Dehydrolithocholic acid is a major metabolite of lithocholic acid .[1] It is formed from LCA by the cytochrome P450 (CYP) isoform CYP3A4. Dehydrolithocholic acid is an agonist of G protein-coupled bile acid activated receptor 1 (GP-BAR1/TGR5; EC50 = 0.27 μM), vitamin D receptor (VDR; EC50 = 3 μM), and farnesoid X receptor (FXR) in cell-based reporter assays.[2],[3] It also binds to the human pregnane X receptor (PXR; IC50 = 15 μM) and activates mouse and human PXRs in cell-based reporter assays when used at a concentration of 100 μM.[4] Dehydrolithocholic acid binds to retinoic acid receptor-related orphan receptor γt (RORγt; Kd = 1.13 μM for the recombinant human ligand-binding domain) and decreases its activity in a cell-based reporter assay when used at a concentration of 10 μM.[5] It inhibits the differentiation of T helper cells that express IL-17a (TH17 cells) when used at a concentration of 20 μM.

Reference:
[1].Deo, A.K., and Bandiera, S.M.3-Ketocholanoic acid is the major in vitro human hepatic microsomal metabolite of lithocholic acidDrug Metab. Dispos.37(9)1938-1947(2009)
[2].Sato, H., Macchiarulo, A., Thomas, C., et al.Novel potent and selective bile acid derivatives as TGR5 agonists: Biological screening, structure-activity relationships, and molecular modeling studiesJ. Med. Chem.51(6)1831-1841(2008)
[3].Makishima, M., Lu, T.T., Xie, W., et al.Vitamin D receptor as an intestinal bile acid sensorScience296(5571)1313-1316(2002)
[4].Staudinger, J.L., Goodwin, B., Jones, S.A., et al.The nuclear receptor PXR is a lithocholic acid sensor that protects against liver toxicityProc. Natl. Acad. Sci. USA98(6)3369-3374(2000)
[5].Hang, S., Paik, D., Yao, L., et al.Bile acid metabolites control TH17 and Treg cell differentiationNature576(7785)143-148(2019)