 4; fold normalized with the minimum concentration for each ligand as 1). Source data is provided as Source Data file.
