Detail of "111025-46-8"

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CAS Number:
111025-46-8
Name:
2,4-Thiazolidinedione,5-[[4-[2-(5-ethyl-2-pyridinyl)ethoxy]phenyl]methyl]-
Superlist Name:
Pioglitazone
Molecular Structure:
Formula:
C₁₉H₂₀N₂O₃S
Molecular Weight:
356.44
Deleted CAS:
105355-27-9|198077-89-3
Synonyms:
5-[4-[2-(5-Ethyl-2-pyridyl)ethoxy]benzyl]thiazolidine-2,4-dione;Pioglitazone;Zactos;
Density:
1.26 g/cm³
Melting Point:
183-184 °C
Boiling Point:
575.4 °C at 760 mmHg
Flash Point:
301.8 °C
Solubility:
Soluble in DMF; slightly soluble in ethanol; practically insoluble in water
Appearance:
Colorless needle crystal
Hazard Symbols:
F,C
Risk Codes:
11-34
Safety:
16-26-36/37/39-45 Details

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Reference

The effect of pioglitazone on hepatic glucose uptake measured with indirect and direct methods in alloxan-induced diabetic dogs: The effect of pioglitazone on hepatic glucose uptake measured with indirect and direct methods in alloxan-induced diabetic dogs. Matsuhisa, Munehide; Shi, Z. Qing; Wan, Calvin; Lekas, Michael; Rodgers, Carol D.; Giacca, Adria; Ryuzo, Kawamori; Vranic, Mladen ( Department of Physiology, University of Toronto, Toronto, Can.). Diabetes, 46(2), 224-231 (English) 1997 American Diabetes Association, Inc. CODEN: DIAEAZ. ISSN: 0012-1797. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Pioglitazone, a thiazolidinedione deriv., ameliorates hyperglycemia by augmenting peripheral glucose disposal and suppressing hepatic glucose prodn. in diabetic animals. However, the effect of this agent on hepatic glucose uptake has not been explored. To det. this, expts. were conducted in alloxan-induced diabetic dogs with (pioglitazone group, n = 7) or without (control group, n = 5) a 10-day oral treatment with pioglitazone (1 mg × kg-1 × day-1). A englycemic-hyperinsulinemic (insulin infusion rate 25.2 pmol × kg-1 × min-1) clamp was maintained by adjusting the peripheral glucose infusion rate (GIR). After a 60-min basal period (period I), portal glucose infusion (Pinf, 33.3 mmol × kg-1 × min-1) was administered for 120 min (period II). This was followed by a 60-min recovery period (period III). Arterial insulin levels were kept stable in the supraphysiol. range throughout the expt. (1,623 ± 52, pioglitazone group; 1,712 ± 52 pmol/l, C group). There was no significant difference in whole-body glucose utilization detd. by [3-3H]glucose between the pioglitazone and C groups in period I (68.4 ± 2.8 vs. 70.1 ± 2.8 mmol × kg-1 × min-1, resp.) and period III (81.2 ± 5.0 vs. 74.5 ± 3.3 mmol × kg-1 × min-1, resp.). Net hepatic glucose uptake (NHGU) detd. by arteriovenous difference method was approx. zero in the basal period (-0.7 ± 1.1, pioglitazone group; 0.1 ± 1.2 mmol × kg-1 × min-1, C group). In period II, hepatic glucose uptake, detd. by the changes in GIR, was significantly higher in the pioglitazone group (6. 50-99-7 and 111025-46-8 which are cas registry numbers of chemicals are mentioned.5 ± 0.6 mmol × kg-1 × min-1) than in the C group (-0.4 ± 0.6 mmol × kg-1 × min-1, P < 0.001). This observation was also confirmed by NHGU during portal glucose infusion (6.9 ± 1.4 vs. 2.1 ± 1.8 mmol × kg-1 × min-1, pioglitazone vs. C, resp.; P < 0.025). We conclude that pioglitazone treatment enhances hepatic glucose uptake during portal glucose loading in alloxan-induced diabetic dogs. However, in hyperinsulinemic conditions, pioglitazone does not enhance the already high peripheral glucose uptake. .

Terminal differentiation of human liposarcoma cells induced by ligands for peroxisome proliferator-activated receptor g and the retinoid X receptor: Terminal differentiation of human liposarcoma cells induced by ligands for peroxisome proliferator-activated receptor g and the retinoid X receptor. Tontonoz, Peter; Singer, Samuel; Forman, Barry M.; Sarraf, Pasha; Fletcher, Jonathan A.; Fletcher, Christopher D. M.; Brun, Regina P.; Mueller, Elisabetta; Altiok, Soner; Oppenheim, Heather; Evans, Ronald M.; Spiegelman, Bruce M. (Dana-Farber Cancer Inst., Harvard Med. Sch., Boston, MA 02115, USA).In this article, certain chemicals are used. Some of their cas registry numbers are 111025-46-8 and 122320-73-4 Proceedings of the National Academy of Sciences of the United States of America, 94(1), 237-241 (English) 1997 National Academy of Sciences. CODEN: PNASA6. ISSN: 0027-8424. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 14 Induction of terminal differentiation represents a promising therapeutic approach to certain human malignancies. The peroxisome proliferator-activated receptor g (PPARg) and the retinoid X receptor a (RXRa) form a heterodimeric complex that functions as a central regulator of adipocyte differentiation. Natural and synthetic ligands for both receptors have been identified. We demonstrate here that PPARg is expressed at high levels in each of the major histol. types of human liposarcoma. Moreover, primary human liposarcoma cells can be induced to undergo terminal differentiation by treatment with the PPARg ligand pioglitazone, suggesting that the differentiation block in these cells can be overcome by maximal activation of the PPAR pathway. We further demonstrate that RXR-specific ligands are also potent adipogenic agents in cells expressing the PPARg/RXRa heterodimer, and that simultaneous treatment of liposarcoma cells with both PPARg- and RXR-specific ligands results in an additive stimulation of differentiation. Liposarcoma cell differentiation is characterized by accumulation of intracellular lipid, induction of adipocyte-specific genes, and withdrawal from the cell cycle. These results suggest that PPARg ligands such as thiazolidinediones and RXR-specific retinoids may be useful therapeutic agents for the treatment of liposarcoma. .

Detail of "111025-46-8"

2,4-Thiazolidinedione,5-[[4-[2-(5-ethyl-2-pyridinyl)ethoxy]phenyl]methyl]-

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Reference