LANREOTIDE IS AN OCTAPEPTIDE ANALOG OF NATURAL SOMATOSTATIN. 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.
THE PRIMARY PHARMACODYNAMIC EFFECT OF LANREOTIDE IS A REDUCTION OF GH AND/OR IGF-1 LEVELS ENABLING NORMALIZATION OF LEVELS IN ACROMEGALIC PATIENTS. 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 INHIBITS MEAL-STIMULATED PANCREATIC SECRETIONS, AND REDUCES DUODENAL BICARBONATE AND AMYLASE CONCENTRATIONS, AND PRODUCES A TRANSIENT REDUCTION IN GASTRIC ACIDITY.