Supplied ready in solution

Gut & Gastrointestinal

At a glance

Ten answers, each one line. Open any row for the detail behind it.

What it does The intestinal counterpart to the GLP-1 drugs.

The intestinal counterpart to the GLP-1 drugs. Where GLP-1 suppresses appetite, GLP-2 makes the remaining bowel physically grow — taller villi, deeper crypts, more absorptive surface. For patients living on intravenous nutrition, that is the difference between a pump every night and a life.

How it works in detail

Half-life ~2 hours in healthy subjects, ~1.3 hours in… — Documented

~2 hours in healthy subjects, ~1.3 hours in short-bowel-syndrome patients, subcutaneously.

Typical studied dose Set on the approved label, which states the starting dose, how it is… — On the label

Set on the approved label, which states the starting dose, how it is increased and the maximum. Read it there rather than anywhere else — including here.

Read the prescribing information

How often it is used The label schedule is once daily. Dosing intervals follow the half-life… — On the label

The label schedule is once daily. Dosing intervals follow the half-life above, and the prescribing information is what sets them.

How it is taken Subcutaneous, once daily — Documented

Subcutaneous, once daily

Main side effects Colorectal cancer surveillance required · Bowel obstruction · Biliary and pancreatic disease — Carries serious risk

Colorectal cancer surveillance required — A drug whose entire mechanism is intestinal growth carries a theoretical neoplasia risk. Colonoscopy is required before starting and periodically thereafter, with polyp removal.

Bowel obstruction — Mucosal growth can narrow an already compromised lumen; stoma stenosis and obstruction are recognised complications.

Biliary and pancreatic disease — Cholecystitis, cholangitis and pancreatitis are labelled risks requiring periodic laboratory assessment.

All benefits and risks, weighed

Storage before mixing Supplied already in solution and kept refrigerated, not frozen. Freezing…

Supplied already in solution and kept refrigerated, not frozen. Freezing a protein solution can aggregate it, which is not always visible.

Shelf life after mixing Nothing to mix — it is not supplied as a powder. The relevant date is…

Nothing to mix — it is not supplied as a powder. The relevant date is the one printed on the product.

Evidence level 5/5 · Very strong — Documented

Multiple phase 3 randomized trials plus regulatory approval in a major market.

How we rate evidence · What the studies found

Regulatory status FDA Approved — Documented

FDA-approved (2012) for short bowel syndrome in patients dependent on parenteral support. Prescription drug, typically prescribed through specialist intestinal failure centres.

Read the prescribing information · The full legal position

Overview

FDA ApprovedFDA-approved (2012) for short bowel syndrome in patients dependent on parenteral support.

At a glance

Regulatory status	FDA-approved (2012) for short bowel syndrome in patients dependent on parenteral support.
Drug class	GLP-2 receptor agonist — 33-amino-acid analog resistant to DPP-4
Route	Subcutaneous, once daily
Half-life	~2 hours in healthy subjects, ~1.3 hours in short-bowel-syndrome patients, subcutaneously.
Evidence rating	5/5 Very strong Evidence rating 5 out of 5: Very strong Multiple phase 3 randomized trials plus regulatory approval in a major market.
Studied in	STEPS phase 3 program and long-term extension studies in short bowel syndrome with intestinal failure.

Teduglutide sequence & structure

Teduglutide is a 33-residue linear peptide with a free C-terminal acid; molecular weight 3,752.1 Da.

Amino acid sequence (N-terminus → C-terminus)

H-HGDGSFSDEMNTILDNLAARDFINWLIQTKITD-OH

Three-letter	`H-His-Gly-Asp-Gly-Ser-Phe-Ser-Asp-Glu-Met-Asn-Thr-Ile-Leu-Asp-Asn-Leu-Ala-Ala-Arg-Asp-Phe-Ile-Asn-Trp-Leu-Ile-Gln-Thr-Lys-Ile-Thr-Asp-OH`
Length	33 amino acid residues
Modifications	Other modification — Ala2→Gly2 point substitution relative to native human GLP-2(1-33) (DPP-4 resistance); no chemical modifications, all 33 residues are standard L-amino acids
Molecular formula	C₁₆₄H₂₅₂N₄₄O₅₅S
Molecular weight	3,752.1 Da (average, free base)
Identifiers	CAS 197922-42-2 · PubChem CID 16139605 · DrugBank DB08900 · UniProt P01275
Sources	KEGG DRUG D06053 (teduglutide: sequence, formula, MW, CAS)EMA EPAR – Revestive (teduglutide) product information, section 5.1 PubChem CID 16139605 (formula, MW)UniProt P01275 GLUC_HUMAN (proglucagon; native GLP-2 = residues 146–178)IUPHAR/BPS Guide to Pharmacology ligand 7049 (InChI, DrugBank/ChEMBL/PubChem links)

Teduglutide is [Gly2]hGLP-2(1-33): native human GLP-2 (proglucagon residues 146–178, HADGSF…) with Ala2 replaced by Gly, otherwise unmodified, free N-terminus and free-acid C-terminus. Gattex/Revestive is recombinant (E. coli) lyophilized teduglutide with L-histidine, mannitol and sodium phosphate excipients. Reported average MW varies slightly by source (KEGG 3752.08, PubChem 3752.1, others up to 3752.14; the labels round to 3752); PubChem also lists a second CAS (287714-30-1) under the same CID, but 197922-42-2 is the registry number used by KEGG, vendors and the label-era literature.

Record confidence: high — two independent authoritative sources agree on the sequence and modifications. Every sequence on the site is listed with its sources on the peptide sequences index.

How it works

Agonises GLP-2 receptors on intestinal subepithelial myofibroblasts and enteric neurons, triggering mucosal growth: increased villus height and crypt depth, slowed gastric emptying and transit, and increased intestinal blood flow. A single alanine-to-glycine substitution blocks DPP-4 degradation, extending half-life from minutes to hours.

Evidence base

Rated 5 of 5 — Very strong. Multiple phase 3 randomized trials plus regulatory approval in a major market.

Phase 3 trials with an objective, hard-to-game endpoint: litres of intravenous nutrition avoided.

Benefits and risks, weighed against the evidence

Every entry below carries the strength of the evidence behind it — three bars for strong human data, two for moderate, one for preliminary or preclinical work. The two columns are not equal by design: where a compound has more documented risk than demonstrated benefit, the lists say so.

Reported benefits

4 entries · 3 on strong human evidence

Reduces parenteral nutrition dependence

A substantial proportion of patients achieved clinically meaningful reductions in weekly parenteral support volume, and some achieved complete independence from it.
Evidence: Strong evidence
Genuine mucosal growth

Biopsy-confirmed increases in villus height and crypt depth — structural change, not just symptom improvement.
Evidence: Strong evidence
Reduces infusion days per week

Fewer nights tethered to a pump, with direct quality-of-life consequences.
Evidence: Strong evidence
Durable with continued therapy

Extension studies show benefit maintained over years of treatment.
Evidence: Moderate evidence

Risks and cautions

6 entries · 3 serious or common

Colorectal cancer surveillance required

A drug whose entire mechanism is intestinal growth carries a theoretical neoplasia risk. Colonoscopy is required before starting and periodically thereafter, with polyp removal.
Evidence: Serious
Bowel obstruction

Mucosal growth can narrow an already compromised lumen; stoma stenosis and obstruction are recognised complications.
Evidence: Serious
Biliary and pancreatic disease

Cholecystitis, cholangitis and pancreatitis are labelled risks requiring periodic laboratory assessment.
Evidence: Serious
Fluid overload

Improved absorption can cause fluid overload if parenteral support is not reduced in step — congestive heart failure has been reported.
Evidence: Moderate evidence
Benefit reverses on stopping

The mucosal changes regress after discontinuation; it is indefinite therapy.
Evidence: Moderate evidence
Very high cost

Among the more expensive chronic therapies in gastroenterology.
Evidence: Minor

Counts are not a score. A single serious risk can outweigh several well-supported benefits, and a long benefit list built on preclinical work outweighs nothing at all.

Opinion — what people actually report

5 themes · 1 reported benefit · 3 reported problems

This is the weakest tier on this site. These are themes drawn from public discussion — forums, subreddits and patient threads — not from trials. There is no control group, no denominator, and no way to confirm that what someone injected matched its label. People post when a result is dramatic and when something goes wrong, and rarely when nothing happens, so treat everything below as a description of the conversation rather than of the compound. The bars count how often a thing is said, not how well it is supported.

Reduced parenteral nutrition dependence Reported benefit. Dominant theme: Comes up in most discussions of this compound.

The benefit that matters, and reports describe it in terms of hours per night freed from an infusion pump rather than in clinical endpoints.
Abdominal pain and distension early on Reported problem. Dominant theme: Comes up in most discussions of this compound.

The most common adverse effect, and reported as difficult in the first weeks.
Colonoscopy surveillance is a source of anxiety Reported problem. Dominant theme: Comes up in most discussions of this compound.

The requirement for scopes because of polyp and neoplasia concerns comes up constantly, and patients find it unsettling.
Stoma changes and site complications Reported problem. Recurring: Raised regularly, though not by everyone.

Enlargement and output changes in patients with stomas are frequently discussed.
Cost is extraordinary and access is fought for Practical note. Dominant theme: Comes up in most discussions of this compound.

Among the most expensive drugs discussed anywhere on this site, and much of the community conversation is about obtaining it.

Where the reports and the evidence part ways

The benefit and the burden both match the trial evidence: STEPS showed reduced parenteral support requirements, and the GI effects and the neoplasia surveillance requirement are labelled and real. The intestinotrophic mechanism that produces the benefit is the same one that drives the polyp concern, which is a genuine trade-off rather than a theoretical one. Patient anxiety about surveillance is proportionate rather than excessive here.

Questions & answers

Readers on Teduglutide

Questions and answers from readers, under generated names. Nothing here has been checked or reviewed by the site and none of it is medical advice. It is the least verified thing on this page — and it is here because people ask each other these things anyway, and most of the other places they can ask are run by sellers.

0 questions · 0 answers

Other readers answer these. Ask about Teduglutide and the people who have actually looked into it can reply. You post under a generated name — two ordinary words — and that is the only thing anyone else sees. Your address is never shown on the page, never sold and never used for marketing. What we keep, and why.

No questions yet. Ask the first one above — it takes one box and an email address.

How names work, and the house rules

Names. Every verified address is given one generated name — two ordinary words — and keeps it. Nobody chooses a name and nobody can take another's. Posts marked desk were written by the site's own editorial desk, usually to open a thread; they carry a generated name like everyone else's and are held to the site's rules, which means they never state an amount.

What is not allowed. Selling, sourcing, vendor names, coupon codes and "message me" — posts that read that way are held and usually removed. Personal medical details you would not want public. Abuse. Instructions framed as what someone else should do.

What this is not. A reader's report of what happened to them is a report, not a finding, and an answer here is one person's view. Nothing in this section changes the evidence rating above it. If something you read here would change what you take, take it to a pharmacist or physician first.

Your data. Delete any post of yours at any time, or remove everything you have written together with your name. Details in the privacy notice.

Who should avoid it

Active gastrointestinal malignancy
Active malignancy elsewhere within the last 5 years (relative)
Known colorectal polyps not yet removed
Pregnancy (insufficient data)

If used under medical supervision, monitor

Colonoscopy before initiation, at 1 year, then every 5 years
Bilirubin, alkaline phosphatase, lipase and amylase every 6 months
Fluid balance and parenteral support volume
Stoma assessment where present

Interactions

Not exhaustive. Always have a pharmacist or physician review your full medication list — including supplements.

Oral medications — increased absorption may require dose reduction of drugs with narrow therapeutic windows
Parenteral nutrition — must be actively reduced as absorption improves

Commonly confused with

These mix-ups cause real harm — two products sold under one name, or two molecules whose effects run in opposite directions.

Semaglutide FDA Approved Evidence 5/5

GLP-1 and GLP-2 are different hormones from the same precursor gene with opposite therapeutic aims: GLP-1 drugs reduce intake and slow the gut, GLP-2 drugs grow the gut to absorb more.

Compare side by side

Regulatory & legal status

Prescription drug, typically prescribed through specialist intestinal failure centres.

Infographic

Teduglutide — benefits & risks at a glance Download SVG

Where to read further

We link to live literature searches rather than a frozen citation list, so you always see current results — including anything published after our last review.

short bowel syndromeGLP-2intestinal growthapprovedrare disease

Related peptides in Gut & Gastrointestinal

Terms used on this page

Intravenous Administration (IV): Intravenous administration delivers drug directly into the bloodstream, giving complete bioavailability by definition and making it the reference route against which all others are measured.
Glucagon-Like Peptide-1 (GLP-1): Glucagon-like peptide-1 is an incretin hormone released by intestinal L-cells after a meal that stimulates glucose-dependent insulin secretion and suppresses appetite.
DPP-4 Cleavage: DPP-4 cleavage is the removal of an N-terminal dipeptide by dipeptidyl peptidase-4, the enzymatic step that inactivates incretin hormones within minutes of their release.
Gastric Emptying: Gastric emptying is the rate at which stomach contents pass into the duodenum, a major determinant of postprandial glucose and of incretin therapy tolerability.
Fibroblast: A fibroblast is the mesenchymal cell that produces and maintains connective tissue matrix, and which differentiates into a contractile myofibroblast during wound repair.
Terminal Half-Life: Terminal half-life is the time taken for drug concentration to fall by half during the final, slowest phase of elimination, and it sets the dosing interval.

This page is educational information, not medical advice. It cannot account for your medical history, medications, or risk factors. Do not start, stop or change any treatment based on it. Speak to a qualified healthcare professional who knows your case.