Skip to search form
Skip to main content
Skip to account menu
Semantic Scholar
Semantic Scholar's Logo
Search 209,973,645 papers from all fields of science
Search
Sign In
Create Free Account
INT 747
Known as:
INT-747
, INT747
National Institutes of Health
Create Alert
Alert
Related topics
Related topics
1 relation
Broader (1)
obeticholic acid
Papers overview
Semantic Scholar uses AI to extract papers important to this topic.
Highly Cited
2015
Highly Cited
2015
The FXR agonist obeticholic acid prevents gut barrier dysfunction and bacterial translocation in cholestatic rats.
L. Verbeke
,
R. Farré
,
+12 authors
W. Laleman
American Journal of Pathology
2015
Corpus ID: 25158244
Highly Cited
2014
Highly Cited
2014
Obeticholic acid, a farnesoid X receptor agonist, improves portal hypertension by two distinct pathways in cirrhotic rats
L. Verbeke
,
R. Farré
,
+8 authors
W. Laleman
Hepatology
2014
Corpus ID: 205891475
The farnesoid X receptor (FXR) is a nuclear bile acid receptor involved in bile acid homeostasis, hepatic and intestinal…
Expand
Highly Cited
2012
Highly Cited
2012
Testosterone protects from metabolic syndrome-associated prostate inflammation: an experimental study in rabbit.
L. Vignozzi
,
A. Morelli
,
+12 authors
M. Maggi
Journal of Endocrinology
2012
Corpus ID: 23004966
Metabolic syndrome (MetS) and benign prostatic hyperplasia (BPH)/lower urinary tract symptoms (LUTS) are often associated. One of…
Expand
Highly Cited
2011
Highly Cited
2011
Farnesoid X receptor activation inhibits inflammation and preserves the intestinal barrier in inflammatory bowel disease
R. Gadaleta
,
K. V. van Erpecum
,
+12 authors
S. V. Mil
Gut
2011
Corpus ID: 23372105
Background & aims Inflammatory bowel disease (IBD) is characterised by chronic intestinal inflammation, resulting from…
Expand
Review
2011
Review
2011
Non-Alcoholic Fatty Liver Disease: The Bile Acid-Activated Farnesoid X Receptor as an Emerging Treatment Target
M. Fuchs
Journal of Lipids
2011
Corpus ID: 18711040
Non-alcoholic fatty liver disease (NAFLD) is currently evolving as the most common liver disease worldwide. It may progress to…
Expand
2011
2011
FXR activation inhibits inflammation and preserves the intestinal barrier in IBD
M. Wildenberg
,
G. R. van den Brink
Gut
2011
Corpus ID: 206952633
Bile salts are produced in the liver and delivered to the duodenum, where they emulsify lipids to facilitate absorption. After…
Expand
Highly Cited
2010
Highly Cited
2010
Functional Characterization of the Semisynthetic Bile Acid Derivative INT-767, a Dual Farnesoid X Receptor and TGR5 Agonist
G. Rizzo
,
D. Passeri
,
+10 authors
L. Adorini
Molecular Pharmacology
2010
Corpus ID: 16576832
Two dedicated receptors for bile acids (BAs) have been identified, the nuclear hormone receptor farnesoid X receptor (FXR) and…
Expand
Highly Cited
2009
Highly Cited
2009
The Bile Acid Receptor FXR Is a Modulator of Intestinal Innate Immunity1
P. Vavassori
,
A. Mencarelli
,
B. Renga
,
E. Distrutti
,
S. Fiorucci
Journal of Immunology
2009
Corpus ID: 1088223
The farnesoid X receptor (FXR) is a bile acid-regulated nuclear receptor expressed in enterohepatic tissues. In this study we…
Expand
Highly Cited
2009
Highly Cited
2009
Antiatherosclerotic effect of farnesoid X receptor.
A. Mencarelli
,
B. Renga
,
E. Distrutti
,
S. Fiorucci
American Journal of Physiology. Heart and…
2009
Corpus ID: 23678290
The farnesoid X receptor (FXR) is a member of the nuclear receptor superfamily that functions as an endogenous sensor for bile…
Expand
Highly Cited
2005
Highly Cited
2005
Protective Effects of 6-Ethyl Chenodeoxycholic Acid, a Farnesoid X Receptor Ligand, in Estrogen-Induced Cholestasis
S. Fiorucci
,
C. Clerici
,
+10 authors
A. Morelli
Journal of Pharmacology and Experimental…
2005
Corpus ID: 13019062
The farnesoid X receptor (FXR), an endogenous sensor for bile acids, regulates a program of genes involved in bile acid…
Expand
By clicking accept or continuing to use the site, you agree to the terms outlined in our
Privacy Policy
(opens in a new tab)
,
Terms of Service
(opens in a new tab)
, and
Dataset License
(opens in a new tab)
ACCEPT & CONTINUE