Octreotide

Octreotide (Sandostatin) is a synthetic cyclic octapeptide analog of somatostatin with a significantly longer half-life (~90 minutes vs ~1-3 minutes). It is a clinically established treatment for acromegaly, carcinoid syndrome, neuroendocrine tumors, and variceal bleeding, available in immediate-release and long-acting depot (LAR) formulations.

Octreotide (Sandostatin) is a synthetic cyclic octapeptide that mimics the pharmacological actions of endogenous somatostatin while offering dramatically improved metabolic stability. Developed by Sandoz (now Novartis) in the early 1980s, octreotide retains the Phe-Trp-Lys-Thr pharmacophore critical for somatostatin receptor binding within a compact 8-amino acid scaffold stabilized by D-amino acid substitutions.

Overview

Octreotide was designed through systematic structure-activity studies of somatostatin-14, identifying the minimal pharmacophore (Phe⁷-Trp⁸-Lys⁹-Thr¹⁰) required for receptor binding and incorporating D-amino acid substitutions and C-terminal reduction to resist enzymatic degradation (Bauer et al., 1982). The resulting octapeptide binds preferentially to somatostatin receptor subtypes 2 and 5 (SSTR2 >> SSTR5 > SSTR3), with minimal activity at SSTR1 and SSTR4.

First approved by the FDA in 1988 for acromegaly and carcinoid syndrome, octreotide has since become one of the most commercially successful peptide therapeutics. The development of the long-acting release (LAR) microsphere formulation in 1998 enabled once-monthly intramuscular injection, transforming patient compliance. In 2020, an oral octreotide formulation (Mycapssa) using transient permeability enhancer (TPE) technology received FDA approval, marking a milestone in oral peptide delivery.

Mechanism of Action

Octreotide replicates the inhibitory actions of native somatostatin through preferential SSTR2/SSTR5 activation:

  • SSTR2-mediated GH suppression: Octreotide's primary clinical effect in acromegaly derives from high-affinity SSTR2 binding on pituitary somatotroph cells, inhibiting adenylyl cyclase, reducing cAMP, and suppressing GH secretion. Tumor shrinkage occurs in approximately 30-50% of patients through SSTR2-mediated antiproliferative signaling (Melmed et al., 2005).
  • Hormone secretion inhibition: Broadly suppresses secretion of serotonin (carcinoid), VIP (VIPomas), gastrin (gastrinomas), insulin (insulinomas), and glucagon (glucagonomas) from neuroendocrine tumor cells.
  • Antiproliferative effects: SSTR2 activation engages phosphotyrosine phosphatases (SHP-1, SHP-2), inducing G1 cell cycle arrest and apoptosis in neuroendocrine tumor cells. The PROMID trial demonstrated that octreotide LAR significantly prolongs time to tumor progression in midgut NETs (Rinke et al., 2009).
  • Splanchnic blood flow reduction: Inhibits release of vasodilatory peptides (glucagon, VIP) and directly reduces portal blood flow, providing efficacy in variceal bleeding.
  • GI motility and secretion: Reduces gastric acid, pancreatic enzyme secretion, and intestinal fluid secretion, underlying both therapeutic effects (diarrhea control) and side effects (steatorrhea, gallstones).

Reconstitution Calculator

Octreotide

**Octreotide** (Sandostatin) is a synthetic cyclic octapeptide that mimics the p

Draw Volume
0.400mL
Syringe Units
40units
Concentration
250mcg/mL
Doses / Vial
5doses
Vial Total
500mcg
Waste / Vial
0mcg
Syringe Cap.
100units · 1mL
Recommended Schedule
M
T
W
T
F
S
S
Frequency2-3 times daily
How to reconstitute
Gather & prepare
1/6Gather & prepare

Set up a clean workspace with all supplies ready.

1.Wash hands thoroughly, put on disposable gloves
2.Your 0.5mg peptide vial (lyophilized powder)
3.Bacteriostatic water (you'll need 2mL)
4.A 3–5mL syringe with 21–25 gauge needle for reconstitution
5.Alcohol swabs (70% isopropyl)
Use bacteriostatic water (0.9% benzyl alcohol) for multi-dose vials. Sterile water is only safe for single-use.
Supply Planner

7x / week for weeks

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60%
6vials
28 doses5 days/vial2 leftover
Cost Breakdown
Vial price
$0.00per dose
$0.00 /week$0 /month
Store 2-8°C30 day shelf lifeSwirl gentlyFor research purposes only

Research

Acromegaly

Octreotide is a first-line medical therapy for acromegaly when surgery is not curative or not feasible. Octreotide LAR (10-40 mg IM monthly) normalizes GH and IGF-1 levels in approximately 50-70% of patients and produces clinically significant tumor shrinkage (>20% volume reduction) in 30-75% of patients depending on SSTR2 expression levels. Primary medical therapy (octreotide before surgery) has gained acceptance for debulking large macroadenomas. Predictors of response include high tumor SSTR2 expression and T2-hypointense MRI signal (Colao et al., 2011).

Carcinoid Syndrome

Octreotide effectively controls the flushing, diarrhea, and bronchoconstriction of carcinoid syndrome by suppressing serotonin and other vasoactive peptide secretion from midgut neuroendocrine tumors. Symptom control is achieved in 60-70% of patients. The LAR formulation provides consistent 28-day symptom control. Breakthrough symptoms are managed with supplemental subcutaneous octreotide (Rubin et al., 1999).

Neuroendocrine Tumor Growth Control

The landmark PROMID trial (2009) randomized patients with well-differentiated metastatic midgut NETs to octreotide LAR 30 mg monthly vs placebo, demonstrating significant prolongation of time to tumor progression (14.3 vs 6.0 months, HR 0.34) (Rinke et al., 2009). This established somatostatin analogs as antiproliferative agents, not merely symptom-control drugs, fundamentally changing NET management paradigms.

VIPomas and Other Secretory Tumors

Octreotide is the treatment of choice for VIP-secreting tumors causing watery diarrhea-hypokalemia-achlorhydria (WDHA/Verner-Morrison) syndrome. It controls diarrhea in the majority of patients and can be used as a bridge to surgery or as long-term palliation for unresectable disease. Similar efficacy is seen in glucagonomas, gastrinomas, and GRFomas (Nikou et al., 2005).

GI Bleeding

Octreotide (50 mcg IV bolus followed by 25-50 mcg/hr infusion) is standard adjunctive therapy for acute variceal bleeding in portal hypertension. It reduces portal pressure by decreasing splanchnic blood flow, and meta-analyses confirm improved bleeding control when combined with endoscopic therapy. It has largely replaced native somatostatin and vasopressin for this indication due to practical advantages and fewer side effects (Corley et al., 2001).

Safety Profile

Octreotide has a well-characterized safety profile from decades of clinical use. The most significant long-term adverse effect is gallstone formation, occurring in 15-30% of patients on chronic therapy due to reduced gallbladder contractility and altered bile composition. Other common adverse effects include:

  • Gastrointestinal: Diarrhea, steatorrhea, abdominal pain, nausea, flatulence (often transient, improving over weeks)
  • Metabolic: Hyperglycemia or hypoglycemia (altered insulin/glucagon balance), vitamin B12 deficiency
  • Hepatobiliary: Gallstones, biliary sludge, rarely cholecystitis
  • Injection site: Pain, nodules (SC); injection site reactions (LAR)
  • Cardiac: Bradycardia, QT prolongation (rare)
  • Endocrine: Hypothyroidism (TSH suppression, rare)

Gallstone screening by ultrasound is recommended before and during long-term therapy. Most GI side effects attenuate with continued use. The oral formulation (Mycapssa) has a similar adverse effect profile with additional transient GI symptoms related to the permeability enhancer.

Pharmacokinetic Profile

Octreotide — Pharmacokinetic Curve

Subcutaneous injection, Intramuscular (LAR depot), Oral (Mycapssa)
0%25%50%75%100%0m1.5h3h4.5h6h7.5hTimeConcentration (% peak)T_max 36mT_1/2 1.5h
Half-life: 1.5hT_max: 36mDuration shown: 7.5h

Quick Start

Route
Subcutaneous injection, Intramuscular (LAR depot), Oral (Mycapssa)

Molecular Structure

2D Structure
Octreotide molecular structure
Molecular Properties
Formula
C₄₉H₆₆N₁₀O₁₀S₂
Weight
1019.3 Da
CAS
83150-76-9
PubChem CID
448601
Exact Mass
1018.4405 Da
LogP
1
TPSA
383 Ų
H-Bond Donors
13
H-Bond Acceptors
14
Rotatable Bonds
17
Complexity
1740
Identifiers (SMILES, InChI)
InChI
InChI=1S/C49H66N10O10S2/c1-28(61)39(25-60)56-48(68)41-27-71-70-26-40(57-43(63)34(51)21-30-13-5-3-6-14-30)47(67)54-37(22-31-15-7-4-8-16-31)45(65)55-38(23-32-24-52-35-18-10-9-17-33(32)35)46(66)53-36(19-11-12-20-50)44(64)59-42(29(2)62)49(69)58-41/h3-10,13-18,24,28-29,34,36-42,52,60-62H,11-12,19-23,25-27,50-51H2,1-2H3,(H,53,66)(H,54,67)(H,55,65)(H,56,68)(H,57,63)(H,58,69)(H,59,64)/t28-,29-,34-,36+,37+,38-,39-,40+,41+,42+/m1/s1
InChIKeyDEQANNDTNATYII-OULOTJBUSA-N

Research Protocols

subcutaneous Injection

Breakthrough symptoms are managed with supplemental subcutaneous octreotide (Rubin et al., 1999).

GoalDoseFrequency
Approximately10-40 mgMonthly
General Research Protocol30 mgMonthly
Acute variceal bleeding in portal hyperte50 mcg, 25-50 mcgPer protocol

intramuscular Injection

The development of the long-acting release (LAR) microsphere formulation in 1998 enabled once-monthly intramuscular injection, transforming patient compliance.

GoalDoseFrequency
Approximately10-40 mgMonthly
General Research Protocol30 mgMonthly
Acute variceal bleeding in portal hyperte50 mcg, 25-50 mcgPer protocol

oral

In 2020, an oral octreotide formulation (Mycapssa) using transient permeability enhancer (TPE) technology received FDA approval, marking a milestone in oral peptide delivery. The oral formulation (Mycapssa) has a similar adverse effect profile with additional transient GI symptoms related to the per

GoalDoseFrequency
Approximately10-40 mgMonthly
General Research Protocol30 mgMonthly
Acute variceal bleeding in portal hyperte50 mcg, 25-50 mcgPer protocol

Interactions

Peptide Interactions

SOMATOSTATINcompatible

It has largely replaced native somatostatin and vasopressin for this indication due to practical advantages and fewer side effects ([Corley et al.

What to Expect

What to Expect

Onset

Effects begin within hours of administration based on half-life of ~90 minutes (SC); ~28 days effective duration (LAR depot)

Week 3-4

The LAR formulation provides consistent 28-day symptom control.

Month 4-6

The landmark PROMID trial (2009) randomized patients with well-differentiated metastatic midgut NETs to octreotide LAR 30 mg monthly vs placebo,...

Ongoing

Continued use as directed

Quality Indicators

What to look for

  • Well-established safety profile
  • Multiple peer-reviewed studies available
  • Oral administration available

Caution

  • Injection site reactions reported

Frequently Asked Questions

References (9)

Updated 2026-03-08Reviewed by Tides Research Team9 citationsSources: peptide-wiki-mdx, pubchem, peptide-wiki-mdx-v2

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