E6910
吡格列酮 盐酸盐
≥98% (HPLC), powder, hepatic gluconeogenesis blocker
别名:
5-[[4-[2-(5-一乙基-2-吡啶)乙氧基]苯基]甲基]-2,4-噻唑烷二酮 单盐酸盐
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关于此项目
经验公式（希尔记法）:
C19H20N2O3S · HCl
化学文摘社编号:
分子量:
392.90
UNSPSC Code:
41106305
PubChem Substance ID:
NACRES:
NA.77
MDL number:
产品名称
吡格列酮 盐酸盐, ≥98% (HPLC)
SMILES string
Cl.CCc1ccc(CCOc2ccc(CC3SC(=O)NC3=O)cc2)nc1
InChI key
GHUUBYQTCDQWRA-UHFFFAOYSA-N
InChI
1S/C19H20N2O3S.ClH/c1-2-13-3-6-15(20-12-13)9-10-24-16-7-4-14(5-8-16)11-17-18(22)21-19(23)25-17;/h3-8,12,17H,2,9-11H2,1H3,(H,21,22,23);1H
assay
≥98% (HPLC)
form
powder
color
white to off-white
solubility
DMSO: ≥10 mg/mL
originator
Takeda
storage temp.
room temp
Quality Level
Gene Information
human ... PPARG(5468)
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Biochem/physiol Actions
盐酸吡格列酮是一种PPARγ激动剂和噻唑烷二酮（TZD）抗糖尿病药物。
盐酸吡格列酮是一种PPARγ激动剂和噻唑烷二酮（TZD）抗糖尿病药物。吡格列酮是一种核受体过氧化物酶体增殖物激活受体γ（PPAR-γ）的选择性激动剂，并在较小程度上是PPAR-α。
Pioglitazone hydrochloride is usually used to treat type-II diabetes. It has the ability to block hepatic gluconeogenesis.
Application
Pioglitazone hydrochloride has been used:
- to administer to mice model and treated the hepatoma cell line to study its effect on regulating insulin-degrading enzyme (IDE) in diet-induced obese (DIO) C57BL/6 mice
- in drug preparation to analyze its effects on shortening and calcium transport in ventricular myocytes from the Goto-Kakizaki (GK) type 2 diabetic rat
- to treat HepG2 cells with peroxisome proliferator-activated receptor γ (PPARγ) agonists to examine its effect on TOMM40-, APOE- and APOC1-mRNA levels
Features and Benefits
This compound is a featured product for ADME Tox research. Click here to discover more featured ADME Tox products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
This compound is featured on the AMPKs and Nuclear Receptors (PPARs) pages of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.
This compound was developed by Takeda. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.
General description
Pioglitazone hydrochloride consists of poly-morphs, form I and form II. It is an oral antidiabetic agent, that is a member of the thiazolidinedione group.
signalword
Warning
hcodes
Hazard Classifications
Acute Tox. 4 Oral - Carc. 2
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
Peter Ochodnicky et al.
European journal of pharmacology, 730, 51-60 (2014-03-04)
Peroxisome proliferator-activated receptor γ (PPARγ) agonists have been shown to ameliorate diabetic nephropathy, but much less are known about their effects in non-diabetic nephropathies. In the present study, metabolic parameters, blood pressure, aortic endothelial function along with molecular and structural
J R Colca et al.
Clinical pharmacology and therapeutics, 93(4), 352-359 (2013-03-07)
It may be possible to achieve insulin sensitivity through the recently identified mitochondrial target of thiazolidinediones (mTOT), thereby avoiding peroxisome proliferator-activated receptor-γ (PPAR-γ)-dependent side effects. In this phase IIb clinical trial, 258 patients with type 2 diabetes completed a 12-week
Andrew Grey et al.
European journal of endocrinology, 170(2), 255-262 (2013-11-13)
Preclinical studies, observational studies, and clinical trials suggest that thiazolidinediones (TZDs) reduce bone mineral density (BMD) and increase fracture risk. Most of the evidence on the skeletal effects of TZDs is from studies of rosiglitazone. We set out to investigate
Romina Lomonaco et al.
Drugs, 73(1), 1-14 (2013-01-19)
Nonalcoholic fatty liver disease (NAFLD) is considered the most common liver disorder in the Western world. It is commonly associated with insulin resistance, obesity, dyslipidaemia, type 2 diabetes mellitus (T2DM) and cardiovascular disease. Nonalcoholic steatohepatitis (NASH) is characterized by steatosis
Julien Lamontagne et al.
Diabetes, 62(6), 2122-2129 (2013-02-05)
Our objective was to determine if the insulin-sensitizing drug pioglitazone acutely reduces insulin secretion and causes metabolic deceleration in vivo independently of change in insulin sensitivity. We assessed glucose homeostasis by hyperinsulinemic-euglycemic and hyperglycemic clamp studies and energy expenditure by
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