What Is Octreotide? The Somatostatin Analog Peptide for Acromegaly and Neuroendocrine Tumors, and What Its Trials Found

Octreotide is a synthetic peptide that copies the action of somatostatin, the hormone your body uses as an off switch for growth hormone, insulin, glucagon and many gut hormones, including the ones released by some tumors. Doctors use octreotide for three main jobs, which are keeping growth hormone in check in acromegaly, controlling the flushing and diarrhea of carcinoid syndrome, and treating the watery diarrhea caused by VIP secreting tumors. The FDA labels for octreotide list an initial U.S. approval in 1988, which makes it one of the oldest peptide drugs still in daily use.

Natural somatostatin makes a poor drug because your body breaks it down very quickly. Octreotide was engineered to resist that breakdown, so a single injection keeps working for hours, and the monthly depot form (Sandostatin LAR Depot) and an oral capsule (Mycapssa) stretch that effect further. If you have been reading about peptides for hormones and metabolism, octreotide is a useful reference point, because it shows what a fully tested, regulator approved peptide looks like. This article explains how octreotide works, what the key trials found in acromegaly and neuroendocrine tumors (NETs), how the drug is dosed and why gallstones are the side effect everyone watches for. It is educational content about published research, not medical advice.

Somatostatin is a hormone made in the brain, the pancreas and the gut that tells other glands to stop releasing their hormones. It slows growth hormone release from the pituitary, cuts insulin and glucagon output from the pancreas and quiets many of the digestive hormones that drive gut secretion and movement, and it does all of this through a family of somatostatin receptors found on normal cells and on many tumor cells.

The problem with somatostatin as a medicine is that it disappears from the blood within minutes, so it would need a continuous drip to be useful. Octreotide was built as a shorter, more stable peptide that keeps the part of somatostatin that binds the receptor while resisting the enzymes that break down the natural hormone. The first clinical report in carcinoid syndrome described it as a long acting analogue of somatostatin ([Kvols and colleagues, New England Journal of Medicine, 1986](https://doi.org/10.1056/NEJM198609113151102)), and that stability is what turned the off switch into a drug people could use at home.

Octreotide works by binding somatostatin receptors and telling the cell to hold back its hormone. In acromegaly, octreotide acts on the pituitary tumor that is overproducing growth hormone, which in turn lowers IGF-1, the liver hormone that drives most of the tissue growth seen in the disease. In neuroendocrine tumors, octreotide acts on tumor cells that carry somatostatin receptors and secrete substances such as serotonin, which cause flushing and diarrhea.

The same off switch explains most of the side effects. Because octreotide also quiets the gut and the pancreas, the label warns about diarrhea, abdominal pain, swings in blood sugar in either direction, a slower heart rate, thyroid changes, reduced vitamin B12 and, since a recent label update, steatorrhea (fatty stools) from poor fat absorption. Octreotide also slows the gallbladder, which is the root of the gallstone problem covered below.

Octreotide is FDA approved for acromegaly, for carcinoid syndrome symptoms and for VIPoma diarrhea. The [Sandostatin LAR Depot label](https://www.accessdata.fda.gov/drugsatfda_docs/label/2024/021008s049lbl.pdf) lists these three uses, and the [Mycapssa label](https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/208232s000lbl.pdf) covers the oral capsule, which is approved for acromegaly maintenance only.

The label adds an important limit. For carcinoid syndrome and VIPomas, it states that the effect of octreotide "on tumor size, rate of growth and development of metastases, has not been determined." That sentence matters because the PROMID trial, covered below, did study tumor growth, which means the label approval is for symptom control while the tumor growth evidence sits in the published trial literature.

Octreotide belongs to a wider group of peptide drugs that mimic or block a hormone signal, such as the bone building peptides in our [teriparatide and abaloparatide explainer](/articles/teriparatide-abaloparatide-bone-building-peptides) and the amylin analog in our [pramlintide article](/articles/pramlintide-symlin-amylin-analog).

Octreotide does control carcinoid syndrome symptoms, and it has done so since its earliest clinical studies. In the study by Kvols and colleagues ([New England Journal of Medicine, 1986](https://doi.org/10.1056/NEJM198609113151102)), 25 patients with metastatic carcinoid tumors and carcinoid syndrome injected octreotide 150 micrograms under the skin three times daily, and flushing and diarrhea were promptly relieved in 22 of them.

The Kvols study also measured urinary 5-HIAA, a breakdown product of serotonin that tracks how much hormone the tumor is releasing. Eighteen of the 25 patients (72 percent) had a decrease of 50 percent or more in urinary 5-HIAA, and the median duration of that biochemical response was more than 12 months. Because the study had no placebo group, it shows a strong signal rather than a controlled comparison, but the effect was large enough that octreotide became standard symptom control.

The PROMID trial showed that octreotide LAR slows the growth of metastatic midgut neuroendocrine tumors. PROMID ([Rinke and the PROMID Study Group, Journal of Clinical Oncology, 2009](https://doi.org/10.1200/JCO.2009.22.8510)) was a placebo controlled, double blind trial in 85 previously untreated patients with well differentiated metastatic midgut NETs, who received octreotide LAR 30 mg into the muscle once a month or placebo until the tumor progressed or the patient died.

Median time to tumor progression was 14.3 months with octreotide LAR and 6 months with placebo, a hazard ratio of 0.34. After 6 months, stable disease was seen in 66.7% of the octreotide group and 37.2% of the placebo group. Tumors that secreted hormones and tumors that did not responded in a similar way, and the best results were seen in patients with a low tumor load in the liver.

A survival benefit was not clearly shown. The long term PROMID follow up ([Rinke and colleagues, Neuroendocrinology, 2017](https://doi.org/10.1159/000443612)) found median overall survival of 84.7 months with octreotide and 83.7 months with placebo, a hazard ratio of 0.83 that was not statistically significant (p = 0.51). The comparison was blurred because 38 of 43 placebo patients (88.4%) switched to octreotide LAR once their disease progressed.

Tumor burden mattered more than the starting arm, since median overall survival was 107.6 months in the low tumor load group (n = 64) and 57.5 months in the high tumor load group (n = 21). The fair reading of PROMID is that octreotide clearly delays tumor progression, while any survival benefit could not be shown because almost everyone ended up on the drug.

Octreotide and its sister drug lanreotide control growth hormone and IGF-1 in roughly half of patients with acromegaly across the published trials. The largest meta analysis ([Carmichael and colleagues, Journal of Clinical Endocrinology and Metabolism, 2014](https://doi.org/10.1210/jc.2013-3757)) pooled trials published from 1974 to 2012 with 4464 patients enrolled, and overall control rates were 56% for mean growth hormone and 55% for IGF-1 normalization.

An earlier meta analysis of 44 trials ([Freda and colleagues, Journal of Clinical Endocrinology and Metabolism, 2005](https://doi.org/10.1210/jc.2005-0260)) found that the overall rate of tumor increase on long acting somatostatin analogs was 1.4%, and that octreotide LAR outperformed the older lanreotide formulation in patients who had not been preselected for a good response. The practical lesson from both analyses is that octreotide works well for many people with acromegaly but not for everyone, which is why the label ties dose changes to measured growth hormone and IGF-1 levels.

Octreotide can be taken by mouth, but only by one group of patients. Oral octreotide capsules (Mycapssa) are approved for long term maintenance in acromegaly patients who have responded to and tolerated octreotide or lanreotide injections, according to the [Mycapssa label](https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/208232s000lbl.pdf). Peptides are normally destroyed in the gut, so the capsule uses a delayed release design and must be taken on an empty stomach, at least 1 hour before a meal or at least 2 hours after.

The CHIASMA OPTIMAL trial ([Samson and colleagues, Journal of Clinical Endocrinology and Metabolism, 2020](https://doi.org/10.1210/clinem/dgaa526)) tested whether people already controlled on injections stayed controlled after switching to capsules. In that trial, 56 patients were randomly assigned to oral octreotide or placebo for 36 weeks, and IGF-1 normalization was maintained in 58.2% on oral octreotide versus 19.4% on placebo, while growth hormone stayed below 2.5 ng/mL in 77.7% versus 30.4%.

On placebo, the median time to losing IGF-1 control was 16 weeks, while on capsules it was not reached during the trial, and 75% of the oral group finished on oral therapy. The capsule result is a maintenance result, which means it shows that people who already respond to injections can often stay controlled on a pill, not that the pill works as a first treatment. For a broader look at how oral peptide drugs get past the gut, see our guide to [oral versus injectable peptides](/articles/oral-vs-injectable-peptides).

Octreotide dosing depends on the formulation and the condition. The monthly depot is injected into the gluteal muscle by a trained healthcare provider at 4 week intervals, the label states that intervals longer than 4 weeks are not recommended, and the depot comes in 10 mg, 20 mg and 30 mg strengths.

The label says depot doses higher than 40 mg are not recommended. Patients usually start on the short acting injection first, to confirm that octreotide works and is tolerated, before switching to the monthly depot. Octreotide is a prescription medicine managed by endocrinologists and oncologists, and it is not a peptide for self directed protocols.

The most common side effects of octreotide are gut related. In pooled phase 3 acromegaly studies of 261 patients on Sandostatin LAR Depot, the [Sandostatin LAR Depot label](https://www.accessdata.fda.gov/drugsatfda_docs/label/2024/021008s049lbl.pdf) lists diarrhea in 35.6%, abdominal pain in 28.7%, flatulence in 25.3%, constipation in 17.6%, headache in 15.3%, injection site pain in 13.8% and cholelithiasis (gallstones) in 13.4%.

The label's warnings also cover blood sugar changes in either direction, hypothyroidism, bradycardia and other heart rhythm changes, reduced vitamin B12 levels and new onset steatorrhea. If you have diabetes, your glucose lowering medicines may need to be adjusted while you take octreotide.

Octreotide causes gallstones because it slows the gallbladder. The Sandostatin LAR label states that octreotide "may inhibit gallbladder contractility and decrease bile secretion, which may lead to gallbladder abnormalities or sludge," and lists postmarketing reports of complications including cholecystitis, cholangitis and pancreatitis. Bile that sits still in the gallbladder becomes concentrated and forms sludge and stones.

The rate depends on the population and the dose. In a phase 4 study of previously untreated acromegaly patients, the label reports cholelithiasis in 38.2% of people on octreotide LAR (N = 76) versus 4.7% after pituitary surgery (N = 64). In an older review of 44 NET patients on chronic injections under the skin ([Trendle and colleagues, Cancer, 1997](https://pubmed.ncbi.nlm.nih.gov/9024721/)), gallstones and/or sludge developed in 52.3%, and 3 of 44 (6.8%) needed emergency gallbladder removal. The incidence was 35.3% at 150 micrograms three times daily and 61.9% at 500 micrograms three times daily.

The Trendle authors concluded that although most patients developed gallstones, a much smaller share had symptoms, and that routine preventive gallbladder removal was not indicated except during other abdominal surgery. The label advises periodic monitoring and stopping octreotide if gallstone complications are suspected. A similar gallbladder story shows up with rapid weight loss on GLP-1 drugs, which we cover in our [GLP-1 and gallstones article](/articles/glp-1-gallbladder-gallstones-rapid-weight-loss).

Octreotide is a well tested peptide drug with clear, narrow purposes. It reliably quiets the hormone excess of acromegaly and carcinoid syndrome, it delayed tumor progression in PROMID, and an oral capsule now lets some acromegaly patients who already respond to injections stay controlled on a pill. Its costs are equally clear, with gut side effects, blood sugar shifts and a high rate of gallstones that calls for periodic monitoring.

If you are curious about octreotide because of a diagnosis, the right next step is a conversation with an endocrinologist or oncologist who can match the formulation and dose to your lab results. If you came across it in wellness circles, it is worth knowing that octreotide is a hormone suppressing medicine for specific diseases and has no role in weight loss or antiaging routines.