tesaglitazar

structure in first source

Also Known As:

(S)-2-ethoxy-3-(4-((4-(methylsulfonyloxy)phenethyl)oxy)phenyl)propanoic acid; (S)-2-ethoxy-3-(4-(2-(4-methylsulphonyloxyphenyl)ethoxy)phenyl)propanoic acid; 2-ethoxy-3-(4-((4-(methylsulfonyloxy)phenethyl)oxy)phenyl)propanoic acid; AZ 242

Networked: 36 relevant articles (11 outcomes, 17 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Organic Chemicals: 133

Experts

1.	Ohman, K Peter: 4 articles (09/2012 - 12/2006)
2.	Gause-Nilsson, Ingrid: 4 articles (03/2008 - 09/2007)
3.	Berg, Anna-Lena: 3 articles (01/2012 - 07/2007)
4.	Blomgren, Bo: 3 articles (01/2012 - 07/2007)
5.	Hellmold, Heike: 3 articles (01/2012 - 07/2007)
6.	Skånberg, Inger: 3 articles (01/2012 - 07/2007)
7.	Westerberg, Rolf: 3 articles (01/2012 - 07/2007)
8.	Tonstad, Serena: 3 articles (03/2008 - 09/2007)
9.	Oakes, Nicholas D: 3 articles (10/2005 - 11/2002)
10.	Boucher, Jeremie: 2 articles (01/2020 - 01/2020)

Related Diseases

1.	Insulin Resistance 12/01/2006 - "Tesaglitazar > or = 0.5 mg improved insulin-resistance measures. " 10/01/2005 - "The present work demonstrates that tesaglitazar ameliorates these abnormalities and enhances insulin sensitivity in this animal model." 11/01/2002 - "Euglycemic hyperinsulinemic clamp studies showed that treatment with AZ 242 (1 micromol/kg/d) restored insulin sensitivity of obese Zucker rats and decreased insulin secretion. " 03/01/2006 - "This article reviews the available data on the clinical efficacy and safety of tesaglitazar in patients with type 2 diabetes and in individuals without diabetes but with insulin resistance." 07/01/2004 - "Tesaglitazar improved the insulin sensitivity of high-fat-fed rats, indicated by an increase in the glucose infusion rate during hyperinsulinemic-euglycemic clamp (P < 0.01). "
2.	Dyslipidemias (Dyslipidemia) 11/01/2005 - "AstraZeneca plc is developing tesaglitazar, an oral dual peroxisome proliferator-activated receptor alpha/gamma agonist, for the potential improvement of dyslipidemia and glycemic control in type 2 diabetic patients." 01/01/2010 - "Tesaglitazar treatment in OZR significantly reduced nonfasting glucose, C-reactive protein levels and improved dyslipidemia. " 12/01/2006 - "Similar numbers of adverse events occurred in the tesaglitazar < or = 1.0 mg, placebo, and pioglitazone arms, but there was an increasing frequency of discontinuations due to pre-specified hematologic and clinical-chemistry criteria with tesaglitazar doses > or = 1.0 mg. In type 2 diabetic patients, tesaglitazar dose-dependently reduced FPG levels at doses > or = 0.5 mg. Other markers of glycemic control, atherogenic dyslipidemia, and measures associated with insulin resistance were improved at doses > or = 0.5 mg or > or = 1.0 mg. Study limitations included that the majority of patients were white, patients had good glycemic control at baseline, and the increased number of early withdrawals in the tesaglitazar 2.0 mg and 3.0 mg doses limits conclusions about the efficacy of these doses. " 09/01/2007 - "In conclusion, the addition of tesaglitazar to a background of atorvastatin therapy further improved the dyslipidemia associated with insulin resistance." 12/01/2012 - "Compound 20 c shows high efficacy in an ob/ob mouse model of T2D and dyslipidemia, similar to that of rosiglitazone and tesaglitazar, but with a significant increase in body weight gain. "
3.	Type 2 Diabetes Mellitus (MODY) 09/01/2012 - "Pharmacokinetic-pharmacodynamic assessment of the interrelationships between tesaglitazar exposure and renal function in patients with type 2 diabetes mellitus." 03/01/2006 - "Tesaglitazar: a promising approach in type 2 diabetes." 03/01/2006 - "This article reviews the available data on the clinical efficacy and safety of tesaglitazar in patients with type 2 diabetes and in individuals without diabetes but with insulin resistance." 09/01/2007 - "A double-blind, randomised trial of tesaglitazar versus pioglitazone in patients with type 2 diabetes mellitus." 09/01/2007 - "Efficacy, safety and tolerability of tesaglitazar when added to the therapeutic regimen of poorly controlled insulin-treated patients with type 2 diabetes."
4.	Abdominal Obesity 09/01/2005 - "A 12-week, multicentre, randomised, double-blind, placebo-controlled, dose-finding study compared the efficacy and safety of oral tesaglitazar (0.1, 0.25, 0.5 and 1.0 mg/day) and placebo in 390 non-diabetic patients with hypertriglyceridaemia (plasma triglyceride concentration >1.7 mmol/l) and abdominal obesity (waist-to-hip ratio >0.90 for men and >0.85 for women). " 09/01/2007 - "This study compared the efficacy of tesaglitazar with that of pioglitazone as adjunctive therapy to atorvastatin in subjects with abdominal obesity and dyslipidemia. "
5.	Atherosclerosis 04/01/2009 - "During the 8 week low-cholesterol diet, atherosclerosis progressed in the control group with respect to lesion area and severity, whereas tesaglitazar inhibited lesion progression during this period. " 11/01/2006 - "Compared with the HC group, tesaglitazar caused a 92% reduction in atherosclerosis, whereas a 56% reduction was seen in the cholesterol-matched LC group. " 12/01/2012 - "Our data suggest that tesaglitazar may be effective in preventing NAFLD and atherosclerosis in a pre-existing diabetic condition by regulating glucose and lipid metabolism, and the inflammatory response." 12/01/2012 - "Tesaglitazar ameliorates non-alcoholic fatty liver disease and atherosclerosis development in diabetic low-density lipoprotein receptor-deficient mice." 12/01/2012 - "The aim of the present study was to determine whether tesaglitazar attenuates NAFLD and atherosclerosis development in diabetic low-density lipoprotein receptor-deficient (LDLr(-/-)) mice. "

Related Drugs and Biologics

1.	Glucose (Dextrose)
2.	Pioglitazone (Actos)
3.	Lipids
4.	LDL Receptors (LDL Receptor)
5.	Iothalamic Acid (Iotalamic Acid)
6.	Atorvastatin (Lipitor)
7.	Rosiglitazone (Avandia)
8.	C-Reactive Protein
9.	PPAR alpha
10.	Peroxisome Proliferator-Activated Receptors (PPAR)

Related Therapies and Procedures

1.	Glycemic Control
2.	Therapeutics