Research information only. PrecisePep is an educational library. It is not medical advice and is not intended to assist, encourage or enable self-administration. The compounds documented here are research chemicals — most are not approved for human use. Read the full disclaimer.
PrecisePep/Peptide Library/Teduglutide
Gastrointestinal & Mucosal
Gattex® · Revestive® · GLP-2 analogue · ALX-0600
The incretin nobody talks about. GLP-2 comes from the same precursor gene as GLP-1 but grows intestine rather than suppressing appetite — and the drug built from it lets people with short bowel syndrome come off intravenous feeding.
Proglucagon is cut into several different hormones depending on which tissue processes it. In the pancreas it yields glucagon. In intestinal L-cells it yields GLP-1, GLP-2 and oxyntomodulin. The GLP-1 arm produced the drug class that reshaped diabetes and obesity medicine. The GLP-2 arm produced teduglutide, and it does something entirely different: it makes intestine grow.
In short bowel syndrome — usually after extensive surgical resection for Crohn's disease, mesenteric infarction, volvulus or trauma — the remaining intestine cannot absorb enough fluid and nutrition, and people depend on parenteral support delivered through a central line. That dependence carries catheter sepsis, venous thrombosis and liver disease, and it structures a person's entire week around infusions.
Teduglutide increases villus height and crypt depth in the remaining bowel, improving absorptive surface area. Randomised trials reported reductions in weekly parenteral support volume, and a proportion of patients achieved complete independence from it.[1] For a rare disease with almost no pharmacological options, that is a genuinely large result.
Teduglutide is a prescription medicine used under specialist supervision, and this page publishes no grey-market dosing for it. It appears because the conditions index covers intestinal disease, and because it is the most direct answer available to the question the BPC-157 discussion is really asking: is there a peptide that repairs gut? There is. It requires endoscopic surveillance and a gastroenterologist, and the reason for both is on this page.
GLP-2 receptor agonism. The GLP-2 receptor sits on enteroendocrine cells, subepithelial myofibroblasts and enteric neurons rather than on enterocytes themselves — so the growth effect is relayed through intermediates including IGF-1, keratinocyte growth factor and nitric oxide signalling, not delivered directly to the absorbing cell.
Structural adaptation. Increased crypt cell proliferation and reduced enterocyte apoptosis produce taller villi and deeper crypts, and therefore more absorptive surface. This is trophic remodelling of tissue, not a transport-level change.
Functional effects alongside the structural ones. Increased mesenteric blood flow, slowed gastric emptying and reduced gastric acid secretion each contribute to absorption independently of villus height.
The DPP-4 substitution. Native GLP-2 is destroyed by dipeptidyl peptidase-4 within minutes. Replacing the alanine at position two with glycine blocks that cleavage and extends the half-life to roughly two hours — the same trick, at the same position, that protects several other peptides in this class.
And the reason for the surveillance. A drug whose entire mechanism is increased intestinal crypt cell proliferation is a drug with a theoretical capacity to accelerate growth of anything already proliferating abnormally. That is not a hypothetical worry layered on afterwards — it is a direct restatement of how it works.[2]
Effects that have been reported. A study-tier entry means a result was published — not that the effect is established, reproducible, or transferable from a rodent to a person.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Randomised placebo-controlled trials in adults dependent on parenteral support reported significantly greater reductions in weekly infusion volume on teduglutide, sustained through open-label extension.
A minority of trial participants came off intravenous support entirely. In a condition where the alternative is lifelong central venous access, that is a change in kind rather than degree.
Biopsy data show increased villus height and crypt depth — the mechanism confirmed histologically rather than inferred from an absorption endpoint.
Paediatric trials supported extension of the licence to children from 12 months, a population where parenteral dependence carries the greatest cumulative burden.
Beyond volume, trials reported fewer days per week requiring infusion — the endpoint patients tend to care about most, because it is the one that returns time.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Radiation enteritis, chronic intestinal pseudo-obstruction and severe malabsorptive states share the mechanistic rationale. None is an approved indication and none has comparable trial evidence.
GLP-2 has anti-inflammatory and barrier effects in animal colitis models. Teduglutide is not an IBD treatment and the mechanism cuts both ways — a trophic agent in an inflamed, dysplasia-prone colon is not obviously desirable.
The mechanism is legitimately relevant to barrier integrity, which is why it surfaces in "leaky gut" discussion. Using an approved trophic drug for an unvalidated syndrome inverts the risk-benefit entirely.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Patient reporting focuses less on absorption numbers than on sleeping without a pump and travelling without a supply chain.
Widely described in the first weeks and consistent with the trophic mechanism and fluid handling changes.
Increased stoma output or a visibly enlarged stoma is commonly reported and is a labelled effect requiring assessment.
A rare-disease orphan drug requiring endoscopic surveillance and specialist prescribing has essentially no research-chemical presence. Anything offered as such warrants full scepticism.
Adverse effects, contraindications and unknowns. The grey-market tier is where under-reporting is worst: uncontrolled use produces no systematic safety surveillance at all, so absence of a reported harm is not evidence of safety.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Intestinal polyps were identified in trials, and colorectal, gastric and small intestinal polyps have been reported after marketing. The label warns of a risk of accelerating neoplastic growth and requires that colorectal cancer be excluded before treatment starts.
Colonoscopy and upper gastrointestinal endoscopy with polyp removal within six months before starting; follow-up at the end of the first year; thereafter at least every five years. In children, faecal occult blood testing within six months of starting, with endoscopy if there is new or unexplained blood in the stool.
A labelled warning, mechanistically consistent with mucosal growth in a bowel that may already have strictures or adhesions.
Gallbladder, biliary tract and pancreatic events are labelled warnings requiring laboratory assessment before starting and periodically during treatment.
Improved fluid absorption in someone still receiving their previous parenteral volume produces overload. Parenteral support must be reduced as absorption improves — congestive heart failure has been reported.
The common adverse events in the trial programme.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Surveillance exists precisely because the long-term consequence of sustained crypt proliferation in a susceptible bowel is not fully characterised. Registry follow-up continues.
Structural adaptation reverses when the trophic stimulus stops. Parenteral requirements return, which makes this an ongoing therapy rather than a course.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most-reported early experience.
Typical for a daily subcutaneous injection.
Patient discussion regularly returns to the scope schedule, which is a real burden alongside a real benefit.
Figures below are documented, not recommended. Study ranges come from published protocols in the stated model; grey-market ranges are what the research community reports using and carry no safety validation of any kind.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Weight-based, once daily, rotating between abdominal quadrants, thighs and upper arms. Reconstituted from a lyophilised single-dose vial with the supplied sterile water diluent.
In moderate or severe renal impairment or end-stage renal disease, the dose is reduced to 0.025 mg/kg daily.
The clinical work is the weaning, not the injection. Infusion volume is reduced stepwise with fluid balance and laboratory monitoring as absorption improves.
| Parameter | Value | Note |
|---|---|---|
| Dose | 0.05 mg/kg once daily | Subcutaneous, weight-based |
| Renal impairment | 0.025 mg/kg once daily | Moderate, severe or ESRD |
| Before starting (adults) | Colonoscopy + upper GI endoscopy | Within 6 months, polyps removed |
| At 1 year | Repeat endoscopy or imaging | Then at least every 5 years |
| Children | Faecal occult blood within 6 months | Endoscopy if new or unexplained blood |
| Reassess | At 6 months | If parenteral support has not fallen |
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Where parenteral support has not fallen after six months, the label directs reassessment of whether treatment should continue.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Use is confined to specialist intestinal failure services. This site publishes no unsupervised dosing for a drug whose principal risk requires colonoscopy to detect.
Combination effects. Almost no peptide combination has been studied as a combination in humans; stack logic is overwhelmingly mechanistic inference and community practice. Each linked compound has its own page.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
The drug and the weaning protocol are one intervention. Trials paired them and the fluid-overload warning exists because the pairing is not optional.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Intestinal failure management is nutritional before it is pharmacological. Teduglutide adds to that; it does not replace it.
The gut-repair rationale people build around BPC-157 has no human evidence, and adding an unvalidated trophic agent to an approved one in a bowel under polyp surveillance is the least defensible combination on this site.
Improved absorption changes exposure to every orally administered medicine the patient takes. Doses of narrow-therapeutic-index drugs may need review.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
It does demonstrate that a peptide can grow intestinal mucosa. It also demonstrates what that capability requires in exchange: specialist supervision and scheduled colonoscopy.
Whole schedules — dosing, titration, cycle length, and off-time — as documented in trials, as proposed from mechanism, and as circulated in the research community. Reproduced for study and comparison only.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Randomised placebo-controlled trials with 24-week primary endpoints and long-term open-label extension, measuring reduction in weekly parenteral support volume against a standardised weaning algorithm.
Pre-treatment endoscopy, one-year follow-up, five-yearly thereafter, with laboratory assessment of bilirubin, alkaline phosphatase, lipase and amylase before starting and periodically after.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
If parenteral support has not fallen by six months, the continued value of treatment should be reassessed rather than assumed.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Patients consistently describe care coordinated by a dedicated unit rather than general gastroenterology, which reflects how narrow and complex the indication is.
The approved indication is covered above. This section exists because teduglutide is the answer to a question this library gets asked constantly in a different form — can a peptide repair gut — and the answer comes with a price tag that the compounds usually asked about do not disclose.
Approved for short bowel syndrome with parenteral dependence, in adults and children from one year. Everything below is off-label extrapolation. The labelled risk of accelerating neoplastic growth is detectable only by endoscopy, which is why the licence is written around a surveillance schedule.
Pathophysiology
Teduglutide increases intestinal crypt cell proliferation. That is how it works and it is not a side effect of how it works.
Mechanistic rationale
A drug whose entire mechanism is increased crypt proliferation carries a labelled risk of accelerating neoplastic growth, and the licence requires colonoscopy and upper GI endoscopy within six months before starting in adults, again at one year, and at least every five years after. That is the actual price of a peptide that grows intestinal mucosa. Compounds marketed for gut repair on rodent data ask readers to accept the benefit claim without the corresponding surveillance.
Community reports
The comparison is rarely made, and it is the most useful thing this page offers a reader of the rest of this library.
Components carrying the argument: GLP-2 receptor — trophic by design
Pathophysiology
IBD involves chronic mucosal inflammation with an elevated risk of colorectal dysplasia in long-standing colitis.
Mechanistic rationale
GLP-2 has anti-inflammatory and barrier effects in animal colitis models, which is the rationale. A trophic agent in an inflamed, dysplasia-prone colon is not obviously desirable, and this is not an approved use. The approved IBD classes have mucosal healing and surgery-avoidance data.
Community reports
Discussed in IBD contexts on the barrier rationale.
Components carrying the argument: GLP-2 — mucosal growth and barrier
Pathophysiology
Intestinal permeability is measurable; the syndrome constructed on top of it is not a diagnosis.
Mechanistic rationale
The barrier mechanism is genuinely relevant, which is why the compound surfaces in this discussion. Using an approved trophic drug with an endoscopic surveillance requirement for an unvalidated syndrome inverts the risk-benefit calculation completely — the surveillance exists because the benefit in short bowel syndrome is large enough to justify it.
Community reports
Occasional interest, generally from people unaware of the endoscopy requirement.
Components carrying the argument: Barrier and tight junction effects
| Question | Position |
|---|---|
| Approved for | Short bowel syndrome with parenteral dependence |
| Mechanism | Increased intestinal crypt proliferation |
| Labelled risk | Acceleration of neoplastic growth |
| Required before starting (adults) | Colonoscopy + upper GI endoscopy |
| Then | Year 1, and at least every 5 years |
| Off-label gut use | Inverts the risk-benefit — surveillance without the indication |
For intestinal failure: specialist management — optimised parenteral nutrition, oral rehydration, antimotility and antisecretory agents, meticulous catheter care, and surgical options in selected cases. For IBD: mesalazine, corticosteroids for induction, thiopurines, and the biologic classes with mucosal healing endpoints. For IBS: structured low-FODMAP with reintroduction, soluble fibre, gut-directed psychological therapy, and excluding coeliac disease and IBD first.
Physical-chemistry reference for laboratory handling of the lyophilised material. Reproduced so that stability and concentration mathematics can be studied — see the calculator for the arithmetic and the reconstitution guide for sterile technique.
The licensed product is a lyophilised single-dose vial reconstituted with the sterile water diluent supplied in the kit, using the supplied syringe. This site publishes no reconstitution arithmetic for teduglutide — the dose is weight-based, prescribed and dispensed as a kit, and the calculator is not an appropriate tool for it.
Store the kit at controlled room temperature per the label; do not freeze. Reconstituted solution is for single use and should be used within the labelled short window and discarded.
Licensed: 5 mg single-dose vial with prefilled diluent syringe (adult kit); paediatric dosing uses the same presentation with weight-based volume.
Single-use presentation with no multi-dose in-use period — the bacteriostatic-water storage logic that applies elsewhere in this library does not apply here.
Regulatory status changes and differs by country. This is a summary for orientation, not legal advice — check your own jurisdiction.
Approved prescription medicine. Licensed as Gattex in the United States and Revestive in Europe for short bowel syndrome in patients dependent on parenteral support, in adults and children from one year of age. An orphan drug, dispensed through restricted distribution, and in the US supported by a manufacturer programme covering the surveillance requirements.
There is no legitimate unlicensed supply. The principal safety concern — acceleration of neoplastic growth — is detectable only by endoscopy, which is why the licence is written around a surveillance schedule rather than a dose.
Regulatory and trial claims re-checked against primary sources on 16 August 2026. Checked: endoscopic surveillance requirement in the current PI. Approvals, trial readouts and compounding decisions move faster than anything else on this page — a date here means someone looked, not that nothing has changed since.
Not a performance compound and not a common target of anti-doping interest, but peptide hormones and growth factors are addressed under the WADA Prohibited List. Verify against the current list.
Links resolve to PubMed records, trial registries, publisher pages or primary documents. Where a body of work rather than a single paper is cited, the link opens a PubMed query so the full result set — including newer papers than this page — can be reviewed. Verify every claim against the primary source before relying on it.
For educational and research reference only. Nothing on this site is medical advice, a recommendation, or an instruction to administer any substance to a human being. Every figure on this page is a record of what has been reported, not a recommendation. Full disclaimer.
