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Larazotide (AT-1001)8 residuesGGVLVQPGEach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: AT-1001, INN-202
Eight amino acids, taken as a capsule, designed to seal the gut barrier from the inside. Larazotide acetate (AT-1001) is a synthetic zonulin receptor antagonist that blocks tight junction disassembly triggered by gluten-derived gliadin peptides. In Phase 2b, 342 celiac patients on a gluten-free diet saw 26% fewer symptomatic days on the 0.5 mg dose. The Phase 3 trial failed at interim analysis in 2022, and the original developer went bankrupt a year later. Still, larazotide remains the most clinically advanced tight junction regulator ever tested; no injection needed, no systemic absorption, and a safety profile that matched placebo across every trial.
A Phase 2b trial put 342 celiac patients on 0.5 mg three times daily, and symptomatic days dropped 26% compared to placebo. That single data point carried larazotide acetate (AT-1001, sequence GGVLVQPG, CAS 258818-34-7) through over a decade of clinical development. Larazotide is a synthetic eight-amino-acid peptide originally derived from Vibrio cholerae's zonula occludens toxin. It blocks zonulin receptors on intestinal epithelial cells, preventing tight junction disassembly that gliadin peptides trigger after gluten exposure. The drug works entirely in the gut lumen. Systemic absorption is negligible, which accounts for its placebo-comparable safety profile across all trials. Roughly 40% of celiac patients keep having symptoms despite strict gluten-free diet adherence. Larazotide was built for that population. You take a capsule 15 minutes before each meal, three times daily. No reconstitution. No needles. The drug reaches the duodenum and proximal jejunum, occupies zonulin binding sites, and keeps the paracellular pathway sealed. The Phase 3 CedLara trial enrolled 525 patients but was discontinued in June 2022 when interim analysis showed the effect size couldn't reach statistical significance with a feasible sample size. 9 Meters Biopharma filed Chapter 7 bankruptcy in July 2023; assets sold to Interlude Biopharma Co. for $1.7 million. A newer thread of research points to MIS-C: Yonker et al. (2025)[1] ran a Phase 2a trial in 12 children and found faster SARS-CoV-2 spike antigen clearance with QID dosing. A Long COVID trial (NCT05747534) is actively recruiting at Massachusetts General Hospital, though enrollment sits well below target.
Gluten reaches the intestinal lumen, and gliadin peptides trigger zonulin release from enterocytes. Zonulin then binds epidermal growth factor receptor (EGFR) and protease-activated receptor 2 (PAR2) on the basolateral side of epithelial cells. That binding transactivates EGFR through PAR2, firing off phospholipase C. The downstream signaling generates inositol 1,4,5-triphosphate and diacylglycerol, which activate PKC-alpha. PKC-alpha phosphorylates tight junction proteins, including ZO-1 and myosin 1C. Actin polymerization follows. The tight junction complex physically pulls apart, and paracellular permeability spikes. This is the cascade that drives celiac symptoms after gluten exposure. Larazotide sits on zonulin binding sites before any of this starts. By occupying those receptors, it prevents the initial receptor activation. It also inhibits myosin light chain kinase (MLCK), reducing cytoskeletal tension on actin filaments. The combined effect is tight junction stabilization: ZO-1, occludin, and claudin proteins redistribute back to the cell membrane rather than getting pulled inward. Because larazotide works in the luminal space and isn't absorbed systemically, it targets the disease mechanism at origin. No immune suppression. No off-target receptor activity outside the gut.
Oral 0.5 mg TID reduces GI symptoms in celiac disease patients on GFD. Phase 2b (n=342) showed 26% fewer symptomatic days and 31% more improved-symptom days vs. placebo. Phase 3 (n=525) failed to reach statistical significance at interim analysis (June 2022). Emerging Phase 2a data supports use in MIS-C (Yonker et al. 2025)[1]: faster spike antigen clearance and GI recovery. Long COVID trial (NCT05747534) recruiting.
Kelly et al., Gastroenterology 2015 (Phase 2b, n=342, PMID 25683116); Yonker et al., Science Translational Medicine July 2025 (MIS-C Phase 2a, n=12, PMID 40737433)
Phase 3 celiac trial (CedLara) failed. Original developer bankrupt (9 Meters, July 2023). IP now held by Interlude Biopharma Co. (patent assignments May and Dec 2024). No FDA approval. MIS-C data is n=12 only. Long COVID trial (NCT05747534) underenrolled (~48 of 150 target as of 2025). Inverted dose-response (1 mg and 2 mg TID performed no better than placebo) limits escalation options.
Extremely niche community use. Discussed primarily in ME/CFS and celiac disease forums. Oral convenience is the main appeal. Community sentiment shifted from hopeful (pre-2022) to cautiously disappointed after Phase 3 failure. Small subset self-experimenting for Long COVID/leaky gut.
Community protocols directly mirror the Phase 2b clinical trial design (0.5 mg TID). The gap is volume: almost no organized community self-experimentation. Use is driven by patients with formal diagnoses (celiac, ME/CFS, Long COVID) seeking access to a clinically studied drug that never received approval.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 0.5mg | 3x Daily |
| Moderate | 0.5mg | 3x Daily |
| Aggressive | 0.5mg | 3x Daily |
Larazotide is oral. No vials, no bacteriostatic water, no syringes. You're swallowing a capsule, 0.5 mg, three times a day, 15 minutes before meals. Timing matters more than most people expect. The capsule needs to be in the lumen before gliadin-derived peptides arrive. Taking it with food instead of before food likely reduces the protective window. Formulation is the real variable here. Clinical trials used delayed-release capsules engineered to dissolve in the duodenum and proximal jejunum. Raw API powder dumped into a standard gelatin capsule may release in the stomach and never reach the target site. If you're sourcing from a research supplier, delayed-release encapsulation is not optional. Don't escalate the dose. Phase 2b tested 0.5 mg, 1 mg, and 2 mg TID. The 1 mg and 2 mg groups performed no better than placebo. The working hypothesis is receptor saturation causing paradoxical loss of efficacy; 0.5 mg TID is the ceiling. Store capsules at room temperature (20 to 25 degrees Celsius). Stable for 24 months when kept dry.
Clinical trials used 12-week continuous dosing periods. Larazotide is intended for ongoing daily use alongside a gluten-free diet, not as a short-term cycle. No evidence of tachyphylaxis or tolerance was observed during 12-week treatment periods. Long-term use patterns haven't been established in controlled trials.
Clinical trials ran 12-week continuous treatment periods with no observed tachyphylaxis or tolerance. Long-term safety data beyond 12 weeks does not exist from controlled trials. The 12-on / 4-off structure mirrors the trial design and enables periodic reassessment. Larazotide's clinical model is ongoing daily use (not short cycles), but absence of long-term data makes the 12-week checkpoint a reasonable precaution.
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Expected: Gradual reduction in bloating and abdominal pain over 4-8 weeks; 50%+ reduction in weekly abdominal pain scores in Phase 2b responders by week 8-12
Monitor: Optional: lactulose/mannitol ratio at baseline and week 12 to objectively assess intestinal permeability change
Obtain larazotide acetate in delayed-release capsule form, 0.5 mg per capsule. Confirm the supplier provides a Certificate of Analysis showing HPLC purity of 98% or higher.
Swallow whole with a full glass of water on an empty stomach. Do not open the capsule or chew it.
Same timing: 15 minutes before eating, on an empty stomach, with water.
Total daily intake is 1.5 mg (three capsules of 0.5 mg).
Optional conservative start: some users begin at 0.25 mg TID for the first one to two weeks to assess GI tolerance before moving to 0.5 mg TID.
Continue this protocol for 12 weeks alongside a strict gluten-free diet. Larazotide is an adjunct, not a replacement for dietary management.
No withdrawal or rebound effects were observed in clinical trials. Symptoms typically return gradually over 2 to 4 weeks after stopping.
Storage: keep capsules at controlled room temperature (20 to 25 degrees Celsius). No refrigeration needed. No reconstitution step applies.
Note: larazotide is not an injectable. No syringe unit calculations apply. If your source provides raw powder rather than pre-made capsules, you'll need access to delayed-release encapsulation equipment or a compounding service. Standard gelatin capsules will release the drug in the stomach rather than the target site.
N/A: this is the sole supported route
No injectable protocol exists or has been studied. Systemic absorption is negligible regardless of route: larazotide acts entirely in the intestinal lumen. No IV or SC formulation has been developed or tested.
Same nominal dose but uncertain luminal distribution; drug may release in stomach
Clinical formulations used delayed-release capsules to deliver drug specifically to the duodenum/proximal jejunum. Loose raw powder bypasses this targeting. Community reports of raw powder use are anecdotal with inconsistent outcomes.
Complementary gut healing: larazotide closes tight junctions acutely (zonulin receptor blockade) while BPC-157 supports mucosal repair and microvascular healing. Sold together in pre-formulated research capsules (Limitless Life Nootropics Gastro Inflammation Research Formula, $199.99/60 caps).
Larazotide 0.5 mg TID + BPC-157 250 mcg TID (oral capsule), both 15 min before meals, 12 weeks
KPV targets NF-κB-mediated gut mucosal inflammation while larazotide addresses upstream barrier dysfunction. Both are oral peptides with local GI activity. Combined in the same vendor formulation (Limitless Life Nootropics: 250 mcg KPV + 250 mcg N-Acetyl Larazotide per capsule).
NSAIDs independently increase intestinal permeability via prostaglandin inhibition and direct mucosal damage: directly counteracting larazotide's barrier-protective mechanism. NSAID users were explicitly excluded from all clinical trials. Treat as a contraindication.
Do not combineConcurrent antibiotic use was an exclusion criterion in clinical trials. Antibiotics alter gut microbiome composition and intestinal permeability independently, confounding larazotide's effect.
Altered gastric pH from PPIs and H2 blockers can affect capsule dissolution timing and alter luminal distribution of larazotide in the duodenum/proximal jejunum.
Pricing updated 2026-04-09
The Phase 3 CedLara trial (n=525) and its predecessor Phase 2b (n=342) both reported adverse event rates that were statistically indistinguishable from placebo. That's the headline, but the details matter because this drug's safety story is shaped more by what's absent than by what's present. Headache occurred in roughly 5 to 7 percent of participants taking larazotide. The placebo group reported headache at the same rate. Urinary tract infections showed up at about 5 percent, again matching placebo. These are the two most commonly flagged events across all published trial data. Mild GI symptoms (nausea, flatulence) appeared occasionally. Given that the entire study population had celiac disease and baseline GI symptoms, attributing any GI complaint specifically to larazotide is difficult. Trial investigators did not flag any GI adverse event as drug-related. No serious adverse events were attributed to larazotide in any completed trial. No clinically meaningful changes in liver enzymes, kidney function, bone markers, hemodynamic measurements, or ECG parameters were observed. This clean profile is expected: larazotide isn't absorbed into the bloodstream. It acts in the intestinal lumen and gets degraded locally without reaching systemic circulation. Pregnancy and breastfeeding represent a gap, not a clearance. No safety data exists for these populations. Clinical trials enrolled adults only; children under 18 were excluded. The MIS-C Phase 2a (Yonker 2025)[1] enrolled 12 pediatric patients with no reported serious adverse events, but that sample is far too small to draw safety conclusions for routine pediatric use. Drug interactions are theoretical rather than documented. NSAIDs independently increase intestinal permeability and were excluded from clinical trials. Proton pump inhibitors and H2 blockers could alter capsule dissolution timing. Immunosuppressants like azathioprine and methotrexate have overlapping effects on intestinal immune responses; combined use was never studied. When to stop: if GI symptoms worsen beyond your pre-treatment baseline, if you develop a new GI infection, or if antibiotic treatment becomes necessary. The trials excluded concurrent antibiotic use entirely.
Verify Larazotide (AT-1001) dosing and safety with a second opinion
No FDA-approved commercial product. All access via research chemical suppliers. Oral route limits systemic contamination risk vs. injectables, but formulation quality (delayed-release capsule technology) critically affects whether drug reaches the target site in the duodenum/proximal jejunum. Chinese bulk API is cheapest but QC varies widely.
| Test | When | Target |
|---|---|---|
| Lactulose/mannitol ratio (intestinal permeability urine test) | Baseline before starting; repeat at week 12 | Normal ratio <0.030; >50% reduction from personal baseline is a meaningful response signal |
| GI symptom diary / Celiac Symptom Index (CSI) | Weekly throughout protocol | — |
| Serum zonulin (optional) | Baseline and week 12 | — |
Objective measure of tight junction integrity used in clinical trials. Confirms functional response independent of subjective symptom reporting.
The CSI tool was used in Phase 2b to define responders. Weekly abdominal pain scoring allows objective comparison to trial responder threshold (≥50% reduction by weeks 8-12).
Anecdotally tracked in ME/CFS self-experimentation. Note: commercial serum zonulin assays have significant cross-reactivity issues; interpret results cautiously. No validated target range for clinical use.
Begin taking 0.5 mg capsules three times daily before meals. No immediate symptom changes expected. Larazotide works locally in the gut and requires consistent dosing to stabilize tight junctions.
Some patients began noticing reduced bloating and abdominal discomfort during this period in clinical trials. Intestinal permeability markers may start to shift.
Measurable symptom improvement becomes more apparent. In Phase 2b, the 0.5 mg group showed a 26% decrease in symptomatic days by this point. Abdominal pain scores typically show the clearest response.
Peak clinical benefit observed in trials. Patients achieving response typically show a 50% or greater reduction in weekly average abdominal pain scores. Symptom improvement plateaus.
Long-term maintenance data is limited since trials capped at 12 weeks. Continued use alongside a gluten-free diet is the intended model. No tolerance development was seen during trial durations.
Days 1 through 7, tolerance establishment: The drug distributes through the intestinal lumen and starts occupying zonulin receptors. Don't expect symptom changes in the first week. Steady-state luminal concentrations probably establish within days given the short activity window. Headache (5 to 7 percent) and UTI (about 5 percent) were the only notable adverse events in trials, both matching placebo rates. Some users report mild nausea or flatulence that resolves within a few days. Weeks 2 through 4, early barrier stabilization: Tight junction proteins (ZO-1, occludin, claudins) begin redistributing back to the cell membrane. Intestinal permeability markers start shifting if you're tracking lactulose/mannitol ratios. A minority of users notice subtle reductions in post-meal bloating. Most describe the improvement as gradual and hard to pin down at this stage. ME/CFS users report mixed results. Weeks 4 through 8, measurable symptom improvement: This is where the Phase 2b data gets concrete. The 0.5 mg TID group logged 26% fewer symptomatic days by this window. Abdominal pain scores showed the clearest response. Users who respond describe this as the most noticeable period: reduced bloating, less cramping, more consistent stool patterns. Non-responders typically decide to stop here. Weeks 8 through 12, peak clinical benefit: Responders in Phase 2b hit 50% or greater reduction in weekly average abdominal pain scores. The trial also recorded 31% more improved-symptom days versus placebo. Benefits plateau; further gains beyond week 8 to 10 are unlikely. Headache and UTI rates stayed at placebo levels through the full 12 weeks. Off-weeks (weeks 13 through 16), washout and reassessment: No tolerance, tachyphylaxis, or withdrawal was observed in any 12-week trial. Intestinal permeability drifts back toward pre-treatment baseline after stopping. Symptoms return gradually over 2 to 4 weeks. Some users skip the formal off period and dose continuously, citing no tolerance buildup, but long-term safety data for continuous use doesn't exist.
Drug distributes to intestinal lumen and begins occupying zonulin receptors. No measurable symptomatic changes expected; steady-state luminal concentrations likely reached within days.
Most users report no noticeable changes in week 1. Occasional mild GI adjustment (nausea, flatulence) at placebo-comparable rates; resolves within days.
Tight junction protein redistribution (ZO-1, occludin, claudins) back to cell membrane. Intestinal permeability markers begin to shift. Some Phase 2b patients noted reduced bloating in this window.
Minority of users report subtle reduction in post-meal bloating and abdominal discomfort. Most describe gradual, difficult-to-attribute improvement. ME/CFS users report mixed results.
Phase 2b: 26% decrease in symptomatic days by week 8 in the 0.5 mg TID group. Abdominal pain scores show clearest response. Permeability markers continue improving.
Users who respond describe this as the most noticeable window. Reduced bloating, less frequent cramping, more consistent stool patterns. Non-responders typically stop here.
Phase 2b peak: 50%+ reduction in weekly average abdominal pain scores in responders; 31% more improved-symptom days. Benefit plateaus: further improvement unlikely beyond this window.
Responders report stable, maintained symptom control. No further incremental gains beyond week 8-10 is the common experience.
No tolerance, tachyphylaxis, or withdrawal observed in 12-week trials. Intestinal permeability returns toward pre-treatment baseline after stopping. No long-term data beyond 12 weeks in controlled trials.
Gradual return of symptoms within 2-4 weeks of stopping. No rebound phenomenon. Some users skip formal off periods and dose continuously, citing no tolerance development; long-term safety unknown.
Source: Estimated luminal activity duration of 1-4 hours based on porcine model showing peak duodenal concentrations at ~1 hour post-dose; larazotide is not systemically absorbed so plasma half-life is not applicable
Loading the interactive decay curve.
Larazotide acetate has no FDA approval. It reached Phase 3 clinical trials for celiac disease (CedLara trial, 525 patients enrolled) before being discontinued in June 2022 after interim futility analysis. The original developer, 9 Meters Biopharma, filed Chapter 7 bankruptcy in July 2023. Patent assets were acquired by Interlude Biopharma Co. through assignments in May and December 2024. No new Phase 3 program has been announced for any indication. Larazotide is available through research chemical suppliers and select peptide vendors as a research compound. It is not a controlled substance. No compounding pharmacy pathway exists comparable to what's available for peptides like BPC-157 or semaglutide. A Long COVID clinical trial (NCT05747534) is actively recruiting at Massachusetts General Hospital under PI Dr. Lael Yonker. Enrollment is well below the 150-patient target. This content is for educational and research purposes only. Larazotide is not approved for human therapeutic use by the FDA or any regulatory agency. Consult a licensed healthcare provider before using any research compound.
Peptide Schedule Research TeamReviewed Apr 20267 Citations
