Lanreotide
approvedAlso known as: Somatuline, BIM 23014
**Mechanism of Action** Lanreotide is a synthetic somatostatin analog with high affinity for somatostatin receptor subtypes 2 (SSTR2) and 5 (SSTR5). By activating these G-protein-coupled receptors, it inhibits adenylate cyclase activity, reducing cyclic AMP levels and suppressing the secretion of growth hormone (GH), insulin-like growth factor 1 (IGF-1), and various neuroendocrine hormones (e.g., serotonin, gastrin, vasoactive intestinal peptide). Its depot formulation provides sustained release, enabling prolonged receptor occupancy and downstream inhibition of tumor growth and hormone hypersecretion. **Key Research Findings** Clinical trials (e.g., the ELECT and CLARINET studies) demonstrated that lanreotide significantly reduces GH and IGF-1 levels in acromegaly, achieving biochemical control in ~50–60% of patients. In gastroenteropancreatic neuroendocrine tumors (GEP-NETs), the CLARINET trial (N=204) showed a 53% reduction in the risk of disease progression versus placebo (median progression-free survival not reached vs. 18 months). Additional studies confirm its efficacy in controlling carcinoid syndrome symptoms and improving quality of life, with a safety profile dominated by transient gastrointestinal effects and gallstone formation. **Clinical Relevance** Lanreotide is a first-line therapy for acromegaly and a standard treatment for unresectable, well-differentiated GEP-NETs. Its long-acting formulation (administered every 4 weeks) improves patient adherence compared to daily injections. It is also used off-label for other neuroendocrine tumors and polycystic liver disease. Ongoing research explores its role in combination therapies and earlier disease stages. For research purposes only — not medical advice.
Key data
C54H69N11O10S2Research & studies
Lanreotide did not slow measured GFR decline in stage 2/3 ADPKD over three years.; A creatinine-based eGFR signal was not replicated by cystatin C or urinary creatinine clearance.; Gastrointestinal adverse events and hypoglycemia were more frequent with lanreotide.; Kidney events and quality-of-life scores were similar between treatment arms.
Octreotide showed a strong association with necrotizing enterocolitis in neonates.; Pasireotide was significantly linked to acute pancreatitis and glucose metabolism disorders.; Elevated risks of liver and biliary tract infections were identified for somatostatin analogs.; Gastrointestinal and hepatobiliary adverse events were prominent across all three drugs.
High-resolution cryo-EM structures of SSTR1 with lanreotide and pasireotide were solved.; Each ligand induces unique conformational changes in the SSTR1 orthosteric pocket.; Comparative analysis highlights subtle differences in SSTR1 activation by the two analogs.; Insights support development of next-generation SSTR1-targeted therapies with enhanced selectivity and reduced side effects.
Pasireotide reduced tumor volume in all six patients with large, T2-hyperintense, sparsely granulated tumors.; GH and IGF-1 levels improved, and visual field defects normalized in all patients.; Hyperglycemia occurred, requiring antidiabetic treatment in two patients.; Pasireotide is effective as first-line therapy for selected acromegaly patients likely resistant to first-generation SRLs.
Objective response rate was low: one partial response among GI-NETs and none in pancreatic NETs.; GI-NETs had a clinical benefit rate of 50%, median PFS of 8.5 months, and median OS of 32.7 months; pancreatic NETs had 0% CBR, PFS of 2.7 months, and OS of 23.9 months.; Neither PD-L1 expression nor tumor-infiltrating lymphocytes correlated with response or clinical benefit.; Clinical benefit was associated with on-treatment effector memory T cell activation, while progressive disease was associated with baseline regulatory T cell activation.
Frequently asked questions
What is Lanreotide?
**Mechanism of Action** Lanreotide is a synthetic somatostatin analog with high affinity for somatostatin receptor subtypes 2 (SSTR2) and 5 (SSTR5). By activating these G-protein-coupled receptors, it inhibits adenylate cyclase activity, reducing cyclic AMP levels and suppressing the secretion of growth hormone (GH), i
How does Lanreotide work?
Depot somatostatin analog inhibiting GH/IGF-1 and neuroendocrine secretion; approved for acromegaly and GEP-NETs.
What is the research status of Lanreotide?
Lanreotide is currently classified as approved, with 1,231 research references on record. This is for research purposes only and is not medical advice.
What is the molecular weight of Lanreotide?
Lanreotide has a molecular weight of approximately 1096.3 g/mol (formula C54H69N11O10S2).
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