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Recent News and Articles on the Keywords: muraglitazar decreased + 2 diabetes + muraglitazar  Related to the article below (Last Update: 7/8/2008)

Muraglitazar, a dual (a/?) PPAR activator: A randomized, double-blind, placebo-controlled, 24-week … -
JB Buse, CJ Rubin, R Frederich, K Viraswami- … - Clinical Therapeutics, 2005 - Elsevier
... 6 (5) Other 16 (14) BMI, kg/m 2. 31.5 (5.1 ... els were observed with both doses of
muraglitazar (P < 0.05 ... HDL cholesterol levels by 10% and 16%, decreased apo B ...

… of Glycemic Control, Triglycerides, and HDL Cholesterol Levels With Muraglitazar, a Dual (a/?) … -
DM Kendall, CJ Rubin, P Mohideen, JM Ledeine, R … - Diabetes Care, 2006 - Am Diabetes Assoc
... lipid abnormalities in individuals with type 2 diabetes inadequately controlled ... is
unknown whether the effects of muraglitazar to decrease high-sensitivity ...

Selling Safety-Lessons From Muraglitazar -
JM Brophy - JAMA, 2005 - Am Med Assoc
... fatty acid oxidation, leading to a decrease in plasma ... Muraglitazar is the first
dual-PPAR agonist to be ... Given the emerging epidemic of type 2 diabetes, it is ...

Muraglitazar Bristol-Myers Squibb/Merck -
D Barlocco - Current Opinion in Investigational Drugs, 2005 - air.unimi.it
... mg/day) or pioglitazone (45 mg/day) was conducted in patients with type 2 diabetes
(six to ... At a dose of = 5 mg, muraglitazar caused a larger decrease in 24 ...

MURAGLITAZAR: AN AGENT FOR THE TREATMENTOF TYPE 2 DIABETES AND ASSOCIATED DYSLIPIDEMIA -
SL Cox - Drugs of Today, 2005 - journals.prous.com
... on the efficacy and safety of muraglitazar in patients ... dyslipidemia in patients with
type 2 diabetes is elevated levels of triglyceride and decreased levels of ...

… of Pancreatic {beta}-Cell Function and Prevention of Type 2 Diabetes by Pharmacological Treatment … -
TA Buchanan, AH Xiang, RK Peters, SL Kjos, A … - Diabetes, 2002 - Am Diabetes Assoc
... R. Gregg, PT Cheng, and N. Hariharan Muraglitazar, a Novel ... ML Cruz, and MI Goran
Decreased {beta}-Cell ... for the prevention of type 2 diabetes and cardiovascular ...

PPARa and PPAR? dual agonists for the treatment of type 2 diabetes and the metabolic syndrome -
C Fi?vet, JC Fruchart, B Staels - Current Opinion in Pharmacology, 2006 - Elsevier
... Moreover, muraglitazar improved lipid abnormalities associated with diabetic
dyslipidemia; decreased TGs, apo ... in Diabetics (GLAD) Phase II trial, tesaglitazar ...

THERAPEUTIC OPTIONS IN DEVELOPMENT FOR MANAGEMENT OF DIABETES: PHARMACOLOGIC AGENTS AND NEW … -
HE Lebovitz - Endocrine Practice, 2006 - AACE
... The effects of muraglitazar were compared with placebo in patients with type 2 diabetes
and a ... muragli- tazar showed a significant decrease in HbA1c and ...

Recent findings concerning thiazolidinediones in the treatment of diabetes -
G Boden, M Zhang - Expert Opin. Investig. Drugs, 2006 - Expert Opinion
... Muraglitazar has completed the required 2-year toxicity ... TZDs have been demonstrated
to decrease hepatic fat ... G, LAAKSO M: Lipids and glucose in Type 2 diabetes. ...

[PDF] Goodbye glitazars
D Conlon - Br J Diabetes Vasc Dis, 2006 - bjdvd.com
... In May 2006 the two glitazars most ... Muraglitazar was associated with an increased
incidence of ... tesaglitazar was associated with decreased glomerular filtration. ...

Source: Google Scholar
 
 

Type 2 diabetes, Muraglitazar decreases HA1c levels

 

 
Results from a Phase III study indicated that Muraglitazar, an investigational compound, significantly decreased hemoglobin A1c ( HA1c ) levels at 24 weeks versus placebo in patients with Type 2 diabetes.
Additional effects were seen on triglycerides and HDL-cholesterol.

The New Drug Application ( NDA ) for Muraglitazar is currently under review by FDA ( Food and Drug Administration ).
If approved, Muraglitazar would become the first agent in a new class of investigational compounds called glitazars, a dual alpha/gamma PPAR ( peroxisome proliferator-activated receptor ) activator, available in the United States.
The glitazars activate PPAR gamma lowering plasma glucose and free fatty acid concentrations and PPAR alpha lowering plasma triglyceride concentrations and increasing HDL cholesterol.

The Phase III trial was a randomized, double-blind, placebo-controlled, multicenter, parallel-group study of 340 men and women aged 18 to 70 years whose type 2 diabetes was inadequately controlled ( defined as having A1c values of 7% to 10% at screening ) with diet and exercise and who had a body mass index ( BMI ) of less than 41.
Patients received a once-daily regimen of Muraglitazar 2.5 mg tablets ( n=111 ), Muraglitazar 5 mg tablets ( n=114 ), or placebo ( n=115 ) for 24 weeks.
In addition, a cohort of patients ( n=109 ) who met all other study criteria, but had higher A1c values at screening ( A1c greater than 10% and up to and including 12% ) were enrolled in a parallel 24- week open-label evaluation of a daily dose of Muraglitazar 5 mg.
In the double-blind study group, mean baseline A1c for all patient groups was 7.89% to 8.02%.
At 24 weeks, mean changes in A1c versus baseline were -0.32%, -1.05%, and -1.23% in the placebo, Muraglitazar 2.5 mg, and Muraglitazar 5 mg groups, respectively ( p < 0.0001, placebo versus either Muraglitazar group ).

In the open-label cohort ( mean baseline A1c 10.68% ), mean change in A1c versus baseline was -2.62% after 24 weeks of treatment with Muraglitazar 5 mg once daily.

The AACE recommended A1c target level of less than or equal to 6.5% was achieved by 18%, 36%, and 58% of patients taking placebo, Muraglitazar 2.5 mg, and Muraglitazar 5 mg, respectively in the double-blind cohort.

In the subgroup of patients with baseline triglyceride levels of 150 mg/dL or more, changes in triglyceride levels were -13.2%, -24.8%, and -30.4% with placebo, Muraglitazar 2.5 mg, and Muraglitazar 5 mg ( p = 0.13 versus placebo for the Muraglitazar 2.5 group and p = 0.0002 versus placebo for the Muraglitazar 5 mg group ).
Mean HDL-cholesterol levels increased 2%, 10%, and 16% from baseline in the placebo, 2.5 mg, and 5 mg groups of the double-blind study ( p < 0.0001 in both Muraglitazar-treated groups versus placebo ) and increased 12% from baseline in the 5 mg open-label group, respectively.

Other secondary endpoints showed that Muraglitazar was associated with significant reductions from baseline in mean fasting plasma glucose ( FPG ), fasting plasma insulin, free fatty acid, apoB, and non-HDL cholesterol levels.
Muraglitazar treatment was also associated with increased insulin sensitivity as measured by a decrease in homeostasis model assessment of insulin resistance ( HOMA-IR ).

In the study, no cases of confirmed hypoglycemia were reported ( confirmed hypoglycemia was defined as symptoms of hypoglycemia accompanied by a fingerstick glucose test result of less than or equal to 50 mg/dl ).
In the double-blind cohort, mean change in body weight versus baseline was -0.8, +1.1, and +2.1 kg in the placebo, Muraglitazar 2.5 mg, and Muraglitazar 5 mg groups, respectively, and was +2.9 kg in the open-label cohort taking Muraglitazar 5 mg.
Edema-related adverse events occurred in 8%, 8%, and 11% of patients taking placebo, Muraglitazar 2.5 mg, and Murgalitazar 5mg, respectively, in the double-blind study and 8% in patients taking Muraglitazar 5 mg in the open-label cohort.
All events were mild or moderate in severity in the Muraglitazar-treated groups.
Incidence of serious adverse events was 3% to 4% across all treatment groups. In the double-blind study, adverse events occurred in 69%, 71%, and 77% of the patients in the placebo, Muraglitazar 2.5 mg, and Muraglitazar 5 mg groups, respectively, and in 70% of the patients in the open-label cohort taking Muraglitazar 5 mg.

Exclusion criteria included triglyceride values greater than 600 mg/dL, symptomatic type 2 diabetes, NYHA Class III/IV cardiac status, or treatment with non-statin cholesterol-lowering medications prior to randomization.
Patients who were taking statins were allowed to continue taking statins if their regimens had been stable for at least 6 weeks prior to enrollment.

Source: 14th Annual Meeting of the American Association of Clinical Endocrinologists ( AACE ), 2005
 
 
 
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