Catalog No.S2046 Synonyms: AD-4833, U-72107E
Molecular Weight(MW): 392.9
Pioglitazone HCl is a selective peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist, used to treat diabetes.
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Primary hepatocytes were treated with or without 20μM Wy14643/Pioglitazone/Rosiglitazone for 24h followed by stimulation with or without 1μg/ml recombinant human FGF21 for 15min. FGF21 signaling was analyzed by phosphorylation of ERK1/2 and FRS2 examination.
Mol Nutr Food Res, 2017. Pioglitazone HCl purchased from Selleck.
Accumulated 7-day BrdU labeling in representative sections of pancreatic islets from mice fed (A) normal chow, (B) HFD, (C) HFD+clodronate, and (D) HFD+pioglitazone. β-Cells were immunostained with anti-insulin Ab (green) and for replication with anti-BrdU Ab (red). Nuclei were stained in blue. Scale bar, 100 μm. The percentage of BrdU-positive β-cells was calculated. Values are means±SE with 5 pancreas samples in each experimental group analyzed and are shown in E. *P<0.05 where significant difference was detected between the HFD mice and other treatment groups. No significant difference was detected between the results of other groups.
Endocrinology and Metabolism, 2016, 311(4): E763-E771.. Pioglitazone HCl purchased from Selleck.
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|Description||Pioglitazone HCl is a selective peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist, used to treat diabetes.|
Pioglitazone inhibits LPS-induced iNOS expression and NO generation, and inhibition of iNOS is sufficient to protect dopaminergic neurons against LPS insult. Pioglitazone protects dopaminergic neurons against LPS insult at least via inhibiting iNOS expression and NO generation, which is potentially mediated via inhibition of p38 MAPK activity. Pioglitazone inhibits LPS-induced phosphorylation of p38 MAPK. 
|In vivo||Pioglitazone administered orally (0.3-3 mg/kg/d for 7 days) dose dependently reduces hyperglycemia, hyperlipidemia, and hyperinsulinemia in male fatty rats. Pioglitazone improves glucose tolerance and augmentes the glycemic response to exogenous insulin and clearance of plasma triglyceride in rats.  Pioglitazone-treated transgenic mice reveals improved muscle strength and body weight, exhibits a delayed disease onset, and survives significantly longer than nontreated SOD1-G93A mice.  Pioglitazone markedly decreases hyperglycemia, hyperlipidemia, hyperinsulinemia, and glucoseintolerance characterized as insulin resistant states in these rats and mice. Pioglitazone potentiates insulin-mediated glucose metabolism in the diaphragm and adipose tissues of yellow KK mice and enhanced the glycemic response to exogenous insulin in Zucker fatty rats.  Pioglitazone results in a reduction in the number of activated microglia and reactive astrocytes in the hippocampus and cortex of APPV717I transgenic mice. Pioglitazone decreases beta-secretase-1 (BACE1) mRNA and protein levels in APPV717I transgenic mice. |
-  Xing B, et al. J Neuroinflammation,?008, 5, 4.
-  Sugiyama Y, et al. Arzneimittelforschung,?990, 40(3), 263-267.
-  Sch黷z B, et al. J Neurosci,?005, 25(34), 7805-7812.
|In vitro||DMSO||79 mg/mL (201.06 mM)|
|Ethanol||4 mg/mL (10.18 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01517165||Terminated||Opioid-Related Disorders||National Institute on Drug Abuse (NIDA)|National Institutes of Health Clinical Center (CC)||January 4, 2012||Phase 1|
|NCT00604578||Withdrawn||Asthma|Airway Inflammation|Airflow Obstruction|Airway Hyperactivity||National Heart, Lung, and Blood Institute (NHLBI)|National Institutes of Health Clinical Center (CC)||January 4, 2008||Phase 2|
|NCT00927290||Terminated||Chronic Hepatitis C|Insulin Resistance||French National Agency for Research on AIDS and Viral Hepatitis|French National Institute for Health and Medical Research-French National Agency for Research on AIDS and Viral Hepatitis (Inserm-ANRS)||December 3, 2009||Phase 3|
|NCT02338999||Recruiting||Systemic Lupus Erthematosus||National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)|National Institutes of Health Clinical Center (CC)||December 29, 2014||Phase 1|Phase 2|
|NCT00994175||Completed||Severe, Refractory Asthma|Airway Inflammation|Airflow Obstruction||National Heart, Lung, and Blood Institute (NHLBI)|National Institutes of Health Clinical Center (CC)||September 23, 2009||Phase 2|
|NCT02942758||Not yet recruiting||Acute Myeloid Leukemia||University Hospital Regensburg|Anticancer Fund, Belgium|Celgene||February 2017||Phase 2|
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