Pramlintide

CAS No.: 151126-32-8
Molecular Formula: C171H267N51O53S2
Molecular Weight: 3949.44
Appearance: White Powder
Purity (HPLC): ≥98.0%

Function
1. Delays gastric emptying:
Slows the rate at which food moves from the stomach to the small intestine, thereby delaying postprandial glucose absorption and lowering peak postprandial blood glucose levels.
2. Inhibits glucagon secretion:
Suppresses glucagon secretion by pancreatic alpha cells after meals, reduces hepatic glucose output, and prevents excessive rises in blood glucose.
3. Increases satiety:
Acts on the central nervous system to generate signals of fullness and reduce food intake, aiding in weight management.

Description About Pramlintide
Pramlintide is the first non-insulin glucose-lowering drug approved by the FDA for use in patients with type 1 and type 2 diabetes as an adjunct to mealtime insulin to improve glycemic control.
Pramlintide is a synthetic amylin analog peptide designed to regulate glucose metabolism and appetite pathways. By mimicking endogenous amylin activity, pramlintide supports post-meal glucose control, delayed gastric emptying, and satiety signaling. It is widely researched in diabetes treatment, metabolic regulation, and peptide-based therapeutic development.
In the treatment of diabetes, pramlintide plays a pivotal regulatory role by mimicking the function of naturally occurring amylin. Co-secreted with insulin by pancreatic beta cells, amylin primarily acts to slow gastric emptying—thereby delaying intestinal glucose absorption—which helps mitigate sharp postprandial spikes in blood glucose levels. This mechanism makes pramlintide an effective tool for managing postprandial hyperglycemia, particularly for patients with type 1 or type 2 diabetes who rely on insulin therapy yet struggle to control blood glucose levels after meals. By reducing glycemic fluctuations, pramlintide also lowers the risk of hypoglycemic events and improves patients' quality of life.
Pramlintide functions by mimicking endogenous amylin; it binds to amylin receptors on cell membranes and activates downstream signaling pathways, thereby delaying gastric emptying, inhibiting glucagon secretion, and increasing satiety, ultimately resulting in lowered postprandial blood glucose levels and weight loss.