Seglitide
One of the first small, long-acting somatostatin mimics: a six-amino-acid ring from Merck that suppressed growth hormone, insulin and glucagon far longer than the natural hormone, but was not developed to approval
Natural somatostatin shuts off growth hormone, insulin and glucagon, but it is gone from the blood in minutes, which makes it hard to use as a drug. In the early 1980s chemists at Merck shrank its active region into a stable six-amino-acid ring, cyclo(N-Me-Ala-Tyr-D-Trp-Lys-Val-Phe), and called it MK-678 (also L-363,586 and, later, seglitide). It was 50 to 100 times more potent than somatostatin and lasted far longer. Small studies gave it to people with diabetes and to human pituitary-tumour tissue, and it suppressed the same hormones for hours rather than minutes. It reached early clinical testing but was not taken to approval, and it is not a marketed medicine; the octapeptide octreotide, developed in parallel, became the somatostatin analogue that reached the clinic.
Used in human trials: 2, 5, 10 or 40 µg/hr, Continuous infusion, Intravenous (Type 1 diabetes, intravenous infusion) Details ↓
Recommended Dosing
Used in human trials
Typical range2–40 µg/hr · continuous infusion Human studyPMID 2872569compare across peptides →
No manufacturer dose exists for this use: these are amounts given in published trials, not recommendations.
What is it?
Somatostatin is the body's off-switch for several hormones. Released in the brain, the gut and the pancreas, it tells the pituitary to stop releasing growth hormone and tells the pancreatic islets to stop releasing insulin and glucagon. As a medicine it has one fatal flaw: enzymes clear it from the blood in about two minutes, so any effect needs a constant drip and vanishes the moment it stops. The search for a small, stable mimic that keeps somatostatin's actions but lasts longer is what produced this molecule.
Merck's chemists found that somatostatin's fourteen amino acids could be cut down to a ring of six while keeping the four residues that do the binding. The result, cyclo(N-Me-Ala-Tyr-D-Trp-Lys-Val-Phe), was reported in 1984 as a 'super active' analogue, 50 to 100 times more potent than somatostatin at inhibiting insulin, glucagon and growth-hormone release. Ring-closing and the unnatural N-methyl-alanine and D-tryptophan residues are what make it resist the enzymes, so its half-life in people is about three quarters of an hour rather than two minutes.
The clearest human data came from diabetes. Infused into the vein of people with type 1 diabetes at 10 micrograms an hour, the analogue suppressed the glucose, glucagon, growth-hormone and triglyceride rises after a meal about as well as natural somatostatin infused at twenty times that rate, and it cleared from the blood six times more slowly. Given into the nose at bedtime, a single dose blunted the overnight rise in growth hormone and the early-morning hyperglycaemia (the 'dawn phenomenon') that makes type 1 diabetes hard to control, which raised the idea of using it as an adjunct to insulin without an extra injection.
It also acted directly on the pituitary. On cells taken from human growth-hormone-secreting pituitary tumours, nanomolar concentrations of the analogue switched off both resting and stimulated growth-hormone release, much as somatostatin does, which is the action that makes somatostatin analogues a treatment for acromegaly. Animal work filled in the rest: in dogs it protected transplanted pancreas tissue by quieting its digestive secretions, and in diabetic-hypertensive rats an oral dose lowered blood pressure.
One finding is a reminder that a receptor agonist in one tissue can behave differently in another. In isolated guinea-pig heart muscle the same molecule acted not as an agonist but as a competitive blocker of somatostatin's effect, because of how that tissue's receptors are coupled, a caution against reading one tissue's result across the body.
Seglitide was never approved and its development did not continue. Octreotide, an eight-amino-acid analogue developed over the same years, became the somatostatin drug that reached the clinic and is still used for acromegaly and hormone-secreting tumours. Seglitide is now mostly of historical and laboratory interest, and is still used in research as a tool to tell somatostatin-receptor subtypes apart. It is not a medicine and nothing on this page is a dose to use.
Mechanism of Action
Seglitide is a small, stable copy of the business end of somatostatin. It switches on the same receptors and so turns off the same hormones, but its ring structure makes it last far longer in the body.
Somatostatin receptors
The molecule keeps the four residues of somatostatin that bind its receptors (the D-tryptophan and lysine among them), so it activates somatostatin receptors and reproduces the hormone's inhibitory actions (PMID 6143233). It is still used in research to tell receptor subtypes apart.
Growth hormone, insulin and glucagon down
Through those receptors it suppresses pituitary growth-hormone release and pancreatic insulin and glucagon release: on human pituitary-tumour cells nanomolar doses switched off growth hormone (PMID 1680212), and in people it blunted the meal-time glucagon, growth-hormone and glucose rises (PMID 2872569).
Tissue-dependent behaviour
In isolated guinea-pig heart the same agonist acted as a competitive antagonist of somatostatin because of local receptor coupling (PMID 8104651) — a reminder that one tissue's result does not carry across the body.
Published Research
These are the studies of seglitide read from their PubMed abstracts on November 5, 2026. The molecule is more often cited as a research tool to classify somatostatin receptors than studied as a drug; the cards below are the studies of seglitide itself: three in people (diabetes and the dawn phenomenon), two on isolated tissue (human pituitary-tumour cells and guinea-pig heart) and two in animals. The 1984 structure-activity paper that first made the molecule names it only by structure and is listed in the references.
Infused in type 1 diabetes
Six people with insulin-dependent diabetes were given a five-hour intravenous infusion of the analogue (at 2, 5, 10 or 40 micrograms an hour), of natural somatostatin (200 micrograms an hour), or of placebo, with a standard meal. The analogue cleared about six times more slowly than somatostatin and its half-life was roughly 45 minutes against somatostatin's two. At 10 micrograms an hour it suppressed the post-meal rises in glucagon, growth hormone, glucose, xylose and triglyceride about as much as somatostatin did at 200 micrograms an hour. The authors concluded it was a long-acting, potent analogue with potential as an adjunct to insulin.
Intravenous and intranasal in diabetes
A report of early clinical experience giving the analogue to people with insulin-dependent diabetes both intravenously and into the nose. Both routes reduced fasting and after-meal high blood sugar, and in patients kept on a closed-loop insulin pump the intranasal dose improved the early-morning glucose rise known as the dawn phenomenon. The authors suggested the analogue, added to standard insulin, could help control unstable diabetes. The abstract gives no milligram amount for the intravenous arm.
A bedtime nasal dose for the dawn phenomenon
Six people with type 1 diabetes were given 600 micrograms of the analogue into the nose at bedtime, to see whether the overnight growth-hormone surge that drives early-morning hyperglycaemia could be blunted without an extra injection. Compared with saline nights, the bedtime nasal dose lowered overnight plasma glucose and growth hormone. The study used the molecule as a tool to test the role of nocturnal growth hormone in the dawn phenomenon.
On human pituitary-tumour cells
Cells from three human growth-hormone-secreting pituitary tumours (somatotrophinomas) were grown in culture and exposed to the analogue. At 1 and 10 nanomolar it inhibited both resting and growth-hormone-releasing-factor-stimulated growth-hormone release from all three tumours over two hours; at 100 nanomolar the effect on resting release outlasted treatment in two of them. Its actions matched those of somatostatin-14, and the authors suggested it might have a role in treating acromegaly, the condition of growth-hormone excess.
An agonist that blocks in heart muscle
In isolated guinea-pig right atria, seglitide, normally a potent somatostatin-receptor agonist, instead behaved as a competitive antagonist of somatostatin's negative effect on contraction (pA2 values around 6.1 to 6.5 against three forms of somatostatin), with little effect on the responses to other agents. The finding is explained by how this tissue's receptors are coupled, and it is a caution that a receptor agonist can present as a blocker in a particular preparation.
Protecting pancreas grafts in dogs
Pancreas transplants can fail early because of their own digestive secretions. In dogs, the analogue at 0.3 micrograms per kilogram per hour, given under the skin by osmotic pump for seven days, cut the serum amylase (a marker of exocrine secretion) of transplanted pancreas tissue significantly compared with untreated dogs, and a single infusion produced a fourfold drop in pancreatic exocrine output after a meal. The work tested it as a way to quiet a new graft while it settles.
Blood pressure in diabetic rats
An oral dose of the analogue lowered blood pressure in a rat model of combined hypertension and diabetes, but not in the ordinary spontaneously hypertensive rat. The blood-pressure fall did not track changes in insulin, glucagon, growth hormone or the renin-angiotensin system, so its mechanism was left unexplained. An incidental observation rather than a developed indication.
Dosing Data
Seglitide has no approved label and is not a medicine. Both rows below are amounts given to people under supervision in published studies, recorded to document the science rather than to be used: an intravenous infusion rate from the diabetes study and a single nasal dose from the dawn-phenomenon study. The amounts are in different units and routes because the studies asked different questions.
Educational information, not medical advice. Each dose above is tagged with its source: an approved label, a published human study, animal data, or amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no label and no published test that says what forms or vial sizes Seglitide is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
No worked example: none of the doses on this page is a fixed amount in mg or mcg injected under the skin or into a muscle (the routes given are: intranasal, intravenous). There is no home-mixing step to show. The reconstitution calculator does the arithmetic for any vial.
Source: the route and amount of each dose row in Dosing Data below.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Seglitide, before or after mixing. The mixing guide sets out the general rules, with their sources: keep a mixed vial in the fridge, and use it promptly, as the bacteriostatic water label says of any drug dissolved in it. The 28 days often quoted is the limit for an opened multiple-dose vial from a manufacturer, an outer limit set for sterility, not a time a mixed solution has been shown to keep. Nobody has published how long Seglitide stays intact once mixed.
How it is taken
As it was given in human studies: Intravenous (Continuous infusion; Type 1 diabetes, intravenous infusion); Intranasal (Once at bedtime; Dawn phenomenon, nasal).
For injection technique, sites and needle disposal, see the mixing guide.
Source: Used in human trials: the route and frequency of each row in Dosing Data below.
What to expect, and when
How long it stays in the body: a half-life of about 45 minutes in people (vs ~2 minutes for somatostatin). After about five half-lives almost none is left.
How long the doses were given: Type 1 diabetes, intravenous infusion: 5 hours; Dawn phenomenon, nasal: Single dose.
When effects appear: unknown; no source on this page gives a time to effect for Seglitide. Results reported in the studies are under Published Research.
Source: half-life: PMID 2872569; Used in human trials, the duration of each row in Dosing Data below.
Side effects, and when to stop or get help
From the Side Effects section: Suppression of growth hormone, glucagon and insulin — its intended actions, which also set its risks (PMID 2872569); Because it suppresses insulin as well as glucagon, its net effect on blood sugar depends on the balance and on background insulin (PMIDs 2872569, 2900206); No approved-label safety profile exists, because development stopped and no large trial was run. Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Seglitide. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“The published human studies are small and focus on hormones and blood sugar rather than on a full safety assessment; they report the drug's intended effects more than its adverse ones”).
Interactions
Unknown: a PubMed search for human interaction studies of Seglitide (reviewed 2026-11-05) found none. Unknown is not the same as safe to combine.
Every peptide's record, with its source: the interaction matrix.
Checking what you bought
Unknown: no published independent test of Seglitide products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder; it checks the measured mass against Seglitide's expected mass, 809.0 Da, from this entry's molecular data. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Discontinued (Never approved anywhere: Drugs@FDA and the openFDA label endpoint hold no record (searched November 5, 2026)). Sport: Prohibited (S0 catch-all).
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
The published human studies are small and focus on hormones and blood sugar rather than on a full safety assessment; they report the drug's intended effects more than its adverse ones.
Contraindications & Cautions
Seglitide has no label and no approved use. These points come from what the molecule does and from the studies.
Legal Status
Seglitide is an investigational compound that was never approved in any country and is not marketed.
Frequently Asked Questions
?What is seglitide?
An experimental drug from the early 1980s, coded MK-678 and L-363,586 by Merck. It is a stable six-amino-acid ring that copies the active part of the hormone somatostatin, so it suppresses growth hormone, insulin and glucagon, but lasts much longer in the body than somatostatin does.
?Was it ever approved or sold?
No. Seglitide reached early clinical testing (ChEMBL records phase 2) but was not developed further and was never approved or marketed anywhere. Octreotide became the somatostatin analogue that reached the clinic instead.
?What was it studied for?
Mostly diabetes: it blunted meal-time and overnight blood-sugar rises in people with type 1 diabetes (PMIDs 2872569, 2892113). It also switched off growth-hormone release from human pituitary-tumour cells, the action behind somatostatin analogues' use in acromegaly (PMID 1680212).
?How is it different from octreotide?
Both are small, long-acting somatostatin analogues developed in the same era. Seglitide is a cyclic hexapeptide (a six-residue ring); octreotide is an octapeptide (eight residues). Octreotide was the one taken to approval and is still used; seglitide was not.
?Is it still used at all?
Not as a medicine. It survives in pharmacology research as a tool compound for telling somatostatin-receptor subtypes apart, which is why it appears in many receptor studies.
?Is it approved or available to buy?
No. Seglitide is not a medicine and is not sold as one. Grey Peptides lists no sellers and recommends no source; this page is a record of the published science.
References
- [clinical-trial] Gottesman I, et al. "Efficacy, pharmacokinetics and tolerability of a somatostatin analogue (L-363,586) in insulin-dependent diabetes mellitus." Life Sci, 1986;38(24):2211-9. PMID: 2872569.
- [clinical-trial] Bolli GB, et al. "Preliminary experience on treatment of insulin-dependent diabetes mellitus with a long-acting somatostatin analogue (L363,586)." Horm Res, 1988;29(2-3):95-8. PMID: 2900206.
- [clinical-trial] Campbell PJ, et al. "Prevention of the Dawn phenomenon (early morning hyperglycemia) in insulin-dependent diabetes mellitus by bedtime intranasal administration of a long-acting somatostatin analog." Metabolism, 1988;37(1):34-7. PMID: 2892113.
- [pubmed] Daniels M, et al. "Actions of L-363,586, a cyclic hexapeptide analogue of somatostatin, on GH secretion by human somatotrophinoma cells in vitro." Life Sci, 1991;49(16):1207-12. PMID: 1680212.
- [animal] Dimech J, et al. "Antagonist effects of seglitide (MK 678) at somatostatin receptors in guinea-pig isolated right atria." Br J Pharmacol, 1993;109(4):898-9. PMID: 8104651.
- [animal] Liu T, et al. "Effect of a cyclic hexapeptide analog (L363,586) of somatostatin on the function of pancreas grafts in dogs." J Surg Res, 1985;39(1):39-45. PMID: 2409352.
- [animal] Hartmann J, et al. "Blood pressure reduction in hypertensive-diabetic rats by the somatostatin analog MK-678." Life Sci, 1989;45(3):267-74. PMID: 2569653.
- [pubmed] Veber DF, et al. "A super active cyclic hexapeptide analog of somatostatin." Life Sci, 1984;34(14):1371-8. PMID: 6143233.
- [other] FDA Global Substance Registration System, Seglitide, UNII 5P57R7IR6J (acetate URM20C99DG; protein; INN 6146, USAN X-96, CAS 81377-02-8, MeSH C040968, PubChem 5311430; codes MK-678 and L-363,586), read November 5, 2026: a cyclic hexapeptide, cyclo(N-methyl-L-alanyl-L-tyrosyl-D-tryptophyl-L-lysyl-L-valyl-L-phenylalanyl) (C44H56N8O7, 808.96 g/mol). https://gsrs.ncats.nih.gov/ginas/app/beta/substances/5P57R7IR6J
- [other] ChEMBL molecule CHEMBL311695 (SEGLITIDE), read November 5, 2026: molecule type Protein; synonyms Seglitide (INN), MK-678, L-363586; highest clinical phase recorded 2. https://www.ebi.ac.uk/chembl/compound_report_card/CHEMBL311695/
- [other] US FDA, Drugs@FDA and the drug label endpoint (openFDA), searched November 5, 2026: no application and no label record for seglitide. It has an FDA substance record (UNII 5P57R7IR6J) and a USAN, which name a molecule and do not approve it.
- [registry] ClinicalTrials.gov API v2, searched November 5, 2026: 0 records for seglitide, MK-678 or L-363,586. The registry began in 2000, after the molecule's 1980s-90s studies, so the absence is expected. https://clinicaltrials.gov/search?term=seglitide
Sources & Citations
The seven studies carded above and the References-only structure-activity paper were read from their PubMed records on November 5, 2026. Structure, codes and identifiers come from the FDA Global Substance Registration System (UNII 5P57R7IR6J) and ChEMBL (CHEMBL311695); the absence of approval from Drugs@FDA and openFDA, and the absence of registered trials from ClinicalTrials.gov, all checked the same day. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.