Lanreotide

Warning

H361 (100%): Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

P203, P280, P318, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 12 reports by companies from 1 notifications to the ECHA C&L Inventory.

In preregistration studies of lanreotide, serum enzyme levels did not change appreciably and there were no reports of clinically apparent acute liver injury. Pooled analyses reported that there were no overall changes in serum ALT, AST or alkaline phosphatase levels during therapy or instances of clinically meaningful elevations with treatment. Prolonged therapy with lanreotide, as with other somatostatin analogues, was associated with a high rate of biliary sludge and cholelithiasis, probably due to inhibition of gall bladder contractility and decrease in bile secretion. In long term studies, cholelithiasis developed in 20% to 33% of lanreotide treated patients. In some instances, symptomatic cholecystitis occurred which can be accompanied by mild-to-moderate elevations in serum enzymes and bilirubin. However, most lanreotide associated gallstones were asymptomatic. Unlike octreotide, lanreotide and other long acting somatostatin analogues have not been liked to cases of clinically apparent liver injury, independent of cholelithiasis or biliary sludge, although they have had more limited use and have not been used in many of the clinical situations that were treated with octreotide (portal hypertension, variceal hemorrhage and infants with congenital hyperinsulinemia).

Drug-Induced Liver Injury Severity and Toxicity (DILIst)

H01CB03

H - Systemic hormonal preparations, excl. sex hormones and insulins

QH - Systemic hormonal preparations, excl. sex hormones and insulin

Lanreotide exhibits antisecretory effects through cAMP suppression, and activation of ion currents such as K+ and Ca2+ which leads to hyperpolarization of the membrane and inhibition of Ca2+ mediated depolarization. Furthermore, through direct and indirect mechanisms, Lanreotide has potent antiproliferative effects.

Lanreotide is a somatostatin analogue (SSA) and has mainly inhibitory effects which are mediated via somatostatin receptors (SSTRs) 2 and 5 and include inhibition of growth hormone release in the brain. Tumor SSTR activation induces downstream cell cycle arrest and/or apoptosis, and also results in blunted production of substances that support tumor growth as well as tumor angiogenesis. This leads to the anti-proliferative effects of Lanreotide.

0G3DE8943Y

LANREOTIDE

Established Pharmacologic Class [EPC] - Somatostatin Analog

Mechanisms of Action [MoA] - Somatostatin Receptor Agonists

Lanreotide is a Somatostatin Analog. The mechanism of action of lanreotide is as a Somatostatin Receptor Agonist.

Lanreotide forms a drug depot at the site of injection; therefore, there are 2 phases that describe the absorption of Lanreotide: 1. Initial rapid subcutaneous release during the first few days of treatment where drug that has not precipitated is rapidly absorbed. 2. Slow release of drug from the depot via passive diffusion. Absorption is independent of body weight, gender, and dosage.