The system's brake. A growth axis with no off-switch would not be a physiology; it would be a tumour.
Identity
- Class
- Cyclic peptide (14 and 28 aa forms)
- Source
- Hypothalamus, pancreatic delta cells, GI tract
- Receptor
- Somatostatin receptors SSTR1–SSTR5
Key properties
Evidence floorClinicalREF1CLIN1Approximate values for the native hormone; engineered analogs are often deliberately larger and far longer-acting. Each figure carries its own provenance tier, and the floor is the weakest of them - the Standard.
Mechanism
Somatostatin inhibits GH (and TSH) release from the pituitary and broadly suppresses endocrine and exocrine secretion across the GI tract and pancreas. It is the inhibitory counterweight that, opposing GHRH, sculpts GH pulses.
Reference notes
- Any account of GH timing has to include somatostatin — it sets the troughs between pulses.
- Its broad inhibitory reach extends well beyond GH, into gut and pancreatic secretion.
- Stable somatostatin analogs are long-established tools in endocrinology.
Regulatory status
United States · reviewed September 2026- Basis
- Native somatostatin is too short-lived to market; octreotide, lanreotide and pasireotide are the approved analogs.
Status describes the molecule as a drug substance under US law and is an editorial reading of the public record — approvals, trial registrations, and the FDA 503A bulk-substances list. It is not legal advice and it changes; the review date above is the last time the table was checked. Other jurisdictions are noted only where they differ materially.
Common questions
- What is Somatostatin (SST)?
- The brake on the growth-hormone axis — and much else. Structurally it is Cyclic peptide (14 and 28 aa forms).
- How does SST work?
- Somatostatin inhibits GH (and TSH) release from the pituitary and broadly suppresses endocrine and exocrine secretion across the GI tract and pancreas. It is the inhibitory counterweight that, opposing GHRH, sculpts GH pulses.
- How strong is the evidence for SST?
- PeptideHormone grades SST at the "Established" evidence tier — its mechanism and core effects are settled across the peer-reviewed literature. It is catalogued as an endogenous signal the body produces itself, and the tier is an editorial judgment about the public literature that can change as the science does.
- What is the half-life of SST?
- The reported circulating half-life of SST is ~1–3 min (very short).
- Is SST FDA-approved?
- No — as of September 2026, SST is a native hormone with no drug product of its own, though engineered analogs may be approved. Native somatostatin is too short-lived to market; octreotide, lanreotide and pasireotide are the approved analogs. Status is US-centric and can change; check the FDA record for the current position.
In the literature
Live registry counts · retrieved- Ph 157
- Ph 284
- Ph 348
- Ph 422
Searched as Somatostatin, somatostatin-14. Counts are search hits from the primary registries, not a curated set and not a grade – a measure of how much work exists on SST, not how it turned out.
Selected literature
Curated peer-reviewed reviews, sourced from PubMed. Selected for relevance, not exhaustive — open any entry on PubMed for the full record and its primary citations.
- 1.Structure and Function of Somatostatin and Its Receptors in Endocrinology · Endocrine reviews, 2025 · PMID 39116368
- 2.Somatostatin · The New England journal of medicine, 1983 · PMID 6139753
External references
SST in the public knowledge graph — the same entity resolved across the authoritative chemistry and protein databases.