Home
Drugs
Targets
Pathways
Ontologies
Cyp450s
Adv.search
Help/FAQ

Drug-Target Interaction

Drug

show drug details
PubChem ID:31401
Structure:
Synonyms:
(3alpha,5beta,7beta)-3,7-dihydroxycholan-24-oic acid
(3alpha,5beta,7beta,8xi)-3,7-dihydroxycholan-24-oic acid
(4R)-4-[(3R,5S,7S,8R,9S,10S,13R,14S,17R)-3,7-dihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoic acid
128-13-2
17-beta-(1-Methyl-3-carboxypropyl)etiocholane-3-alpha,7-beta-diol
3 alpha,7 beta-Dihydroxy-5 beta-cholan-24-oic Acid
3,7-Dihydroxycholan-24-oic acid
3-alpha,7-beta-Dihydroxy-5-beta-cholanoic acid
3-alpha,7-beta-Dihydroxycholanic acid
3-alpha,7-beta-Dioxycholanic acid
3alpha,7beta-Dihydroxy-5beta-cholan-24-oic acid
4-10-00-01604 (Beilstein Handbook Reference)
5-beta-Cholan-24-oic acid, 3-alpha,7-beta-dihydroxy-
50809-41-1
5beta-Cholan-24-oic acid-3alpha,7beta-diol
7-beta-Hydroxylithocholic acid
7beta-Hydroxylithocholic acid
80225-86-1
AB00513977
Acide ursodesoxycholique [INN-French]
Acido ursodeossicolico [Italian]
Acido ursodeoxicolico [INN-Spanish]
Acidum ursodeoxycholicum [INN-Latin]
Actigall
Actigall (TN)
Antigall
Arsacol
BPBio1_001052
BRN 3219888
BSPBio_000956
C07880
C24H40O4
CCRIS 5502
CHEBI:9907
Chenodeoxycholic acid
Cholan-24-oic acid, 3,7-dihydroxy-, (3-alpha,5-beta,7-beta)-
Cholan-24-oic acid, 3,7-dihydroxy-, (3-alpha,5-beta,7-beta)- (9CI)
Cholan-24-oic acid, 3,7-dihydroxy-, (3alpha,5beta,7beta)-
Cholit-ursan
D00734
DB01586
Delursan
Deoxyursocholic Acid
Destolit
Deursil
Dom-ursodiol c
EINECS 204-879-3
ISO-URSODEOXYCHOLIC ACID
IU5
Litursol
LMST04010033
LS-53033
Lyeton
MLS000028461
MLS001066373
NCGC00179363-01
NCI60_028904
NSC 657950
NSC 683769
Peptarom
PHL-ursodiol c
PMS-ursodiol c
Prestwick0_000958
Prestwick1_000958
Prestwick2_000958
Prestwick3_000958
SMP2_000012
SMR000058403
Sodium Ursodeoxycholate
Solutrat
SPBio_003105
U-9000
U5127_SIGMA
UDCA
UDCS
Urosiol
Ursacholic Acid
Ursacol
UrSO
Urso (TN)
Urso 250
Urso DS
Urso Forte
Ursobilin
Ursochol
Ursocholic acid, deoxy-
Ursodamor
ursodeoxycholate
Ursodeoxycholic acid
Ursodeoxycholic acid (JP15/INN)
Ursodeoxycholic acid, UDCA, Ursosan, Ursofalk, Urso Forte, Udiliv,
Ursodesoxycholic acid
Ursodiol
Ursodiol (USP)
Ursodiol [USAN]
Ursofalk
Ursolvan
Ursosan
ATC-Codes:

Target

show target details
Uniprot ID:MK01_HUMAN
Synonyms:
ERK-2
ERT1
Extracellular signal-regulated kinase 2
MAP kinase 2
MAPK 2
Mitogen-activated protein kinase 1
Mitogen-activated protein kinase 2
p42-MAPK
EC-Numbers:2.7.11.24
Organism:Homo sapiens
Human
PDB IDs:1PME 1TVO 1WZY 2E14 2OJG 2OJI 2OJJ 3D42 3D44
Structure:
3D44

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

19085950
Bile acids activate fibroblast growth factor 19 signaling in human hepatocytes to inhibit cholesterol 7alpha-hydroxylase gene expression.. Kwang-Hoon Song; Tiangang Li; Erika Owsley; Stephen Strom; John Y L Chiang (2009) Hepatology (Baltimore, Md.) display abstract
Mouse fibroblast growth factor 15 (FGF15) and human ortholog FGF19 have been identified as the bile acid-induced intestinal factors that mediate bile acid feedback inhibition of cholesterol 7alpha-hydroxylase gene (C YP7A1) transcription in mouse liver. The mechanism underlying FGF15/FGF19 inhibition of bile acid synthesis in hepatocytes remains unclear. Chenodeoxycholic acid (CDCA) and the farnesoid X receptor (FXR)-specific agonist GW4064 strongly induced FGF19 but inhibited CYP7A1 messenger RNA (mRNA) levels in primary human hepatocytes. FGF19 strongly and rapidly repressed CYP7A1 but not small heterodimer partner (SHP) mRNA levels. Kinase inhibition and phosphorylation assays revealed that the mitogen-activated protein kinase/extracellular signal-regulated kinase 1/2 (MAPK/Erk1/2) pathway played a major role in mediating FGF19 inhibition of CYP7A1. However, small interfering RNA (siRNA) knockdown of SHP did not affect FGF19 inhibition of CYP7A1. Interestingly, CDCA stimulated tyrosine phosphorylation of the FGF receptor 4 (FGFR4) in hepatocytes. FGF19 antibody and siRNA specific to FGFR4 abrogated GW4064 inhibition of CYP7A1. These results suggest that bile acid-activated FXR is able to induce FGF19 in hepatocytes to inhibit CYP7A1 by an autocrine/paracrine mechanism. Conclusion: The hepatic FGF19/FGFR4/Erk1/2 pathway may inhibit CYP7A1 independent of SHP. In addition to inducing FGF19 in the intestine, bile acids in hepatocytes may activate the liver FGF19/FGFR4 signaling pathway to inhibit bile acid synthesis and prevent accumulation of toxic bile acid in human livers.