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Vasopressin, also known as arginine vasopressin (AVP), antidiuretic hormone (ADH), or argipressin, is a neurohypophysial hormone found in most mammals. Its two primary functions are to retain water in the body and to constrict blood vessels.
Pramlintide is an analogue of amylin, a small peptide hormone that is released into the bloodstream by the β-cells of the pancreas along with insulin, after a meal. Like insulin, amylin is completely absent in individuals with Type I diabetes.
Glucagon-like peptide-1 (GLP-1) is an incretin derived from the transcription product of the proglucagon gene. The major source of GLP-1 in the body is the intestinal L cell that secretes GLP-2 as a gut hormone.
Antide acetate (Ac-AA10-NH2) is an LHRH antagonist and represses LH and FSH release from the pituitary gland. It shows a high antiovulatory activity and releases negligible histamine.
Enfuvirtide is a 36 amino acid peptide corresponding to a region of gp41, the transmembrane subunit of HIV-1 envelope protein. It belongs to the therapeutic class of fusion inhibitors and acts by binding to gp41 and impeding the conformational changes in gp41 necessary for fusion of the virus with the cell.
Aviptadil, also known as vasoactive intestinal polypeptide (VIP), is a 28 amino acid neuropeptide that belongs to the glucagon-growth hormone-releasing factor secretion superfamily. Aviptadil acts as a potent systemic vasodilator and bronchodilator. It inhibits the proliferation of vascular and bronchial smooth muscle cells and decreases platelet aggregation. These biological effects are mediated by specific VIP receptors.
Histrelin acetate is a potent LHRH agonist. After a transient increase, continuous administration results in downregulation of LH and FSH levels followed by a suppression of ovarian and testicular steroid biosynthesis.
Buserelin Acetate is an agonist of gonadotropin-releasing hormone receptor(GnRHR). Buserelin is a synthetic luteinizing hormone–releasing hormone (LHRH) analog.
A 39-amino acid peptide originally isolated from the salivary glands of the Gila monster (Heloderma suspectum), differs from exendin-3 only in two positions close to the N-terminus. Application of exenatide causes an increase in acinar cAMP without stimulating amylase release. As an incretin mimetic, exenatide acts as agonist of the glucagon-like peptide-1 (GLP-1) receptor.