Octreotide

Sandostatin, Sandostatin LAR Depot, Mycapssa (oral), Bynfezia Pen, SMS 201-995, octreotide acetate

Sexual health, hormones & signalling

Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates

Note on this profile. Octreotide is an approved prescription medicine used mainly in endocrinology and oncology, not a research-only compound. This page explains the published science. Community/self-directed use is essentially none documented, and the compound has no plausible place in body-composition or longevity protocols — its main metabolic effect is to suppress growth hormone and insulin.

Summary

Class: Synthetic cyclic octapeptide (8 amino acids, one disulfide bridge, D-amino acids and a reduced C-terminus) — a stabilised analogue of the natural 14-amino-acid hormone somatostatin
Mechanism: Activates somatostatin receptors (mainly SSTR2, also SSTR5) to switch off secretion of growth hormone, many gut hormones and tumour peptides, and to slow gut motility and splanchnic blood flow
Routes studied: Subcutaneous injection 2–4 times daily (Sandostatin); intravenous infusion (hospital); intramuscular depot every 4 weeks (Sandostatin LAR); oral delayed-release capsules (Mycapssa); radiolabelled forms for imaging
Half-life: ~1.7–1.9 h subcutaneous (versus ~2–3 min for natural somatostatin); LAR releases over ~4 weeks with steady state after 3 injections; oral ~2–3 h
Storage: Ampoules/vials: refrigerate 2–8 °C, protect from light; may be at room temperature for up to 14 days. LAR kit: refrigerate, bring to room temperature 30–60 min before mixing. Mycapssa capsules: room temperature
Regulatory status: Approved medicine worldwide (US 1988 SC; 1998 LAR; 2020 oral). Multiple generics

Doses are as reported in studies or by the community — never recommendations.

1What it is

Somatostatin is a 14-amino-acid hormone discovered in 1973 in the hypothalamus, where it blocks growth hormone release. It is also made throughout the gut and pancreas, where it acts as a general "off switch" for hormone secretion and digestion. The natural hormone lasts only a couple of minutes in blood, which makes it useless as a drug. Octreotide, developed by Sandoz in the early 1980s, keeps the four amino acids somatostatin needs to bind its receptor and wraps them in a protected ring, extending the action to hours. It was approved in the US in 1988.

It is one of the most important peptide drugs in medicine: the standard treatment for acromegaly (growth hormone excess) when surgery fails, the standard symptom control for hormone-secreting neuroendocrine tumours, and an off-label workhorse for bleeding oesophageal varices, high-output fistulas, dumping syndrome and sulfonylurea overdose. A radioactively tagged version (octreoscan, and the later DOTATATE agents) is how neuroendocrine tumours are imaged, and the related radioligand lutetium-177 DOTATATE is a treatment.

2How it's thought to work

Octreotide binds SSTR2 strongly, SSTR5 moderately and SSTR3 weakly, with little activity at SSTR1 and SSTR4. Pituitary GH-secreting tumours and most well-differentiated neuroendocrine tumours express SSTR2 densely, which is why they respond.

Receptor activation lowers cAMP and calcium entry in secretory cells, suppressing release of GH, TSH, insulin, glucagon, gastrin, VIP, serotonin, secretin and others.

It reduces splanchnic (gut) blood flow, lowering portal pressure — the basis for use in variceal bleeding.

It slows gastric emptying and intestinal transit and reduces fluid secretion, which helps secretory diarrhoea but also causes steatorrhoea and gallbladder stasis.

In some tumours it has a direct anti-proliferative effect via SSTR2 signalling and indirectly via lowered IGF-1.

Somatostatin receptor activation on a secretory cell, mainly the SSTR2 subtype. The receptor lowers cAMP and calcium entry, and the granules of growth hormone, insulin, glucagon, gastrin and VIP stay where they are.Schematic — not to scale

3What the research shows

Acromegaly

Decades of trials show biochemical control (normal IGF-1 and GH <2.5 µg/L) in roughly 40–60% of patients, with tumour shrinkage in a majority, depending on selection (Freda 2005 meta-analysis, J Clin Endocrinol Metab; Melmed 2018 consensus, Nat Rev Endocrinol). Oral octreotide (Mycapssa) maintained control in 58% vs 19% on placebo in patients previously controlled on injectables in the MPOWERED/CH-ACM-01 programme (Samson 2020, J Clin Endocrinol Metab; Fleseriu 2022, Lancet Diabetes Endocrinol). [4][5][8]

Graded A/B

Carcinoid syndrome symptom control

Flushing and diarrhoea improve in 60–80% of patients (Kvols 1986, NEJM, the original 25-patient series; many since). LAR is the standard first-line therapy. [2]

Anti-proliferative effect in neuroendocrine tumours

PROMID (n=85 with metastatic midgut NETs) found octreotide LAR 30 mg every 4 weeks lengthened time to tumour progression from 6.0 to 14.3 months vs placebo (HR 0.34) (Rinke 2009, J Clin Oncol). Lanreotide's CLARINET (profile 125) extended this to pancreatic and other GEP-NETs. [3]

Graded A (meta-analyses)

Variceal bleeding

Octreotide infusion plus endoscopic therapy improves initial haemostasis and reduces rebleeding compared with endoscopy alone, with no clear mortality effect (Corley 2001 meta-analysis, Gastroenterology). [6]

Sulfonylurea overdose, dumping syndrome, hyperinsulinism, chylothorax, high-output fistulas

Case series and small trials support each; all off-label. In sulfonylurea poisoning, octreotide reliably suppresses insulin release and reduces dextrose requirements (Fasano 2008, Ann Emerg Med ). [7]

Graded B/A

Diabetic retinopathy, polycystic liver and kidney disease, TSH-secreting adenomas

Mixed or modest. Somatostatin analogues slow liver volume growth in polycystic liver disease (Hogan 2010, J Am Soc Nephrol).

4Reported side effects and interactions

Literature-reported

gastrointestinal effects dominate — diarrhoea, loose fatty stools, abdominal cramps, nausea and bloating (30–60% early, usually easing over weeks). Gallstones or biliary sludge develop in up to half of long-term users, mostly asymptomatic. Blood glucose can go either way: it suppresses insulin (hyperglycaemia) and also glucagon and GH (hypoglycaemia), so people with diabetes need close monitoring early. Bradycardia and conduction changes; hypothyroidism from TSH suppression; vitamin B12 deficiency with long use; hair thinning; injection-site pain (LAR especially). Pancreatitis rare. Oral form adds headache and more GI effects.

Community-reported

none documented.

Theoretical. chronic GH/IGF-1 suppression in someone without GH excess would be expected to lower lean mass and bone density over time; this is why the compound has no rational enhancement use.

Interactions. reduces cyclosporine absorption (transplant rejection reported); increases bromocriptine bioavailability; slows absorption of many oral drugs; insulin and oral hypoglycaemic doses often need reduction; additive bradycardia with beta-blockers and calcium-channel blockers; QT-prolonging drugs (modest QT effect); reduced clearance of drugs metabolised by CYP3A4 is possible via GH suppression.

Markers researchers commonly monitor

Per label and endocrine/oncology practice:

Marker	Why it's watched
IGF-1 and GH (random or post-glucose)	the targets in acromegaly; also show whether a non-acromegalic person's GH axis is being suppressed.
Fasting glucose and HbA1c	glucose can rise or fall; checked at baseline and within the first weeks.
TSH and free T4	TSH suppression can cause hypothyroidism over months.
Gallbladder ultrasound	at baseline and periodically (every 6–12 months) in long-term users.
Vitamin B12	long-term use reduces absorption.
Resting heart rate and ECG	bradycardia and modest QT effects.
Chromogranin A, urinary 5-HIAA, and imaging	in neuroendocrine tumour patients, to track disease rather than drug effect.
Faecal fat / weight and nutritional status	steatorrhoea and malabsorption with chronic use.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Short-acting octreotide is a ready-to-use solution (50, 100, 500 µg/mL; 200 and 1,000 µg/mL multi-dose vials) — no . The LAR depot is a microsphere powder that must be suspended with the supplied immediately before deep (gluteal) injection, by a trained person, following the kit instructions exactly; it cannot be given subcutaneously or intravenously. Mycapssa capsules are taken on an empty stomach, at least 1 h before or 2 h after food. The calculator is not applicable.

6Commonly studied alongside

Lanreotide (profile 125) and pasireotide (profile 126), the other somatostatin analogues; pegvisomant (GH-receptor blocker, combined in resistant acromegaly); cabergoline; lutetium-177 DOTATATE and everolimus in neuroendocrine tumours; terlipressin and endoscopic therapy in variceal bleeding. Relevant context in this library: growth hormone secretagogues (Ipamorelin, CJC-1295, sermorelin, tesamorelin) do the opposite of octreotide at the GH axis.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	FDA-approved: Sandostatin (1988), Sandostatin LAR (1998), Bynfezia pen (2020), Mycapssa oral (June 2020, for acromegaly in patients controlled on injectables); generics of the injection and LAR
European Union	EMA/national authorisations for Sandostatin and Sandostatin LAR; Mycapssa approved by the European Commission in 2022 for acromegaly †
United Kingdom	MHRA-licensed; prescription-only; NHS use for acromegaly, NETs and variceal bleeding
Australia	TGA-registered; PBS-listed for acromegaly and NETs
South Africa	SAHPRA-registered; prescription-only
Sport	Not on the WADA Prohibited List (it lowers GH rather than raising it)

8Open questions

Which patients respond: SSTR2 expression predicts response but is not routinely measured before treatment.
Optimal interval extension (6–8 weeks) for stable patients on depot forms.
Whether oral octreotide can fully replace injections across the acromegaly population rather than only in pre-controlled patients.

9References

1Bauer W et al. (1982). SMS 201-995: a very potent and selective octapeptide analogue of somatostatin with prolonged action. Life Sci. PubMed · DOI
2Kvols LK et al. (1986). Treatment of the malignant carcinoid syndrome: evaluation of a long-acting somatostatin analogue. NEJM. PubMed · DOI
3Rinke A et al. (2009). Placebo-controlled, double-blind, prospective, randomized study on the effect of octreotide LAR in the control of tumor growth in patients with metastatic neuroendocrine midgut tumors (PROMID). J Clin Oncol. PubMed · DOI
4Freda PU et al. (2005). Long-acting somatostatin analog therapy of acromegaly: a meta-analysis. J Clin Endocrinol Metab. PubMed · DOI
5Fleseriu M et al. (2022). Maintenance of response to oral octreotide compared with injectable somatostatin receptor ligands in patients with acromegaly (MPOWERED). Lancet Diabetes Endocrinol. PubMed
6Corley DA et al. (2001). Octreotide for acute esophageal variceal bleeding: a meta-analysis. Gastroenterology. PubMed · DOI
7Fasano CJ et al. (2008). Comparison of octreotide and standard therapy versus standard therapy alone for the treatment of sulfonylurea-induced hypoglycemia. Ann Emerg Med. PubMed · DOI
8Melmed S et al. (2018). A consensus statement on acromegaly therapeutic outcomes. Nat Rev Endocrinol. PubMed · DOI
9Novartis. Sandostatin / Sandostatin LAR Depot prescribing information; Chiesi/Amryt. Mycapssa prescribing information (current labels). PubMed

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

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11Page history

30 Oct 2026Profile published — awaiting medical review

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