| Reference | [1]. Curr Opin Investig Drugs. 2005 Apr;6(4):427-34.<br />
Muraglitazar (Bristol-Myers Squibb/Merck).<br />
Barlocco D(1).<br />
Author information: (1)University of Milan, Istituto di Chimica Farmaceutica e Tossicologica, Viale Abruzzi 42, 20131 Milano, Italy. [email protected]<br />
Bristol-Myers Squibb and Merck & Co are co-developing muraglitazar, a dual peroxisome proliferator-activated receptor-alpha/gamma agonist, for the potential treatment of type 2 diabetes and other metabolic disorders. In November 2004, approval was anticipated as early as mid-2005.<br />
PMID: 15898350 [Indexed for MEDLINE]<br />
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[2]. Prev Cardiol. 2006 Spring;9(2):110-4. doi: 10.1111/j.1520-037x.2000.5474.x.<br />
Muraglitazar and the FDA: what constitutes drug safety?<br />
Liebson PR(1).<br />
Author information: (1)Section of Cardiology, Rush Medical College, Rush University Medical Center, Chicago, IL 60612, USA. [email protected]<br />
DOI: 10.1111/j.1520-037x.2000.5474.x PMID: 16603830 [Indexed for MEDLINE]<br />
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[3]. Drugs Today (Barc). 2005 Sep;41(9):579-87. doi: 10.1358/dot.2005.41.9.925347.<br />
Muraglitazar: an agent for the treatment of type 2 diabetes and associated dyslipidemia.<br />
Cox SL(1).<br />
Author information: (1)Medical Information Department, Prous Science, Barcelona, Spain. [email protected]<br />
Many studies indicate that postprandial metabolic abnormalities, such as hyperglycemia and dyslipidemia, which are exaggerated and prolonged in type 2 diabetes, are important risk factors for cardiovascular disease. Different pharmacotherapies have been developed to specifically target these risk factors associated with type 2 diabetes. The peroxisome proliferator-activated receptor (PPAR) agonists, which are potent insulin sensitizers, have been the focus of much research during the past decade. Since their development, PPAR agonists have emerged as an important target for the treatment of insulin resistance and dyslipidemia. The more recent development of agonists that selectively target both the alpha and gamma PPARs has provided a potential treatment of global risk in patients with the metabolic syndrome or type 2 diabetes. Muraglitazar is a non-thiazolidinedione, oxybenzylglycine dual PPARalpha/gamma agonist that is in advanced clinical development for the treatment of type 2 diabetes and its associated dyslipidemia. This article summarizes the available clinical data on the efficacy and safety of muraglitazar in patients with type 2 diabetes.<br />
DOI: 10.1358/dot.2005.41.9.925347 PMID: 16341289 [Indexed for MEDLINE]<br />
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[4]. J Vasc Interv Radiol. 2015 Jan;26(1):124-30. doi: 10.1016/j.jvir.2014.10.005. Epub 2014 Nov 18.<br />
Muraglitazar-eluting bioabsorbable vascular stent inhibits neointimal hyperplasia in porcine iliac arteries.<br />
Uurto I(1), Hämäläinen M(2), Suominen V(3), Laurila M(4), Kotsar A(3), Isotalo T(5), Tammela TL(3), Kellomäki M(6), Salenius JP(3).<br />
Author information: (1)Divisions of Vascular Surgery and Urology, Department of Surgery, Tampere University Hospital, Tampere, Finland. Electronic address: [email protected]. (2)Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, Tampere, Finland. (3)Divisions of Vascular Surgery and Urology, Department of Surgery, Tampere University Hospital, Tampere, Finland. (4)Department of Pathology, Tampere University Hospital, Tampere, Finland. (5)Department of Surgery, Päijät-Häme Central Hospital, Lahti, Finland. (6)Biomaterials and Tissue Engineering Group, Department of Electronics and Communications Engineering, Tampere University of Technology, Tampere, Finland; BioMediTech-Institute of Biosciences and Medical Technology, Tampere, Finland.<br />
PURPOSE: To evaluate the biocompatibility of a new muraglitazar-eluting polylactide copolymer stent and investigate its ability to prevent the formation of intimal hyperplasia. MATERIALS AND METHODS: Ten self-expandable muraglitazar-eluting poly-96 L/4D-lactic acid (PLA96) stents and 10 self-expandable control PLA96 stents were implanted into porcine common iliac arteries. After 28 days follow-up, all stent-implanted iliac arteries were harvested and prepared for quantitative histomorphometric analysis. RESULTS: Angiographic analysis revealed that one control PLA96 stent had occluded and one had migrated. Histomorphometric analysis demonstrated that, with the control PLA96 stent, the luminal diameter and area were decreased versus the muraglitazar-eluting PLA96 stents (means ± standard error of the mean, 3.58 mm ± 0.34 vs 4.16 mm ± 0.14 and 9.83 mm(2) ± 2.41 vs 13.75 mm(2) ± 0.93, respectively). The control PLA96 stent induced more intimal hyperplasia than the bioactive muraglitazar-eluting PLA96 stent (557 µm ± 122 vs 361 µm ± 32). Vascular injury scores demonstrated only mild vascular trauma for both stents (muraglitazar-eluting, 0.68 ± 0.07; control, 0.75 ± 0.08). Inflammation scores also showed mild inflammation for both stents (muraglitazar-eluting, 1.05 ± 0.17; control, 1.23 ± 0.19). CONCLUSIONS: This new muraglitazar-eluting PLA96 stent was shown to be biocompatible with a tendency for better patency and less intimal hyperplasia compared with the control PLA96 stents.<br />
DOI: 10.1016/j.jvir.2014.10.005 PMID: 25454655 [Indexed for MEDLINE]<br />
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[5]. Diabetes. 2006 Jan;55(1):240-8.<br />
Muraglitazar, a novel dual (alpha/gamma) peroxisome proliferator-activated receptor activator, improves diabetes and other metabolic abnormalities and preserves beta-cell function in db/db mice.<br />
Harrity T(1), Farrelly D, Tieman A, Chu C, Kunselman L, Gu L, Ponticiello R, Cap M, Qu F, Shao C, Wang W, Zhang H, Fenderson W, Chen S, Devasthale P, Jeon Y, Seethala R, Yang WP, Ren J, Zhou M, Ryono D, Biller S, Mookhtiar KA, Wetterau J, Gregg R, Cheng PT, Hariharan N.<br />
Author information: (1)Dept. of Metabolic Diseases, HWP-21-2.02, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, NJ 08543, USA.<br />
Muraglitazar, a novel dual (alpha/gamma) peroxisome proliferator-activated receptor (PPAR) activator, was investigated for its antidiabetic properties and its effects on metabolic abnormalities in genetically obese diabetic db/db mice. In db/db mice and normal mice, muraglitazar treatment modulates the expression of PPAR target genes in white adipose tissue and liver. In young hyperglycemic db/db mice, muraglitazar treatment (0.03-50 mg . kg(-1) . day(-1) for 2 weeks) results in dose-dependent reductions of glucose, insulin, triglycerides, free fatty acids, and cholesterol. In older hyperglycemic db/db mice, longer-term muraglitazar treatment (30 mg . kg(-1) . day(-1) for 4 weeks) prevents time-dependent deterioration of glycemic control and development of insulin deficiency. In severely hyperglycemic db/db mice, muraglitazar treatment (10 mg . kg(-1) . day(-1) for 2 weeks) improves oral glucose tolerance and reduces plasma glucose and insulin levels. In addition, treatment increases insulin content in the pancreas. Finally, muraglitazar treatment increases abnormally low plasma adiponectin levels, increases high-molecular weight adiponectin complex levels, reduces elevated plasma corticosterone levels, and lowers elevated liver lipid content in db/db mice. The overall conclusions are that in db/db mice, the novel dual (alpha/gamma) PPAR activator muraglitazar 1) exerts potent and efficacious antidiabetic effects, 2) preserves pancreatic insulin content, and 3) improves metabolic abnormalities such as hyperlipidemia, fatty liver, low adiponectin levels, and elevated corticosterone levels.<br />
PMID: 16380499 [Indexed for MEDLINE]
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