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Rosiglitazone 目录号 GC16444

Potent PPARγ agonist

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10mM (in 1mL DMSO)

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Sample solution is provided at 25 µL, 10mM.


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Cell experiment [1]:

Cell lines

Non–small cell lung carcinoma (NSCLC) cells (H1792 and H1838)

Preparation method

The solubility of this compound in DMSO is >17.9 mg/mL. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months.

Reacting condition

10 μmol/L, 48 hours


Rosiglitazone reduced the phosphorylation of Akt and increased phosphatase and tensin homologue (PTEN) protein expression in non–small cell lung carcinoma (NSCLC) cells (H1792 and H1838), and this was associated with inhibition of NSCLC cell proliferation. Rosiglitazone increased the phosphorylation of AMP-activated protein kinase α (AMPKα), a downstream kinase target for LKB1, whereas it decreased phosphorylation of p70 ribosomal protein S6 kinase (p70S6K), a downstream target of mammalian target of rapamycin (mTOR).

Animal experiment [2]:

Animal models

C57/BL6 mice

Dosage form

8 mg/kg per day


In C57/BL6 mice underwent femoral angioplasty, treatment with rosiglitazone (8 mg/kg per day) attenuated neointimal formation. In a BM transplantation model, Rosiglitazone caused a 6-fold increase in colony formation by human endothelial progenitor cells, promoted the differentiation of APCs toward the endothelial lineage in mouse BM in vivo and in human peripheral blood in vitro, and inhibited the differentiation toward the smooth muscle cell lineage. Within the neointima, rosiglitazone stimulated APCs to differentiate into mature endothelial cells and caused earlier reendothelialization.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.


[1]. Han S W, Roman J. Rosiglitazone suppresses human lung carcinoma cell growth through PPARγ-dependent and PPARγ-independent signal pathways[J]. Molecular cancer therapeutics, 2006, 5(2): 430-437.

[2]. Wang C H, Ciliberti N, Li S H, et al. Rosiglitazone facilitates angiogenic progenitor cell differentiation toward endothelial lineage[J]. Circulation, 2004, 109(11): 1392-1400.

Chemical Properties

Cas No. 122320-73-4 SDF
别名 Brl-49653,Brl 49653
化学名 5-[[4-[2-[methyl(pyridin-2-yl)amino]ethoxy]phenyl]methyl]-1,3-thiazolidine-2,4-dione
Canonical SMILES CN(CCOC1=CC=C(C=C1)CC2C(=O)NC(=O)S2)C3=CC=CC=N3
分子式 C18H19N3O3S 分子量 357.43
溶解度 ≥ 17.85 mg/mL in DMSO 储存条件 Store at 2-8°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
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Rosiglitazone is a potent agonist of peroxisome proliferator-activated receptor γ (PPARγ), a subfamily of the nuclear-receptor superfamily which is predominately expressed in adipose tissue and regulates gene expression responding to ligand binding. Belonging to the thiazolidinedione (TZD) class, rosiglitazone, like other TZD members, binds to PPARγ DNA as heterodimers and activate transcription of various metabolic regulators involved in the differentiation of stem cells into adipocytes and increased expression of genes regulating the metabolism of glucose and lipid. Rosiglitazone is used to treat patients with type II diabetes mellitus for its strong ability to improve insulin sensitization through its effects either on fatty acid uptake and storage in adipose tissue or on adiokines.


[1].Peter J. Cox, David A. Ryan, Frank J. Hollis, Ann-Marie Harris, Ann K. Miller, Marika Vousden and Hugh Cowley. Absorption, disposition, and metabolism of rosiglitazone, a potent thiazolidinedione insulin sensitizer, in humans. Drug Metabolism and Disposition 2000; 28(7): 772-780
[2].Adie Vilioen and Alan Sinclair. Safety and efficacy of rosiglitazone in the elderly diabetic patient. Vascular Health and Risk Management 2009:5 389-395