CiglitazoneCAS# 74772-77-3 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 74772-77-3 | SDF | Download SDF |
PubChem ID | 2750 | Appearance | Powder |
Formula | C18H23NO3S | M.Wt | 333.44 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 100 mM in 1eq. NaOH | ||
Chemical Name | 5-[[4-[(1-methylcyclohexyl)methoxy]phenyl]methyl]-1,3-thiazolidine-2,4-dione | ||
SMILES | CC1(CCCCC1)COC2=CC=C(C=C2)CC3C(=O)NC(=O)S3 | ||
Standard InChIKey | YZFWTZACSRHJQD-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C18H23NO3S/c1-18(9-3-2-4-10-18)12-22-14-7-5-13(6-8-14)11-15-16(20)19-17(21)23-15/h5-8,15H,2-4,9-12H2,1H3,(H,19,20,21) | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Selective agonist at PPARγ (peroxisome proliferator-activated receptor γ). Activates PPARγ with an EC50 value of 3 μM in vitro, and is at least 33-fold selective over PPARα and δ. Antihyperglycemic in vivo. |
Ciglitazone Dilution Calculator
Ciglitazone Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.999 mL | 14.9952 mL | 29.9904 mL | 59.9808 mL | 74.976 mL |
5 mM | 0.5998 mL | 2.999 mL | 5.9981 mL | 11.9962 mL | 14.9952 mL |
10 mM | 0.2999 mL | 1.4995 mL | 2.999 mL | 5.9981 mL | 7.4976 mL |
50 mM | 0.06 mL | 0.2999 mL | 0.5998 mL | 1.1996 mL | 1.4995 mL |
100 mM | 0.03 mL | 0.15 mL | 0.2999 mL | 0.5998 mL | 0.7498 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Autonomous inhibition of apoptosis correlates with responsiveness of colon carcinoma cell lines to ciglitazone.[Pubmed:25502518]
PLoS One. 2014 Dec 11;9(12):e114158.
Colorectal cancer is a leading cause of mortality worldwide. Resistance to therapy is common and often results in patients succumbing to the disease. The mechanisms of resistance are poorly understood. Cells basically have two possibilities to survive a treatment with potentially apoptosis-inducing substances. They can make use of their existing proteins to counteract the induced reactions or quickly upregulate protective factors to evade the apoptotic signal. To identify protein patterns involved in resistance to apoptosis, we studied two colorectal adenocarcinoma cell lines with different growth responses to low-molar concentrations of the thiazolidinedione Ciglitazone: HT29 cells underwent apoptosis, whereas SW480 cells increased cell number. Fluorescence detection and autoradiography scans of 2D-PAGE gels were performed in both cell lines to assess protein synthesis and turnover, respectively. To verify the data we performed shotgun analysis using the same treatment procedure as in 2D-experiments. Biological functions of the identified proteins were mainly associated with apoptosis regulation, chaperoning, intrinsic inflammation, and DNA repair. The present study suggests that different growth response of two colorectal carcinoma cell lines after treatment with Ciglitazone results from cell-specific protein synthesis and differences in protein regulation.
A novel polymer-free ciglitazone-coated vascular stent: in vivo and ex vivo analysis of stent endothelialization in a rabbit iliac artery model.[Pubmed:27613845]
Oncotarget. 2016 Sep 6;7(36):57571-57580.
AIM: Peroxisome proliferator-activated receptor-gamma (PPARg) agonists have known pleiotropic cardiovascular effects with favourable properties in vascular remodeling, and specifically in suppression of vascular smooth muscle cell proliferation. A novel vascular stent coating using the PPARg ligand Ciglitazone (CCS) was investigated regarding its effects on endothelialization after 7 and 28 days. METHODS: Microporous bare metal stents (BMS) were coated with Ciglitazone by ultrasonic flux with a load of 255 mug Ciglitazone/stent. SixteenNew Zealand white rabbits, fed a with high cholesterol diet, underwent stent implantation in both iliac arteries. Everolimus-eluting stents (EES) and BMS were comparators. Histology (CD 31 immunostaining, confocal and scanning electron microscopy, morphometry) was performed after 7 and 28 days and by OCT (optical coherence tomography) in vivo after 28 days. RESULTS: Microscopy showed comparable results with near complete endothelialization in CCS and BMS (%CD31 above stent struts after 7 days: 67.92+/-36.35 vs. 84.48+/-23.86; p = 0.55; endothel % above stent struts: 77.22+/-27.9 vs. 83.89+/-27.91; p = 0.78). EES were less endothelialized with minimal fibrin deposition, not found in BMS and CCS (% CD 31 above struts after 28 days, BMS: 100.0+/-0.0 vs. EES: 95.9+/-3.57 vs. CCS: 100.0+/-0.0; p = 0.0292). OCT revealed no uncovered struts in all stents after 28 days. CONCLUSIONS: Polymer-free coating with Ciglitazone, a PPARg agonist is feasible and stable over time. Our data prove unimpaired endothelial coverage of a Ciglitazone-coated vascular stent system by histology and OCT. Thus, this PPARg agonist coating deserves further investigation to evaluate its potency on local neointimal suppression.
A protective role of ciglitazone in ox-LDL-induced rat microvascular endothelial cells via modulating PPARgamma-dependent AMPK/eNOS pathway.[Pubmed:25388834]
J Cell Mol Med. 2015 Jan;19(1):92-102.
Thiazolidinediones, the antidiabetic agents such as Ciglitazone, has been proved to be effective in limiting atherosclerotic events. However, the underlying mechanism remains elucidative. Ox-LDL receptor-1 (LOX-1) plays a central role in ox-LDL-mediated atherosclerosis via endothelial nitric oxide synthase (eNOS) uncoupling and nitric oxide reduction. Therefore, we tested the hypothesis that Ciglitazone, the PPARgamma agonist, protected endothelial cells against ox-LDL through regulating eNOS activity and LOX-1 signalling. In the present study, rat microvascular endothelial cells (RMVECs) were stimulated by ox-LDL. The impact of Ciglitazone on cell apoptosis and angiogenesis, eNOS expression and phosphorylation, nitric oxide synthesis and related AMPK, Akt and VEGF signalling pathway were observed. Our data showed that both eNOS and Akt phosphorylation, VEGF expression and nitric oxide production were significantly decreased, RMVECs ageing and apoptosis increased after ox-LDL induction for 24 hrs, all of which were effectively reversed by Ciglitazone pre-treatment. Meanwhile, phosphorylation of AMP-activated protein kinase (AMPK) was suppressed by ox-LDL, which was also prevented by Ciglitazone. Of interest, AMPK inhibition abolished Ciglitazone-mediated eNOS function, nitric oxide synthesis and angiogenesis, and increased RMVECs ageing and apoptosis. Further experiments showed that inhibition of PPARgamma significantly suppressed AMPK phosphorylation, eNOS expression and nitric oxide production. Ciglitazone-mediated angiogenesis and reduced cell ageing and apoptosis were reversed. Furthermore, LOX-1 protein expression in RMVECs was suppressed by Ciglitazone, but re-enhanced by blocking PPARgamma or AMPK. Ox-LDL-induced suppression of eNOS and nitric oxide synthesis were largely prevented by silencing LOX-1. Collectively, these data demonstrate that Ciglitazone-mediated PPARgamma activation suppresses LOX-1 and moderates AMPK/eNOS pathway, which contributes to endothelial cell survival and function preservation.
Ciglitazone, a peroxisome proliferator-activated receptor gamma ligand, inhibits proliferation and differentiation of th17 cells.[Pubmed:25593646]
Biomol Ther (Seoul). 2015 Jan;23(1):71-6.
Peroxisome proliferator-activated receptor gamma (PPARgamma) was identified as a cell-intrinsic regulator of Th17 cell differentiation. Th17 cells have been associated with several autoimmune diseases, including experimental autoimmune encephalomyelitis (EAE), inflammatory bowel disease (IBD), and collagen-induced arthritis. In this study, we confirmed PPARgamma-mediated inhibition of Th17 cell differentiation and cytokine production at an early stage. Treatment with Ciglitazone, a PPARgamma ligand, reduced both IL-1beta-mediated enhancement of Th17 differentiation and activation of Th17 cells after polarization. For Th17 cell differentiation, we found that Ciglitazone-treated cells had a relatively low proliferative activity and produced a lower amount of cytokines, regardless of the presence of IL-1beta. The inhibitory activity of Ciglitazone might be due to decrease of CCNB1 expression, which regulates the cell cycle in T cells. Hence, we postulate that a pharmaceutical PPARgamma activator might be a potent candidate for treatment of Th17-mediated autoimmune disease patients.
Thiazolidinediones--the new insulin enhancers.[Pubmed:10052651]
Clin Exp Hypertens. 1999 Jan-Feb;21(1-2):157-66.
Insulin resistance, characterized by reduced responsiveness to normal circulating levels of insulin, leads to hyperglycemia and hyperinsulinemia resulting in a deadly quartet of non-insulin dependent diabetes mellitus, obesity, hypertension and dyslipidemia These complications, also referred to as 'Syndrome X' have been associated with an increased risk of coronary heart disease. A number of non-pharmacological and pharmacological interventions are available for prevention and treatment of insulin resistance. However, introduction of thiazolidinediones, the new orally active class of drug, has proved to be a major breakthrough in this field. These agents have been shown to reduce insulin resistance by a novel mechanism of action. By interacting with a family of nuclear receptors known as peroxisome proliferator activated receptors thiazolidinediones are thought to enhance the actions of insulin, thereby increasing insulin dependent glucose disposal and reducing hepatic glucose output. A series of animal and clinical studies in patients with impaired Glucose Tolerance and NIDDM have demonstrated the safety and effect of various thiazolidinediones including Ciglitazone, pioglitazone and troglitazone. Thus, thiazolidinediones by unlocking insulin resistance act as a key to glycemic control and hence are likely to prove a useful and rational therapy in NIDDM and possibly other disorders resulting from insulin resistance.
Peroxisome proliferator-activated receptor gamma ligands are potent inhibitors of angiogenesis in vitro and in vivo.[Pubmed:10085162]
J Biol Chem. 1999 Mar 26;274(13):9116-21.
Peroxisome proliferator-activated receptor gamma (PPARgamma) is a nuclear receptor that functions as a transcription factor to mediate ligand-dependent transcriptional regulation. Activation of PPARgamma by the naturally occurring ligand, 15-deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2), or members of a new class of oral antidiabetic agents, e.g. BRL49653 and ciglitizone, has been linked to adipocyte differentiation, regulation of glucose homeostasis, inhibition of macrophage and monocyte activation, and inhibition of tumor cell proliferation. Here we report that human umbilical vein endothelial cells (HUVEC) express PPARgamma mRNA and protein. Activation of PPARgamma by the specific ligands 15d-PGJ2, BRL49653, or ciglitizone, dose dependently suppresses HUVEC differentiation into tube-like structures in three-dimensional collagen gels. In contrast, specific PPARalpha and -beta ligands do not affect tube formation although mRNA for these receptors are expressed in HUVEC. PPARgamma ligands also inhibit the proliferative response of HUVEC to exogenous growth factors. Treatment of HUVEC with 15d-PGJ2 also reduced mRNA levels of vascular endothelial cell growth factor receptors 1 (Flt-1) and 2 (Flk/KDR) and urokinase plasminogen activator and increased plasminogen activator inhibitor-1 (PAI-1) mRNA. Finally, administration of 15d-PGJ2 inhibited vascular endothelial cell growth factor-induced angiogenesis in the rat cornea. These observations demonstrate that PPARgamma ligands are potent inhibitors of angiogenesis in vitro and in vivo, and suggest that PPARgamma may be an important molecular target for the development of small-molecule inhibitors of angiogenesis.