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Glucagon (Porcine glucagon) is a peptide hormone, produced by pancreatic α-cells. Glucagon stimulates gluconeogenesis. Glucagon decreases the activity of HNF-4. Glucagon increases HNF4α phosphorylation.
Teduglutide is a polypeptide consisting of 33 amino acids. It is glucagon-like peptide-2 (GLP-2) analogue that is used for the treatment of short bowel syndrome.
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.
Alarelin acetate is a synthetic LH-RH agonist, and stimulates the release of FSH and LH from the pituitary gland. It is known for its induction of ovulation and used to treat endmometriosis.
Fertirelin 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.
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.
Deslorelin acetate is an injectable gonadotropin releasing hormone super-agonist (GnRH agonist) also known as an LHRH agonist. It stops the production of sex hormones (testosterone and oestrogen).
Angiotensin II is an octapeptide that produced from angiotensin I after the removal of two amino acids at the C-terminal by angiotensin-converting enzyme (ACE). Angiotensin II is mediated by AT1 and AT2 receptors, which are seven transmembrane glycoproteins with 30% sequence similarity.
Terlipressin is a synthetic triglycyllysine derivative of vasopressin with vasoconstrictive, antihemorrhagic, and antidiuretic properties. Upon intravenous administration, terlipressin, an inactive prodrug, is biotransformed to its active moiety, lysine vasopressin (LVP), a nonselective vasopressin analogue with affinity for vasopressin receptors V1 (V1a), V2 and V3 (V1b). As a V1 agonist, terlipressin increases systemic vascular resistance, particularly in the splanchnic area, resulting in a decrease of portal pressure. V1 binding also promotes platelet aggregation and glycogenolysis, while V3 binding induces adrenocorticotropic hormone (ACTH) secretion. Compared to vasopressin, terlipressin has a minimal effect on V2 receptors, which are responsible for promotion of water reabsorption in the collecting ducts of the kidney via stimulation of cyclic AMP production.