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Somatostatin (SST-14 and SST-28)14 residuesAGCKNFFWKTFTSCEach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: SST-14, SST-28, SRIF
Fourteen amino acids, a disulfide bridge, and a half-life measured in seconds. Somatostatin (SST-14) is the body's master inhibitory hormone, produced in the hypothalamus, pancreas, and gut to suppress growth hormone, insulin, glucagon, and gastric acid simultaneously. Roger Guillemin's lab isolated it from sheep brains in 1973. The catch: it disappears from your bloodstream in under three minutes. That ultrashort duration forced pharmacologists to engineer octreotide, lanreotide, and pasireotide as longer-lasting clinical substitutes. Native somatostatin stays in the research lab and ICU, where continuous IV infusion is the only delivery method that works.
A 120-patient double-blind RCT proved native somatostatin could stop variceal bleeding better than placebo (36% failure vs. 59%)[1]. Then octreotide made the finding nearly irrelevant. Somatostatin (somatotropin release-inhibiting factor, SRIF, CAS 38916-34-6) is a cyclic peptide hormone that exists as SST-14 (14 amino acids, Cys3-Cys14 disulfide bridge) and SST-28 (an N-terminally extended 28-amino-acid form). The mechanism is broad-spectrum inhibition. Somatostatin binds all five G protein-coupled somatostatin receptor subtypes (SSTR1 through SSTR5) at roughly equal nanomolar affinity. That receptor coverage shuts down growth hormone release from the pituitary, insulin and glucagon secretion from pancreatic islets, gastric acid output, and splanchnic blood flow. No other single endogenous peptide hits that many secretory targets at once. Endocrinologists and gastroenterologists used continuous IV infusions (250 to 500 mcg per hour) for acute esophageal variceal hemorrhage through the 1990s. A European multicenter RCT [2] and a separate sclerotherapy comparison trial [3] confirmed equivalent efficacy. The peptide also appears in diagnostic provocative testing for insulinoma localization and GH axis studies. PubMed lists over 39,000 citations. The practical limitation is straightforward: enzymatic degradation at the Trp8-Lys9 and Phe7-Trp8 bonds wipes out circulating somatostatin in 1 to 3 minutes after IV delivery. No subcutaneous or oral route produces meaningful plasma levels. The pharmaceutical industry responded with octreotide (1.8-hour half-life), lanreotide (depot lasting 4 weeks), and pasireotide (12-hour half-life). Those analogs carry FDA approvals; native somatostatin does not. It remains research-only in the United States.
Five receptor subtypes, one peptide, and an inhibitory signal that touches nearly every secretory organ in the body. SST-14 locks onto SSTR1 through SSTR5 with roughly equal nanomolar binding. SST-28 skews toward SSTR5 with about 10-fold selectivity. All five receptors couple to inhibitory G proteins (Gi/Go). The downstream cascade starts with the Gi alpha subunit suppressing adenylyl cyclase. Intracellular cyclic AMP drops. Protein kinase A activity falls. In pituitary somatotrophs, that kills GH gene transcription and blocks exocytosis of stored hormone. In pancreatic beta cells and alpha cells, the same pathway suppresses insulin and glucagon release. The beta-gamma subunit does separate work. It opens G protein-coupled inwardly rectifying potassium (GIRK) channels, hyperpolarizing the cell membrane. It also inhibits voltage-gated N-type and L-type calcium channels. Less calcium entry means fewer secretory granules fuse with the membrane. The antisecretory effect is therefore double-locked: reduced cAMP signaling plus electrical silencing of the cell. SSTR2 and SSTR5 engage protein tyrosine phosphatases SHP-1 and SHP-2, which strip phosphate groups from growth factor receptors. This produces the antiproliferative effects that make somatostatin receptors valuable targets in neuroendocrine tumor therapy (Lutetium-177 DOTATATE, FDA-approved for NETs). Degradation happens fast. Endopeptidases cleave the Trp8-Lys9 bond and the Phe7-Trp8 bond within the disulfide-constrained ring. Plasma half-life: 1 to 3 minutes. The synthetic analogs survive by incorporating D-amino acids and shrinking the ring structure to shield those cleavage sites.
Native somatostatin (SST-14/SST-28) has strong clinical evidence for IV use in acute variceal hemorrhage and diagnostic GH suppression. The 1-3 min half-life makes all self-administered or outpatient protocols pharmacologically impossible. Synthetic analogs (octreotide, lanreotide, pasireotide) have superseded native SST for all routine clinical applications. 2024-2026 research focus has shifted to SSTR subtype roles in Alzheimer's disease (neprilysin regulation) and PRRT in NETs.
Calès P et al. PMID 1976563: double-blind RCT (n=120): variceal bleeding failure rate 36% SST vs 59% placebo. Confirmed by PMID 7913907 (SST vs sclerotherapy, equivalent efficacy) and PMID 9388396 (ABOVE European multicenter RCT).
All clinical evidence is for supervised IV infusion in hospital/ICU settings. No valid self-administration protocol exists. Analogs have superseded native SST in most applications. No 2024-2026 clinical trials using native somatostatin for new indications were identified.
No self-administration community exists for native somatostatin. Zero self-injection protocols found on r/peptides or bodybuilding forums. The biohacker community discusses inhibiting endogenous somatostatin (to enhance GH pulses): the opposite of exogenous dosing.
No biohacker or self-administration community exists. All evidence comes from supervised IV clinical/research protocols. The 1-3 minute half-life eliminates any practical self-administration pathway: this peptide cannot be made to work outside a hospital IV setting.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 250mcg | Continuous IV infusion (mcg/hour) |
| Moderate | 250mcg | Continuous IV infusion (mcg/hour) |
| Aggressive | 500mcg | Continuous IV infusion (mcg/hour) |
This peptide does not belong in anyone's home refrigerator. Native somatostatin requires continuous IV infusion through a hospital pump because the 1-3 minute half-life means a single subcutaneous injection produces no meaningful blood levels. There is no self-administration protocol that works. For the reconstitution math in clinical settings: a standard 3 mg vial dissolved in 50 mL of 0.9% NaCl gives 60 mcg per mL. Running at 250 mcg per hour means 4.2 mL per hour on the IV pump. Running at 500 mcg per hour means 8.3 mL per hour. Research-grade vials (0.25 mg) reconstituted in 0.5 mL bacteriostatic water yield 500 mcg per mL for bench studies. The detail most people miss: rebound monitoring is just as important as infusion monitoring. Stopping the drip isn't the end of the clinical event. GH, insulin, and glucagon all spike above baseline for one to two hours after cessation. Have dextrose 50% drawn up before you turn off the pump. Store lyophilized powder at minus 20 degrees Celsius; reconstituted solution lasts 24 hours at 2-8 degrees Celsius maximum. Do not refreeze.
Native somatostatin is not used in cycling protocols due to its ultrashort half-life. Research and diagnostic applications typically involve single-session continuous IV infusions lasting minutes to hours. For variceal hemorrhage, infusions of 250-500 mcg/hour are maintained for 2-5 days. There is no established cycling regimen. Patients requiring long-term somatostatin receptor suppression should use FDA-approved analogs (octreotide, lanreotide, or pasireotide) under medical supervision.
Cycling protocols are not applicable to native somatostatin. The 1-3 min half-life restricts all use to single-session IV infusions lasting minutes to days. No chronic or cyclical self-administration regimen exists or is clinically appropriate. Long-term somatostatin receptor suppression requires switching to approved analogs (octreotide LAR, lanreotide Autogel, pasireotide) with established long-term safety frameworks.
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Expected: Control of acute esophageal variceal bleeding via reduction of splanchnic blood flow and portal pressure. PMID 1976563 demonstrated 36% failure rate vs 59% placebo; comparable efficacy to sclerotherapy with fewer complications (PMID 7913907).
Monitor: Continuous ECG; blood glucose q1-2h during infusion and q30min for 2h post-cessation; hemodynamic monitoring (BP, HR); watch for rebound hypoglycemia at infusion stop.
Confirm the clinical indication (acute variceal hemorrhage, diagnostic GH suppression, or approved research protocol). Native somatostatin is not used outside supervised clinical or research settings.
Establish IV access with continuous hemodynamic monitoring: ECG, automated blood pressure cuff (every 15-30 minutes), and pulse oximetry. Draw up atropine for bradycardia backup.
Reconstitute the 3 mg lyophilized vial with 50 mL of 0.9% NaCl. This yields a concentration of 60 mcg per mL. For research applications, a 0.25 mg vial in 0.5 mL bacteriostatic water gives 500 mcg per mL.
For variceal hemorrhage: administer a 250 mcg IV bolus over 3 to 5 minutes. Follow immediately with continuous infusion at 250 mcg per hour (4.2 mL per hour at 60 mcg/mL concentration). Rate may increase to 500 mcg per hour (8.3 mL per hour) based on clinical response.
For diagnostic infusion: administer 1 to 5 mcg per kg IV bolus, followed by continuous infusion at 1 to 5 mcg per kg per minute. For a 70 kg adult, that translates to a 70 to 350 mcg bolus.
Treat any reading below 70 mg/dL with IV dextrose immediately.
Continue glucose checks every 30 minutes for 2 hours. Watch for rebound hypoglycemia, GH overshoot, and gastric acid rebound.
Discard any unused reconstituted solution after 24 hours.
Reference route; 100% bioavailability; the only route capable of maintaining therapeutic plasma concentrations
Requires IV pump, hospital access, and continuous monitoring. Single bolus provides only ~3-5 min of activity before plasma levels decay to sub-therapeutic levels.
No established therapeutic dose; no meaningful sustained effect at any SC dose
Used in research PK studies only. Rapid degradation by tissue endopeptidases at injection site prevents sustained plasma levels. SST-28 is modestly more resistant than SST-14 but still impractical for SC therapy. All self-injection protocols are pharmacologically unfounded.
Somatostatin suppresses both insulin and glucagon simultaneously; blood glucose effects are unpredictable. Rebound hypoglycemia risk at infusion cessation (glucagon suppression lifts before insulin recovers). Requires intensive glucose monitoring if co-administered in clinical setting.
Do not combineAdditive bradycardia; continuous ECG monitoring required during co-administration. Concurrent use requires careful hemodynamic oversight in hospital setting.
Enhanced negative chronotropic effects from additive calcium channel inhibition; avoid combination without continuous ECG monitoring.
Theoretical additive arrhythmia risk from somatostatin's cardiac electrophysiological effects (SSTR2/5 on cardiac conduction). Avoid combination without ECG monitoring.
Pricing updated 2026-04-09
Rebound hypersecretion after stopping the IV drip is the safety concern that matters most. When a continuous somatostatin infusion ends, GH, insulin, glucagon, and gastric acid all overshoot their baseline levels within minutes. In diabetic patients, the risk is specific: glucagon suppression lifts before insulin secretion fully recovers, opening a window for dangerous hypoglycemia. Dextrose 50% should be available at bedside. Blood glucose monitoring needs to continue every 30 minutes for at least two hours after cessation. Bradycardia during IV infusion is the second priority. Somatostatin activates SSTR2 and SSTR5 on cardiac tissue. Heart rate can drop below the threshold where intervention is needed (sustained HR below 50 bpm). Patients on beta-blockers or non-dihydropyridine calcium channel blockers face additive risk. Continuous ECG monitoring is standard protocol, and atropine should be drawn up before the infusion starts. Gastrointestinal effects are common during infusion. Nausea, abdominal cramping, and diarrhea reflect the abrupt suppression of GI motility and enzyme secretion. These tend to be transient because the half-life is so short; stop the drip and symptoms resolve in minutes. Hyperglycemia from insulin suppression occurs during active infusion. Blood glucose can spike, especially in patients with pre-existing insulin resistance. Monitoring every one to two hours during infusion is the minimum standard. Hypotension results from reduced splanchnic blood flow. That same vascular effect is therapeutically useful in variceal bleeding, but it creates problems in patients who are already hemodynamically unstable. Fluid resuscitation and vasopressor access are required for actively bleeding patients. Prolonged continuous infusion (days, as in variceal hemorrhage protocols) carries the same chronic risks seen with somatostatin analogs: gallbladder stasis leading to sludge formation, fat malabsorption (steatorrhea), and potential vitamin B12 deficiency. IV site pain and flushing are common with extended infusions but resolve quickly after the line is removed. Pregnancy and breastfeeding: insufficient safety data exists. Avoid unless the clinical situation is life-threatening and no analog alternative is available. All use requires direct medical supervision in a facility equipped for hemodynamic and glucose monitoring. When to get emergency help: sustained heart rate below 50 bpm, symptomatic hypoglycemia that doesn't respond to dextrose, signs of anaphylaxis, or hemodynamic collapse. When to stop the infusion: confirmed arrhythmia, refractory hypotension, or allergic reaction.
Verify Somatostatin (SST-14 and SST-28) dosing and safety with a second opinion
No compounding market exists for native somatostatin in the US (not on FDA 503A/503B approved bulk lists). Research-grade suppliers (AbMole, Bachem, Cayman Chemical) provide laboratory-grade material only. Any self-administration attempt bypasses the continuous monitoring required for safe clinical use.
| Test | When | Target |
|---|---|---|
| Blood glucose | Every 1-2 hours during infusion; at cessation; every 30 min for 2 hours post-cessation | 80-180 mg/dL; treat hypoglycemia (<70 mg/dL) aggressively with IV dextrose |
| Heart rate / continuous ECG | Continuous monitoring during entire infusion period | HR >50 bpm; pause infusion if sustained bradycardia or conduction changes |
| Blood pressure | Every 15-30 minutes during infusion | SBP >90 mmHg; SBP >100 mmHg preferred in high-risk patients |
| Serum GH (research/diagnostic use only) | Baseline; during infusion peak; 30-60 min and 90-120 min post-cessation | — |
Insulin suppression causes hyperglycemia during infusion; rebound hypoglycemia risk when glucagon suppression lifts before insulin recovers at infusion stop
Bradycardia risk via cardiac SSTR2/5; additive effect with beta-blockers, CCBs, and any bradycardic agents
Splanchnic vasodilation reduction can cause hypotension; risk elevated in actively bleeding patients with pre-existing hemodynamic compromise
Confirms GH suppression efficacy for diagnostic purposes; documents rebound hypersecretion kinetics
Rapid onset of GH suppression and reduction of splanchnic blood flow. Peak plasma concentration achieved almost immediately with IV administration.
Plasma levels decline rapidly (half-life ~1-3 min). GH, insulin, and glucagon secretion are acutely suppressed. Gastric acid output decreases measurably.
Sustained suppression of GH, insulin, glucagon, and GI hormones for the duration of infusion. Steady-state plasma levels achieved within 10-15 minutes. Portal pressure reduction evident in variceal bleeding applications.
Rapid clearance from plasma. Rebound hypersecretion of GH and other hormones may occur within minutes of cessation. Blood glucose may fluctuate: monitor for rebound hypoglycemia or hyperglycemia.
All direct hormonal effects fully reversed. No residual activity expected beyond 15-30 minutes. Rebound GH elevation typically normalizes within 1-2 hours.
Seconds to 1 minute (IV bolus): The peptide reaches peak plasma concentration almost instantly. GH suppression kicks in. Splanchnic blood flow starts dropping. Insulin and glucagon output falls within the first minute. Transient flushing and brief hypotension can occur at this stage. 1-15 minutes (bolus only, no infusion): Without a continuous drip, plasma levels halve every 1-3 minutes. All hormonal suppression reverses within 15 to 20 minutes of a single bolus. This window confirms why a bolus alone has no therapeutic staying power. During continuous infusion (minutes to hours): Steady-state plasma levels land within 10-15 minutes of starting the pump. Portal pressure drops measurably. GH, insulin, glucagon, and the full GI hormone panel stay suppressed for as long as the infusion runs. Common side effects during this phase include nausea, abdominal cramping, bradycardia, hyperglycemia, and mild hypotension. 0-30 minutes post-infusion: Plasma levels become undetectable within 15-20 minutes of turning off the pump. Then the rebound hits. GH, insulin, and glucagon all overshoot baseline. Blood glucose can swing in either direction. This is the highest-risk window for hypoglycemia in diabetic patients. 1-2 hours after cessation: All direct pharmacological effects are fully reversed. The GH rebound normalizes. Gastric acid secretion returns to baseline. No residual somatostatin activity remains beyond 30 minutes in most patients.
Peak plasma concentration within seconds of IV bolus. GH suppression and splanchnic blood flow reduction begins within 1 minute. Insulin and glucagon secretion acutely inhibited.
No community data available.
Plasma half-life ~1-3 min; levels halve rapidly without continuous infusion. All hormone suppression reverses within 15-20 minutes of a single bolus.
No community data available.
Steady-state plasma levels reached within 10-15 min of starting continuous infusion. Sustained reduction of portal pressure, GH, insulin, glucagon, and GI hormones for infusion duration.
No community data available.
Plasma levels undetectable within 15-20 min of cessation. Rebound hypersecretion of GH, insulin, and glucagon above baseline. Blood glucose may fluctuate dangerously: highest risk window for hypoglycemia in diabetic patients.
No community data available.
All direct pharmacological effects fully reversed. Rebound GH elevation normalizes. No residual somatostatin activity expected. Gastric acid secretion returns to baseline.
No community data available.
Source: Sheppard M et al. Multiple IV studies; SST-14 half-life 1-3 minutes (mean ~3 min). Patel YC. Front Neuroendocrinol. 1999;20(3):157-198. PMID: 10433861
Loading the interactive decay curve.
Native somatostatin (SST-14, SST-28) has no FDA approval for any therapeutic indication in the United States. The regulatory classification is research-only. Somatostatin does not appear on FDA 503A or 503B approved bulk drug substance lists, which means no US compounding pharmacy can legally produce it for patient use. Stilamin (somatostatin 3 mg per vial) is a pharmaceutical product manufactured by Merck KGaA and registered in select European markets (Italy and others). It is not available through US distribution channels. Research-grade somatostatin acetate is available from laboratory suppliers (AbMole, Bachem, Cayman Chemical) for in vitro and animal studies. These products are labeled "for research use only" and are not manufactured under cGMP for human administration. WADA status: somatostatin itself is not currently listed as a prohibited substance, but manipulation of growth hormone secretion pathways may fall under the prohibited methods category depending on context. Athletes should verify with their governing body. All information on this page is for educational and research reference only. It does not constitute medical advice. Somatostatin use in any clinical setting requires direct physician supervision, hospital-grade IV delivery equipment, and continuous monitoring.
Peptide Schedule Research TeamReviewed Apr 20269 Citations
