Compounds > saroglitazar
Page last updated: 2024-11-13

saroglitazar

Description

saroglitazar: a PPARalpha and PPARgamma agonist [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

saroglitazar : A monocarboxylic acid that is (2S)-2-ethoxy-3-(p-ethoxyphenyl)propanoic acid in which one of the methyl hydrogens of the p-ethoxy substituent has been replaced by the nitrogen of 2-methyl-5-[4-(methylthio)phenyl]-1H-pyrrole. An agonist at the subtypes alpha and gamma of the peroxisome proliferator-activated receptor (PPAR) with predominant PPARalpha activity, it is used in the treatment of type 2 diabetes. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID60151560
CHEMBL ID4297530
CHEBI ID134708
SCHEMBL ID16346340
MeSH IDM000594724

Synonyms (35)

Synonym
495399-09-2
saroglitazar
lipaglyn
(2s)-2-ethoxy-3-[4-(2-{2-methyl-5-[4-(methylthio)phenyl]-1h-pyrrol-1-yl}ethoxy)phenyl]propanoic acid
CHEBI:134708
saroglitazarum
S9674
unii-e0ymx3s4jd
zyh1
e0ymx3s4jd ,
saroglitazar [inn]
(2s)-2-ethoxy-3-(4-(2-(2-methyl-5-(4-(methylsulfanyl)phenyl)-1h-pyrrol-1-yl(ethoxy)phenyl)propanoic acid
benzenepropanoic acid, .alpha.-ethoxy-4-(2-(2-methyl-5-(4-(methylthio)phenyl)-1h-pyrrol-1-yl)ethoxy)-, (.alpha.s)-
saroglitazar [who-dd]
c25h29no4s
SCHEMBL16346340
CS-6149
HY-19937
DTXSID10197819
AKOS027337115
mfcd28502034
(s)-2-ethoxy-3-(4-(2-(2-methyl-5-(4-(methylthio)phenyl)-1h-pyrrol-1-yl)ethoxy)phenyl)propanoic acid
MRWFZSLZNUJVQW-DEOSSOPVSA-N
(s)-alpha-ethoxy-4-[2-[-methyl-5-[4-(methylthio) phenyl]-1h-pyrrol-1-yl]ethoxy]benzene-propanoic acid
DB13115
BCP25470
495399-09-2 (free)
EX-A7122
Q15269693
P14958
CHEMBL4297530
A913988
MS-27899
(2s)-2-ethoxy-3-[4-[2-[2-methyl-5-(4-methylsulfanylphenyl)pyrrol-1-yl]ethoxy]phenyl]propanoic acid
VUA39909

Research Excerpts

Overview

Saroglitazar is a drug for the treatment of Type II diabetes. It is a novel peroxisome proliferator-activated receptor (PPAR) agonist with dual agonistic properties (α/γ)

ExcerptReferenceRelevance
"Saroglitazar is a novel peroxisome proliferator-activated receptor (PPAR) agonist with dual agonistic properties (α/γ). "( Proof-of-concept study to evaluate the safety and efficacy of saroglitazar in patients with primary biliary cholangitis.
Bainbridge, JD; Caldwell, SH; Chalasani, NP; deLemos, AS; Goldberg, DS; Levy, C; Mena, EA; Parmar, DV; Pyrsopoulos, N; Ravinuthala, R; Rossi, S; Shaikh, F; Sheikh, A; Vuppalanchi, R, 2022)		2.4
"Saroglitazar is a novel PPAR-α/γ agonist with predominant PPAR-α activity. "( Saroglitazar suppresses the hepatocellular carcinoma induced by intraperitoneal injection of diethylnitrosamine in C57BL/6 mice fed on choline deficient, l-amino acid- defined, high-fat diet.
Bhoi, B; Giri, SR; Ingale, K; Jain, MR; Kadam, S; Nyska, A; Patel, H; Ranvir, R; Rath, A; Rathod, R; Sharma, A; Trivedi, C, 2023)		3.8
"Saroglitazar is a dual PPAR-α/γ agonist approved for the treatment of diabetic dyslipidemia. "( Effect of a Dual PPAR α/γ agonist on Insulin Sensitivity in Patients of Type 2 Diabetes with Hypertriglyceridemia- Randomized double-blind placebo-controlled trial.
Bhansali, A; Bhansali, S; Hawkins, M; Jain, N; Kaur, S; Kurpad, AV; Rastogi, A; Sharma, A, 2019)		1.96
"Saroglitazar is a novel peroxisome proliferator-activated receptor (PPAR) agonist with dual PPAR agonistic properties (α/γ)."( A Multicenter, Open-Label, Single-Arm Study to Evaluate the Efficacy and Safety of Saroglitazar in Patients With Primary Biliary Cholangitis.
González-Huezo, MS; Muñoz-Espinosa, LE; Parmar, D; Payan-Olivas, R; Pio Cruz-Lopez, JL; Shaikh, F; Vuppalanchi, R, 2021)		1.57
"Saroglitazar. Saroglitazar is a drug for the treatment of Type II diabetes."( The first approved agent in the Glitazar's Class: Saroglitazar.
Agrawal, R, 2014)		1.38
"Saroglitazar (ZYH1) is a novel peroxisome proliferator-activated receptor (PPAR) agonist with predominant PPARα and moderate PPARγ activity."( Pharmacokinetics, safety, and tolerability of saroglitazar (ZYH1), a predominantly PPARα agonist with moderate PPARγ agonist activity in healthy human subjects.
Jain, MR; Jani, RH; Kansagra, K; Patel, H, 2013)		1.37
"Saroglitazar appeared to be an effective and safe therapeutic option for improving hypertriglyceridemia in patients with T2DM."( A multicenter, prospective, randomized, double-blind study to evaluate the safety and efficacy of Saroglitazar 2 and 4 mg compared with placebo in type 2 diabetes mellitus patients having hypertriglyceridemia not controlled with atorvastatin therapy (PRES
Bhansali, A; Jani, RH; Jariwala, G; Jha, P; Joshi, S; Mukhopadhyay, S; Pai, V, 2014)		2.06
"Saroglitazar is a dual PPAR α/γ agonist approved in India for the management of diabetic dyslipidemia."( Observational study to evaluate the safety and efficacy of saroglitazar in Indian diabetic dyslipidemia patients.
Jaiswal, AD; Kumar, S; Mathur, RP; Sharma, KH; Shetty, SR, )		1.82
"Saroglitazar is a potential therapeutic option in type 2 diabetic patients with high TG levels, not controlled by statins, for comprehensive control of lipid and glycemic parameters with acceptable safety profile."( Observational study to evaluate the safety and efficacy of saroglitazar in Indian diabetic dyslipidemia patients.
Jaiswal, AD; Kumar, S; Mathur, RP; Sharma, KH; Shetty, SR, )		1.82

Treatment

Saroglitazar treatment significantly reduced the liver injury markers (serum ALT and AST), reversed hepatic steatosis and decreased the levels of pro-inflammatory cytokines like TNF-α in liver. Treatment with sarog litazar resulted in a rapid reduction of ALP concentration at Week 4 that was sustained through the study duration. Treatment also led to increase in the C-peptide (percent change: 59.42, 95% CI: 48.78, 70.06)

ExcerptReferenceRelevance
"Saroglitazar treatment significantly reduced the liver injury markers (serum ALT and AST), reversed hepatic steatosis and decreased the levels of pro-inflammatory cytokines like TNF-α in liver. "( Saroglitazar suppresses the hepatocellular carcinoma induced by intraperitoneal injection of diethylnitrosamine in C57BL/6 mice fed on choline deficient, l-amino acid- defined, high-fat diet.
Bhoi, B; Giri, SR; Ingale, K; Jain, MR; Kadam, S; Nyska, A; Patel, H; Ranvir, R; Rath, A; Rathod, R; Sharma, A; Trivedi, C, 2023)		3.8
"Saroglitazar treatment led to a reduction in MRI-PDFF from 10.3±10.5% at baseline to 8.1±7.6%."( Saroglitazar improves nonalcoholic fatty liver disease and metabolic health in liver transplant recipients.
Boyett, S; Bui, AT; Forsgren, M; Parmar, D; Patel, S; Patel, V; Sanyal, AJ; Shaikh, F; Siddiqui, MS, 2023)		3.07
"The saroglitazar treatment significantly improved postprandial TGs in people with diabetic dyslipidemia."( Abrogation of postprandial triglyceridemia with dual PPAR α/γ agonist in type 2 diabetes mellitus: a randomized, placebo-controlled study.
Bhatt, J; Dunbar, RL; Parmar, DV; Parmar, K; Rastogi, A; Thacker, HP, 2020)		1.12
"Saroglitazar treatment led to increase in the C-peptide (percent change: 59.42, 95% CI: 48.78, 70.06), fasting insulin levels (percent change: 47.10; 95% CI: 38.63, 55.57), HOMA of beta cell function for C-peptide (percent change: 71.67; 95% CI: 39.09, 104.26) and HOMA of insulin resistance for C-peptide (percent change: 58.29, 95% CI: 46.74, 69.83) at week 12 from baseline."( A Prospective, Multicentre, Open-Label Single-Arm Exploratory Study to Evaluate Efficacy and Safety of Saroglitazar on Hypertriglyceridemia in HIV Associated Lipodystrophy.
Deshpande, A; Jani, RH; Joshi, S; Toshniwal, H, 2016)		1.37
"Treatment with saroglitazar resulted in a rapid reduction of ALP concentration at Week 4 that was sustained through the study duration."( Proof-of-concept study to evaluate the safety and efficacy of saroglitazar in patients with primary biliary cholangitis.
Bainbridge, JD; Caldwell, SH; Chalasani, NP; deLemos, AS; Goldberg, DS; Levy, C; Mena, EA; Parmar, DV; Pyrsopoulos, N; Ravinuthala, R; Rossi, S; Shaikh, F; Sheikh, A; Vuppalanchi, R, 2022)		1.3
"Treatment with saroglitazar significantly improved total cholesterol (-17 mg/dL, 95% confidence interval [CI], -24 to 9; P < .001), triglyceride (-45 mg/dL, 95% CI, -60 to 31; P < .001), low-density lipoprotein cholesterol (-8 mg/dL, 95% CI, -15 to -1; P = .01), and VLDL-C (-8 mg/dL, -14 to -3; P < .001). "( Saroglitazar, a Dual PPAR α/γ Agonist, Improves Atherogenic Dyslipidemia in Patients With Non-Cirrhotic Nonalcoholic Fatty Liver Disease: A Pooled Analysis.
Cisneros, L; Duseja, A; Gawrieh, S; Momin, T; Parmar, D; Sanyal, AJ; Sarin, SK; Sheikh, F; Siddiqui, MS, 2023)		2.71
"Treatment of saroglitazar (1 and 4 mg/kg, oral) for 12 weeks significantly ameliorated retinal vascular leakage and leukostasis in the diabetic rats."( Effect of dual PPAR-α/γ agonist saroglitazar on diabetic retinopathy and oxygen-induced retinopathy.
Jain, M; Joharapurkar, A; Kshirsagar, S; Patel, MS; Patel, V; Savsani, H, 2021)		1.26
"Treatment with saroglitazar 4 mg resulted in a rapid and sustained decrease of ALP levels at week 4 (-84 ± 47 U/L, P = 0.003)."( A Multicenter, Open-Label, Single-Arm Study to Evaluate the Efficacy and Safety of Saroglitazar in Patients With Primary Biliary Cholangitis.
González-Huezo, MS; Muñoz-Espinosa, LE; Parmar, D; Payan-Olivas, R; Pio Cruz-Lopez, JL; Shaikh, F; Vuppalanchi, R, 2021)		1.19

Toxicity

Saroglitazar appeared to be an effective therapeutic option for improving hypertriglyceridemia in patients with T2DM. The drug was found to be safe and well tolerated by patients.

ExcerptReferenceRelevance
" No serious adverse events were reported."( Pharmacokinetics, safety, and tolerability of saroglitazar (ZYH1), a predominantly PPARα agonist with moderate PPARγ agonist activity in healthy human subjects.
Jain, MR; Jani, RH; Kansagra, K; Patel, H, 2013)		0.65
" Saroglitazar was found to be safe and well tolerated in this study."( Pharmacokinetics, safety, and tolerability of saroglitazar (ZYH1), a predominantly PPARα agonist with moderate PPARγ agonist activity in healthy human subjects.
Jain, MR; Jani, RH; Kansagra, K; Patel, H, 2013)		1.56
" Saroglitazar was found to be safe and well tolerated by patients."( A multicenter, prospective, randomized, double-blind study to evaluate the safety and efficacy of Saroglitazar 2 and 4 mg compared with placebo in type 2 diabetes mellitus patients having hypertriglyceridemia not controlled with atorvastatin therapy (PRES
Bhansali, A; Jani, RH; Jariwala, G; Jha, P; Joshi, S; Mukhopadhyay, S; Pai, V, 2014)		1.53
"Saroglitazar appeared to be an effective and safe therapeutic option for improving hypertriglyceridemia in patients with T2DM."( A multicenter, prospective, randomized, double-blind study to evaluate the safety and efficacy of Saroglitazar 2 and 4 mg compared with placebo in type 2 diabetes mellitus patients having hypertriglyceridemia not controlled with atorvastatin therapy (PRES
Bhansali, A; Jani, RH; Jariwala, G; Jha, P; Joshi, S; Mukhopadhyay, S; Pai, V, 2014)		2.06
" No serious adverse events, alteration in liver or renal enzymes and edema or weight gain were reported."( Observational study to evaluate the safety and efficacy of saroglitazar in Indian diabetic dyslipidemia patients.
Jaiswal, AD; Kumar, S; Mathur, RP; Sharma, KH; Shetty, SR, )		0.37
" Saroglitazar treatment was safe and well tolerated in this study."( A Prospective, Multicentre, Open-Label Single-Arm Exploratory Study to Evaluate Efficacy and Safety of Saroglitazar on Hypertriglyceridemia in HIV Associated Lipodystrophy.
Deshpande, A; Jani, RH; Joshi, S; Toshniwal, H, 2016)		1.56
" At least 1 treatment-emergent adverse event occurred in 11 (84."( Proof-of-concept study to evaluate the safety and efficacy of saroglitazar in patients with primary biliary cholangitis.
Bainbridge, JD; Caldwell, SH; Chalasani, NP; deLemos, AS; Goldberg, DS; Levy, C; Mena, EA; Parmar, DV; Pyrsopoulos, N; Ravinuthala, R; Rossi, S; Shaikh, F; Sheikh, A; Vuppalanchi, R, 2022)		0.96
" Treatment-emergent adverse events for safety were also evaluated."( Pharmacokinetics and Safety Evaluation of Single-Dose Saroglitazar Magnesium in Subjects with Hepatic Impairment.
Hayes, H; Lawitz, E; Momin, T; Parmar, D; Patel, H; Shaikh, F; Swint, K, 2023)		1.16

Pharmacokinetics

Saroglitazar was rapidly and well absorbed across all doses in the single-dose pharmacokinetic study. Food effect (high-calorie and high-fat breakfast) was examined.

ExcerptReferenceRelevance
" Food effect (high-calorie and high-fat breakfast) was examined by comparing pharmacokinetic data of saroglitazar and its metabolite saroglitazar sulfoxide in plasma samples collected pre-dose and serially up to 72 h post-dose."( Effect of Food on the Pharmacokinetics of Saroglitazar Magnesium, a Novel Dual PPARαγ Agonist, in Healthy Adult Subjects.
Gujarathi, SS; Kansagra, KA; Parikh, DP; Parmar, DV; Parmar, KV; Patel, HB; Patel, HV; Patel, JA; Patel, MR; Patil, US; Soni, MM; Srinivas, NR, 2018)		0.96
"Healthy subject pharmacokinetic data from a well-powered food-effect study (fasted vs fed treatments; n = 50) was used in this work."( Limited Sampling Strategy for Accurate Prediction of Pharmacokinetics of Saroglitazar: A 3-point Linear Regression Model Development and Successful Prediction of Human Exposure.
Joshi, SN; Parmar, DV; Srinivas, NR, 2018)		0.71

Bioavailability

ExcerptReferenceRelevance
" In vivo studies included oral bioavailability and pharmacokinetic assessment in mouse, rat and dog."( Preclinical evaluation of saroglitazar magnesium, a dual PPAR-α/γ agonist for treatment of dyslipidemia and metabolic disorders.
Giri, P; Gupta, L; Jain, MR; Modi, N; Patel, H; Patel, P; Patel, U; Shah, K; Singh, S; Srinivas, NR, 2018)		0.78

Dosage Studied

ExcerptRelevanceReference
" The pharmacokinetics of saroglitazar support a once daily dosage schedule."( Pharmacokinetics, safety, and tolerability of saroglitazar (ZYH1), a predominantly PPARα agonist with moderate PPARγ agonist activity in healthy human subjects.
Jain, MR; Jani, RH; Kansagra, K; Patel, H, 2013)		0.95
"7%) patients reported taking ursodiol at baseline and continued throughout the study with a mean daily dosage of 417 mg."( A Multicenter, Open-Label, Single-Arm Study to Evaluate the Efficacy and Safety of Saroglitazar in Patients With Primary Biliary Cholangitis.
González-Huezo, MS; Muñoz-Espinosa, LE; Parmar, D; Payan-Olivas, R; Pio Cruz-Lopez, JL; Shaikh, F; Vuppalanchi, R, 2021)		0.85
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (3)

RoleDescription
PPARgamma agonistA PPAR modulator which activates the peroxisome proliferator-activated receptor-gamma.
hypoglycemic agentA drug which lowers the blood glucose level.
PPARalpha agonistA PPAR modulator which activates the peroxisome proliferator-activated receptor-alpha.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (4)

ClassDescription
pyrrolesAn azole that includes only one N atom and no other heteroatom as a part of the aromatic skeleton.
monocarboxylic acidAn oxoacid containing a single carboxy group.
methyl sulfideAny aliphatic sulfide in which at least one of the organyl groups attached to the sulfur is a methyl group.
aromatic etherAny ether in which the oxygen is attached to at least one aryl substituent.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Research

Studies (56)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's0 (0.00)18.2507
2000's0 (0.00)29.6817
2010's26 (46.43)24.3611
2020's30 (53.57)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 69.87

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index69.87 (24.57)
Research Supply Index4.28 (2.92)
Research Growth Index4.73 (4.65)
Search Engine Demand Index117.31 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (69.87)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials12 (20.34%)5.53%
Reviews10 (16.95%)6.00%
Case Studies1 (1.69%)4.05%
Observational2 (3.39%)0.25%
Other34 (57.63%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]
SubstanceRelationship StrengthStudiesTrialsClassesRoles
choline
[no description available]		7.610cholinesallergen;
Daphnia magna metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
neurotransmitter;
nutrient;
plant metabolite;
Saccharomyces cerevisiae metabolite
palmitic acid
Palmitic Acid: A common saturated fatty acid found in fats and waxes including olive oil, palm oil, and body lipids.. hexadecanoic acid : A straight-chain, sixteen-carbon, saturated long-chain fatty acid.		2.1310long-chain fatty acid;
straight-chain saturated fatty acid		algal metabolite;
Daphnia magna metabolite;
EC 1.1.1.189 (prostaglandin-E2 9-reductase) inhibitor;
plant metabolite
berberine
[no description available]		3.0310alkaloid antibiotic;
berberine alkaloid;
botanical anti-fungal agent;
organic heteropentacyclic compound		antilipemic drug;
antineoplastic agent;
antioxidant;
EC 1.1.1.141 [15-hydroxyprostaglandin dehydrogenase (NAD(+))] inhibitor;
EC 1.1.1.21 (aldehyde reductase) inhibitor;
EC 1.13.11.52 (indoleamine 2,3-dioxygenase) inhibitor;
EC 1.21.3.3 (reticuline oxidase) inhibitor;
EC 2.1.1.116 [3'-hydroxy-N-methyl-(S)-coclaurine 4'-O-methyltransferase] inhibitor;
EC 2.1.1.122 [(S)-tetrahydroprotoberberine N-methyltransferase] inhibitor;
EC 2.7.11.10 (IkappaB kinase) inhibitor;
EC 3.1.1.4 (phospholipase A2) inhibitor;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
EC 3.1.3.48 (protein-tyrosine-phosphatase) inhibitor;
EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
geroprotector;
hypoglycemic agent;
metabolite;
potassium channel blocker
fenofibrate
Pharmavit: a polyvitamin product, comprising vitamins A, D2, B1, B2, B6, C, E, nicotinamide, & calcium pantothene; may be a promising agent for application to human populations exposed to carcinogenic and genetic hazards of ionizing radiation; RN from CHEMLINE		9.2731aromatic ether;
chlorobenzophenone;
isopropyl ester;
monochlorobenzenes		antilipemic drug;
environmental contaminant;
geroprotector;
xenobiotic
hydroxychloroquine
Hydroxychloroquine: A chemotherapeutic agent that acts against erythrocytic forms of malarial parasites. Hydroxychloroquine appears to concentrate in food vacuoles of affected protozoa. It inhibits plasmodial heme polymerase. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p970). hydroxychloroquine : An aminoquinoline that is chloroquine in which one of the N-ethyl groups is hydroxylated at position 2. An antimalarial with properties similar to chloroquine that acts against erythrocytic forms of malarial parasites, it is mainly used as the sulfate salt for the treatment of lupus erythematosus, rheumatoid arthritis, and light-sensitive skin eruptions.		3.0310aminoquinoline;
organochlorine compound;
primary alcohol;
secondary amino compound;
tertiary amino compound		anticoronaviral agent;
antimalarial;
antirheumatic drug;
dermatologic drug
metformin
Metformin: A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289). metformin : A member of the class of guanidines that is biguanide the carrying two methyl substituents at position 1.		5.2521guanidinesenvironmental contaminant;
geroprotector;
hypoglycemic agent;
xenobiotic
pioglitazone
Pioglitazone: A thiazolidinedione and PPAR GAMMA agonist that is used in the treatment of TYPE 2 DIABETES MELLITUS.. pioglitazone : A member of the class of thiazolidenediones that is 1,3-thiazolidine-2,4-dione substituted by a benzyl group at position 5 which in turn is substituted by a 2-(5-ethylpyridin-2-yl)ethoxy group at position 4 of the phenyl ring. It exhibits hypoglycemic activity.		5.3931aromatic ether;
pyridines;
thiazolidinediones		antidepressant;
cardioprotective agent;
EC 2.7.1.33 (pantothenate kinase) inhibitor;
EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
geroprotector;
hypoglycemic agent;
insulin-sensitizing drug;
PPARgamma agonist;
xenobiotic
diethylnitrosamine
Diethylnitrosamine: A nitrosamine derivative with alkylating, carcinogenic, and mutagenic properties.. N-nitrosodiethylamine : A nitrosamine that is N-ethylethanamine substituted by a nitroso group at the N-atom.		7.610nitrosaminecarcinogenic agent;
hepatotoxic agent;
mutagen
pyrroles
1H-pyrrole : A tautomer of pyrrole that has the double bonds at positions 2 and 4.. pyrrole : A five-membered monocyclic heteroarene comprising one NH and four CH units which forms the parent compound of the pyrrole group of compounds. Its five-membered ring structure has three tautomers. A 'closed class'.. azole : Any monocyclic heteroarene consisting of a five-membered ring containing nitrogen. Azoles can also contain one or more other non-carbon atoms, such as nitrogen, sulfur or oxygen.		13.524812pyrrole;
secondary amine
atorvastatin
[no description available]		8.4811aromatic amide;
dihydroxy monocarboxylic acid;
monofluorobenzenes;
pyrroles;
statin (synthetic)		environmental contaminant;
xenobiotic
glucose, (beta-d)-isomer
beta-D-glucose : D-Glucopyranose with beta configuration at the anomeric centre.. (1->4)-beta-D-glucan : A beta-D-glucan in which the glucose units are connected by (1->4) linkages.. (1->3)-beta-D-glucan : A beta-D-glucan in which the glucose units are connected by (1->3) linkages.		2.1310D-glucopyranoseepitope;
mouse metabolite
lubiprostone
[no description available]		3.710
D-fructopyranose
[no description available]		2.3110cyclic hemiketal;
D-fructose;
fructopyranose		sweetening agent
thioacetamide
Thioacetamide: A crystalline compound used as a laboratory reagent in place of HYDROGEN SULFIDE. It is a potent hepatocarcinogen.. thioacetamide : A thiocarboxamide consiting of acetamide having the oxygen replaced by sulfur.		7.2110thiocarboxamidehepatotoxic agent
dapagliflozin
[no description available]		2.1310aromatic ether;
C-glycosyl compound;
monochlorobenzenes		hypoglycemic agent;
sodium-glucose transport protein subtype 2 inhibitor
empagliflozin
[no description available]		2.1310aromatic ether;
C-glycosyl compound;
monochlorobenzenes;
tetrahydrofuryl ether		hypoglycemic agent;
sodium-glucose transport protein subtype 2 inhibitor
scopolamine hydrobromide
[no description available]		2.610
leptin
Leptin: A 16-kDa peptide hormone secreted from WHITE ADIPOCYTES. Leptin serves as a feedback signal from fat cells to the CENTRAL NERVOUS SYSTEM in regulation of food intake, energy balance, and fat storage.		7.2110
ConditionIndicatedRelationship StrengthStudiesTrials
Dyslipidemia
[description not available]		09.08152
Fatty Liver, Nonalcoholic
[description not available]		09.6211
Diabetes Mellitus, Adult-Onset
[description not available]		09.99174
Diabetes Mellitus, Type 2
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.		09.99174
Dyslipidemias
Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.		09.08152
Non-alcoholic Fatty Liver Disease
Fatty liver finding without excessive ALCOHOL CONSUMPTION.		113.95422
Biliary Cirrhosis
[description not available]		05.5421
Liver Cirrhosis, Biliary
FIBROSIS of the hepatic parenchyma due to obstruction of BILE flow (CHOLESTASIS) in the intrahepatic or extrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC; BILE DUCTS, EXTRAHEPATIC). Primary biliary cholangitis involves the destruction of small intra-hepatic bile ducts and decreased bile secretion. Secondary biliary cholangitis is produced by prolonged obstruction of large intrahepatic or extrahepatic bile ducts from a variety of causes.		17.5421
Disease Models, Animal
Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases.		03.2140
Cirrhosis, Liver
[description not available]		05.7170
Liver Cirrhosis
Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules.		17.7170
Liver Steatosis
[description not available]		03.5720
Insulin Sensitivity
[description not available]		07.2562
Fatty Liver
Lipid infiltration of the hepatic parenchymal cells resulting in a yellow-colored liver. The abnormal lipid accumulation is usually in the form of TRIGLYCERIDES, either as a single large droplet or multiple small droplets. Fatty liver is caused by an imbalance in the metabolism of FATTY ACIDS.		15.5720
Insulin Resistance
Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.		07.2562
Obesity
A status with BODY WEIGHT that is grossly above the recommended standards, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).		02.9130
Hyperlipemia
[description not available]		04.6722
Hyperlipidemias
Conditions with excess LIPIDS in the blood.		04.6722
Hypertriglyceridemia
A condition of elevated levels of TRIGLYCERIDES in the blood.		05.8254
Alloxan Diabetes
[description not available]		02.7620
Innate Inflammatory Response
[description not available]		04.0740
Inflammation
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.		04.0740
Cardiovascular Diseases
Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.		06.8261
Hepatocellular Carcinoma
[description not available]		07.610
Cancer of Liver
[description not available]		02.610
Carcinoma, Hepatocellular
A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.		02.610
Liver Neoplasms
Tumors or cancer of the LIVER.		02.610
Acute Kidney Failure
[description not available]		02.610
Acute Kidney Injury
Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.		02.610
Blood Pressure, High
[description not available]		03.5210
Hypertension
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.		03.5210
Acute Confusional Senile Dementia
[description not available]		02.610
Alzheimer Disease
A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)		02.610
Liver Dysfunction
[description not available]		02.610
Liver Diseases
Pathological processes of the LIVER.		14.610
Diabetes Mellitus
A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.		03.0840
Cirrhosis
[description not available]		02.2510
Ureteral Obstruction
Blockage in any part of the URETER causing obstruction of urine flow from the kidney to the URINARY BLADDER. The obstruction may be congenital, acquired, unilateral, bilateral, complete, partial, acute, or chronic. Depending on the degree and duration of the obstruction, clinical features vary greatly such as HYDRONEPHROSIS and obstructive nephropathy.		07.2510
Fibrosis
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.		07.2510
Kidney Diseases
Pathological processes of the KIDNEY or its component tissues.		14.2510
Cognitive Decline
[description not available]		02.3110
Diseases, Metabolic
[description not available]		02.3110
Metabolic Diseases
Generic term for diseases caused by an abnormal metabolic process. It can be congenital due to inherited enzyme abnormality (METABOLISM, INBORN ERRORS) or acquired due to disease of an endocrine organ or failure of a metabolically important organ such as the liver. (Stedman, 26th ed)		02.3110
Cognitive Dysfunction
Diminished or impaired mental and/or intellectual function.		02.3110
Hyperoxia
An abnormal increase in the amount of oxygen in the tissues and organs.		02.3110
Neovascularization, Optic Disc
[description not available]		02.3110
Diabetic Retinopathy
Disease of the RETINA as a complication of DIABETES MELLITUS. It is characterized by the progressive microvascular complications, such as ANEURYSM, interretinal EDEMA, and intraocular PATHOLOGIC NEOVASCULARIZATION.		07.3110
Retinal Neovascularization
Formation of new blood vessels originating from the retinal veins and extending along the inner (vitreal) surface of the retina.		02.3110
Hypertrophy
General increase in bulk of a part or organ due to CELL ENLARGEMENT and accumulation of FLUIDS AND SECRETIONS, not due to tumor formation, nor to an increase in the number of cells (HYPERPLASIA).		02.1710
Prediabetes
[description not available]		08.9721
Prediabetic State
The time period before the development of symptomatic diabetes. For example, certain risk factors can be observed in subjects who subsequently develop INSULIN RESISTANCE as in type 2 diabetes (DIABETES MELLITUS, TYPE 2).		03.9721
Diabetic Angiopathies
VASCULAR DISEASES that are associated with DIABETES MELLITUS.		03.4811
Atherogenesis
[description not available]		03.0310
Atherosclerosis
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.		03.0310
HIV Lipodystrophy Syndrome
[description not available]		03.5111
HIV-Associated Lipodystrophy Syndrome
Defective metabolism leading to fat maldistribution in patients infected with HIV. The etiology appears to be multifactorial and probably involves some combination of infection-induced alterations in metabolism, direct effects of antiretroviral therapy, and patient-related factors.		03.5111
Fasting Hypoglycemia
HYPOGLYCEMIA expressed in the postabsorptive state, after prolonged FASTING, or an overnight fast.		02.1110
Hypoglycemia
A syndrome of abnormally low BLOOD GLUCOSE level. Clinical hypoglycemia has diverse etiologies. Severe hypoglycemia eventually lead to glucose deprivation of the CENTRAL NERVOUS SYSTEM resulting in HUNGER; SWEATING; PARESTHESIA; impaired mental function; SEIZURES; COMA; and even DEATH.		02.1110
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