| In Vivo | After a single dose of albiglutide, glucose lowering effects occurs within 24 h, as a result of binding of the molecule to the GLP-1 receptor. The reduction in both fasting and postprandial glucose levels is dose related. Albiglutide is less potent than GLP-1. In animal models of diabetes, albiglutide administration stimulates increased β-cell mass. Following SC administration of a single 30-mg dose to patients with type 2 diabetes, maximum concentration is reached in 3-5 days with half-life of 3.6-6.8 days. The apparent volume of distribution after a single dose of albiglutide was 8.2-18.5 L. The eventual fate of albiglutide in the circulation is degradation into small peptides and individual amino acids. Albiglutide had no apparent effects on cardiovascular function, heart rate, electrocardiographic intervals, or respiratory function and did not produce any evidence of electrocardiographic abnormalities or arrhythmias in male cynomolgus monkeys. Furthermore, there were no albiglutide-related effects on neurobehavioral functional assessments. Albiglutide does not cross the blood–brain barrier to reach the satiety centers. Albiglutide reduced myocardial infarct size and improved cardiac function and energetics following myocardial I/R injury which are associated with enhanced myocardial glucose uptake and a shift toward a more energetically favorable substrate metabolism by increasing both glucose and lactate oxidation. |
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