Somatostatin (also known as growth hormone-inhibiting hormone) is a naturally-occurring peptide hormone that regulates the endocrine system. Somatostatin is produced in gastrointestinal (GI) tract, pancreas, hypothalamus, and central nervous system (CNS) and some other organs. Somatostatin is initially secreted as a 116 amino acid precursor, preprosomatostatin, which undergoes endoproteolytic cleavage to prosomastatin. Prosomastatin is further process into two active forms, shorter isoform somatostatin-14 works primarily in the brain, while the longer somatostatin-28 (SST-28) form operates in the GI tract. Somatostatin produces predominantly neuroendocrine inhibitory effects across multiple systems. It is known to inhibit GI, endocrine, exocrine, pancreatic, and pituitary secretions, as well as modify neurotransmission and memory formation in the CNS. Somatostatin binds to six different receptors in various systems and cells throughout the body to produce its regulatory effect. These receptors are specific to somatostatin and classify as G-protein coupled receptors (GPCR). Somatostatin half-life is between 1 to 3 minutes. Due to its short half-life, somatostatin has been formulated exogenously in much more stable forms with a longer half-life; this allows for its primary clinical use, which is the treatment of neuroendocrine tumors.

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.

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.