Lanreotide (Somatuline)
General information
Class/mechanism: Octapeptide somatostatin analog which suppresses multiple endocrine, neuroendocrine, exocrine, and paracrine functions. Lanreotide binds with high affinity to somatostatin receptors (SSTR) 2 and 5, with lower binding affinity for SSTR1, SSTR3, and SSTR4. Binding to SSTR2 and SSTR5 is believed to cause growth hormone (GH) inhibition. Lanreotide also results in reduction of IGF-1 (somatomedin C), motilin, gastric inhibitory peptide, pancreatic polypeptide, gastrin, cholecystokinin (CCK), duodenal bicarbonate and amylase concentrations, gastric acidity, gallbladder contractility, bile secretion, glucagon, and prolactin. It also causes transient decreases in post-prandial insulin secretion and nocturnal release of thyroid-stimulating hormone (TSH).[1][2][3]
Route: SC
Extravasation: n/a
For conciseness and simplicity, HemOnc.org currently will focus on treatment regimens and not list information such as: renal/hepatic dose adjustments, metabolism (including CYP450), excretion, monitoring parameters (although this will be considered for checklists), or manufacturer. Instead, for the most current information, please refer to your preferred pharmacopeias such as Micromedex, Lexicomp, UpToDate (courtesy of Lexicomp), or the prescribing information.[1]
Diseases for which it is used
Patient drug information
- Some patient information is available at the Somatuline manufacturer's website[3]
- Lanreotide (Somatuline) patient drug information (UpToDate)[4]
History of changes in FDA indication
- 8/30/2007: FDA approved for "the long-term treatment of acromegalic patients who have had an inadequate response to or cannot be treated with surgery and/or radiotherapy."[1]
Also known as
Ipstyl, Lanreotide, Lanreotide Acetate, lanreotide injection, Somatuline Autogel, Somatuline Depot, Somatuline LA, Somatuline LP, Somatuline P.R, Somatuline PR.