Octreotide

Mechanism

Octreotide is a synthetic octapeptide (sequence: H-D-Phe-Cys-Phe-D-Trp-Lys-Thr-Cys-Thr-ol, with a disulphide bridge between the two Cys residues) that binds with high affinity to somatostatin receptor subtypes 2 (SSTR2) and 5 (SSTR5), and with lower affinity to SSTR3. These Gᵢ/o-coupled receptors are expressed on the cell surface of various endocrine and neuroendocrine cells. Upon binding, octreotide: (1) inhibits adenylate cyclase, reducing cAMP; (2) activates potassium channels, hyperpolarising the cell membrane; and (3) inhibits voltage-gated calcium channels, reducing intracellular calcium. The net effect is suppression of hormone and neurotransmitter release — including growth hormone, insulin, glucagon, gastrin, vasoactive intestinal peptide (VIP), and serotonin. In acromegaly, octreotide suppresses GH secretion from pituitary somatotroph adenomas, thereby reducing hepatic IGF-1 production. In neuroendocrine tumours, it inhibits secretion of serotonin and other vasoactive amines responsible for carcinoid syndrome symptoms. The SSTR2 selectivity also enables radiolabelled octreotide analogues (e.g., ⁶⁸Ga-DOTATATE for imaging, ¹⁷⁷Lu-DOTATATE for therapy — PRRT) to target SSTR-expressing tumours.

Evidence base

Key Evidence

1. Acromegaly — meta-analysis: Freda PU, et al. Pituitary. 2009. Pooled data from 64 studies showed octreotide LAR normalised IGF-1 in ~55–70% of patients.

2. CLARINET trial (NETs): Caplin ME, et al. New England Journal of Medicine. 2014;371(3):224-233. Lanreotide (related SSTA) significantly prolonged PFS in enteropancreatic NETs (HR 0.47; 95% CI 0.30–0.73).

3. PROMID trial (midgut NETs): Rinke A, et al. Journal of Clinical Oncology. 2009;27(28):4656-4663. Octreotide LAR significantly prolonged time to tumour progression vs. placebo in well-differentiated midgut NETs.

4. Variceal bleeding: Seo YS, et al. Journal of Hepatology. 2014. Meta-analysis supporting vasoactive agents (including octreotide) as adjunctive therapy for acute variceal haemorrhage.

Regulatory Status

• FDA approval: 1988 (immediate-release); 1995 (LAR depot)
• EMA/MHRA: Licensed for acromegaly, NET symptom control, and other indications
• Generic formulations available

Protocols

Octreotide is supplied as a sterile injectable solution (not lyophilised powder):

• Immediate-release (Sandostatin): 50–100 µg subcutaneously, 2–3 times daily. Titrate based on clinical and biochemical response.
• Long-acting release (Sandostatin LAR): 10–30 mg intramuscularly every 4 weeks. Start at 20 mg; adjust based on IGF-1 and symptoms at 3-month intervals.

These details are for research documentation. Octreotide is a prescription-only medicine and is not available for self-directed research use. No research peptide vendor sells octreotide.

UK legal status

Octreotide is a prescription-only medicine (POM) in the UK under the Human Medicines Regulations 2012. It is not a controlled substance under the Misuse of Drugs Act. It is not legally available as a research chemical.

Key points:

• MHRA status: Licensed medicinal product (Sandostatin, Sandostatin LAR; Novartis)
• Prescription requirement: Requires a valid prescription from a registered medical practitioner, typically in endocrinology or oncology
• NHS availability: Widely available through the NHS for licensed indications
• Importation: Personal importation without a prescription is not legal

This compound is included in the Peptide Data knowledge base for educational completeness, given its significance as a somatostatin-pathway peptide. It is not available through any UK research peptide vendor.

Vendor notes

Octreotide is not available through any UK research peptide vendor. It is a licensed prescription medicine dispensed exclusively through pharmacies with a valid prescription. No vendor profile on Peptide Data lists octreotide, and none should.