Cat# : THP-0119
|Product Name:||Exenatide, Glucagon-Like peptide-1 (GLP-1)|
|Description:||This product is a glucagon-like peptide-1 (GLP-1) analog that functions to activate the GLP-1 receptor and increases insulin secretion, decrease glucagon secretion, and slow gastric emptying to improve glycemic control.|
|Molecular Weight:||4186.6 Da|
|Purity:||>99% by SDS-Page and HPLC analysis|
|Endotoxin Level:||<0.001 EU per 1 μg of the protein by the LAL method|
|Applications:||Indicated as adjunctive therapy to improve glycemic control in patients with Type 2 diabetes mellitus who are taking metformin, a sulfonylurea, or a combination of both, but have not achieved adequate glycemic control.|
|Examples of Clinical Use:||Type 2 diabetes mellitus|
|Pharmacodynamics:||The product is an incretin mimetic, which has glucoregulatory effects. While it is has blood-sugar lowering actions alone, it can also be combined with other medications such as pioglitazone, metformin, sulfonylureas, and/or insulin to improve glucose control. The approved use of the product is with either sulfonylureas, metformin and thiazolinediones. The medication is injected twice per day using a pre-filled pen device. Typical human responses to the product plus eating include improvements in the initial rapid release of endogenous insulin, suppression of glucagon release by the pancreas, regulation of gastric empyting and reduced appetite; all behaviors more typical of individuals without blood sugar control problems. The product is self-regulating in that in lowers blood sugar when levels are elevated but does not continue to lower blood sugar when levels return to normal, unlike with sulfonylureas or insulins.|
|Mechanism of action:||Exenatide is a functional analog of the human incretin Glucagon-Like Peptide-1 (GLP-1). Incretins enhance glucose-dependent insulin secretion and exhibit other antihyperglycemic actions following their release into the circulation from the gut. The GLP-1 system increases insulin secretion only in the presence of elevated plasma glucose levels, avoiding inappropriately high insulin levels during fasting. The drug also moderates peak serum glucagon levels during hyperglycemic periods following meals, but does not interfere with glucagon release in response to hypoglycemia. Secondary effects of drug administration reduces the rate of gastric emptying and decreases food intake, mitigating the potential severity of hyperglycemic events after meals.|
|Affected organisms:||Humans and other mammals|
|Targets:||Target 1. Glucagon-like peptide 1 receptor; Enzyme 1. Serum albumin|
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