Lanreotide is a medication used in the management of acromegaly and symptoms caused by neuroendocrine tumors, most notably carcinoid syndrome. It is a long-acting analog of somatostatin. It is available in several countries, including the United Kingdom, Australia and Canada, and was approved for sale in the United States by the Food and Drug Administration on August 30, 2007. Lanreotide was developed in the lab of Dr. David H. Coy, School of Medicine. Dr. Coy serves as Director of the Peptide Laboratory. Lanreotide (as lanreotide acetate) is manufactured by Ipsen, and marketed under the trade name Somatuline. The mechanism of action of lanreotide is believed to be similar to that of natural somatostatin. Lanreotide has a high affinity for human somatostatin receptors (SSTR) 2 and 5 and a reduced binding affinity for human SSTR1, 3, and 4. Activity at human SSTR 2 and 5 is the primary mechanism believed responsible for GH inhibition. Like somatostatin, lanreotide is an inhibitor of various endocrine, neuroendocrine, exocrine and paracrine functions. Lanreotide inhibits the basal secretion of motilin, gastric inhibitory peptide and pancreatic polypeptide, but has no significant effect on the secretion of secretin. Lanreotide inhibits postprandial secretion of pancreatic polypeptide, gastrin and cholecystokinin (CCK). In healthy subjects, lanreotide produces a reduction and a delay in post-prandial insulin secretion, resulting in transient, mild glucose intolerance.

Exenatide (exendin-4) is sold under the brand name BYETTA to improve glycemic control in people with type 2 diabetes mellitus. Exenatide is a glucagon-like peptide 1 (GLP-1) receptor agonist that enhances glucose-dependent insulin secretion by the pancreatic beta cell, suppresses inappropriately elevated glucagon secretion, and slows gastric emptying. The drug also moderates peak serum glucagon levels during hyperglycemic periods following meals but does not interfere with glucagon release in response to hypoglycemia.

Pramlintide is an analog of human amylin. Amylin is co-secreted with insulin from pancreatic beta cells and acts centrally to slow gastric emptying, suppress postprandial glucagon secretion, and decrease food intake. These actions complement those of insulin to regulate blood glucose concentrations. Amylin is relatively deficient in patients with type 2 diabetes, depending on the severity of beta-cell secretory failure, and is essentially absent in patients with type 1 diabetes. Through mechanisms similar to those of amylin, pramlintide improves overall glycemic control, reduces postprandial glucose levels, and reduces bodyweight in patients with diabetes using mealtime insulin. SYMLIN® (pramlintide acetate) is indicated for patients with type 1 or type 2 diabetes who use mealtime insulin and have failed to achieve desired glycemic control despite optimal insulin therapy.

Insulin detemir, a long-acting human insulin analog, is sold under the brand name LEVEMIR to improve glycemic control in adults and children with diabetes mellitus. Insulin detemir binds to the insulin receptor. Receptor-bound insulin lowers blood glucose by facilitating cellular uptake of glucose into skeletal muscle and adipose tissue and by inhibiting the output of glucose from the liver. The primary activity of insulin detemir is the regulation of glucose metabolism. Insulin detemir crosses the BBB and reduces food intake, it improves weight management by an enhanced and prolonged centrally mediated reduction of energy intake.

Human secretin is a gastrointestinal peptide hormone that regulates secretions in the stomach, pancreas, and liver. Synthetic human secretin displays equivalent biological activity and properties as naturally occurring secretin. Acetate salt of synthetic secretin was marketed under the name ChiRhoStim. ChiRhoStim is indicated for the stimulation of pancreatic secretions, including bicarbonate, to aid in the diagnosis of pancreatic exocrine dysfunction, for the gastrin secretion to aid in the diagnosis of gastrinoma. ChiRhoStim is also used for the pancreatic secretions to facilitate the identification of the ampulla of Vater and accessory papilla during endoscopic, retrograde cholangiopancreatography (ERCP). When secretin binds to secretin receptors on pancreatic duct cells it opens cystic fibrosis transmembrane conductance regulator (CFTR) channels, leading to secretion of bicarbonate-rich-pancreatic fluid.

Ziconotide (PRIALT; SNX-111) is a neuroactive peptide, which was approved by FDA in 2004 for the management of severe chronic pain in adult patients for whom intrathecal therapy is warranted, and who are intolerant of or refractory to other treatment, such as systemic analgesics, adjunctive therapies, or intrathecal morphine. Ziconotide acts as a selective N-type voltage-gated calcium channel blocker, which leads to a blockade of excitatory neurotransmitter release from the primary afferent nerve terminals.

Secretin porcine stimulates pancreatic and gastric secretions to aid in the diagnosis of pancreatic exocrine dysfunction and the diagnosis of gastrinoma. Porcine Secretin for Injection administered intravenously stimulates gastrin release in patients with gastrinoma whereas only small changes in serum gastrin concentrations occur in healthy subjects and patients with peptic ulcer disease. The primary action of secretin is to stimulate pancreatic ductal cells to secrete pancreas fluid in large volumes that contain bicarbonate. Secretin is a hormone that is normally released from the duodenum upon exposure of the proximal intestinal lumen to gastric acid, fatty acids, and amino acids. Secretin is released from enterochromaffin cells in the intestinal mucosa. Secretin receptors have been identified in the pancreas, stomach, liver, colon, brain and other tissues. When secretin binds to secretin receptors on pancreatic duct cells it opens cystic fibrosis transmembrane conductance regulator (CFTR) channels, leading to secretion of bicarbonate-rich pancreatic fluid. Secretin may also work through vagal-vagal neural pathways since stimulation of the efferent vagus nerve stimulates bicarbonate secretion and atropine blocks secretin-stimulated pancreatic secretion.