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. Author manuscript; available in PMC: 2012 Mar 1.
Published in final edited form as: Mol Cell Endocrinol. 2010 Jul 6;334(1-2):39–48. doi: 10.1016/j.mce.2010.06.016

Fig. 1.

Fig. 1

Endogenous and synthetic ligands for NR1H and NR1I receptors. A. Most of the known endogenous ligands for LXR, FXR, VDR, PXR, and CAR are products formed from cholesterol, which can be converted to oxysterols, steroid hormones, bile salts, and vitamin D. B. Endogenous ligands for NR1H and NR1I receptors include: 5α-bile alcohols (planar structure, ‘ancestral’ bile salts; FXRs, PXRs), 5β-bile acids (bent structure, evolutionarily ‘recent’ bile salts; FXRs, VDRs, PXRs), calcitriol (VDRs), 5β-pregnan-3,20-dione (PXRs), 5α-androstan-3α-ol (PXRs, CARs), farnesol (FXRs), and 3-aminoethylbenzoate (frog PXRs). The bile alcohol shown is 5α-myxinol disulfate (3β,7α,16α,27-tetrahydroxy-5α-cholestan-3,27-disulfate) from the hagfish. The bile acid shown is taurochenodeoxycholic acid, a common bile acid found in teleost fish, birds, and mammals. C. Synthetic ligands for NR1H and NR1I receptors include: GW4064 (mammalian and zebrafish FXRs), fexaramine (mammalian FXRs), T-0901317 (LXRs, FXRs, PXRs), GW3965 (LXRs), and TCPOBOP (PXRs, CARs).