Larazotide (larazotide) is a synthetic octapeptide, a molecule composed of eight amino acid residues. It was developed to investigate the potential to influence the integrity and regulation of epithelial barriers. A significant portion of clinical studies concerns larazotide acetate, analyzed as an experimental substance administered orally to individuals with celiac disease.
The history of research on larazotide includes laboratory experiments, animal models, randomized clinical trials, and a Phase 3 program for celiac disease that was completed ahead of schedule.
The available results require cautious interpretation. Changes in epithelial permeability under experimental conditions, improvement in symptoms reported by patients and confirmed clinical efficacy are separate issues. They cannot be combined into a general statement that larazidone „rehabilitates leaky gut” [1–3].
More recent studies also include a small randomized study in children with multi-organ inflammatory syndrome associated with COVID-19 and a separate study regarding post-COVID syndrome (long COVID) [4,5].
However, the common biological hypothesis regarding the epithelial barrier does not mean that the substance will be effective in various diseases of the gastrointestinal tract or inflammatory conditions.
The article discusses the identity of larazotide, its classification, the amino acid sequence, the mechanisms of action studied, the results of clinical trials, and the limitations of the available evidence.
What is larazotide? Names, synonyms and identity of the substance
Larazotide is a specific peptide substance developed for research on the regulation of the epithelial barrier.
In the scientific literature it is referred to by several names:
- larazotide;
- larazotide;
- larazotide acetate;
- larazotide acetate;
- AT-1001;
- AT1001.
Distinguishing between names is important because publications may identify the substance under investigation using a development code, whereas analytical documentation may focus on its chemical form or amino acid sequence.
Just matching the abbreviated name is not sufficient to confirm that the two documents relate to identical material.
The molecular identity, the formulation being studied, and the context of the experiment should be taken into account.
Do larazotide and larazotide acetate mean the same thing?
Larazotide refers to the peptide substance itself, whereas the larazotide acetate refers to its acetate form.
The word „octane” does not mean a second peptide with a distinct amino acid sequence.
It describes the chemical form of the material.
The name larazotide acetate has been used in many clinical studies, so keeping this term helps to correctly identify the substance being studied.
However, it should not be automatically assumed that different preparations containing the same chemical form are equivalent.
The active substance, the salt form and the finished pharmaceutical formulation require separate descriptions.
What does the code AT-1001 mean?
AT-1001 is a development code used in research on larazotide.
In the study registry for long COVID, the designation AT1001 was directly associated with larotrectinib acetate [5].
However, it is worth checking the full context of the publication, because short research codes may also appear in documents concerning other substances.
Is larazotide the same as zonulin?
No.
Larazotide and zonulin are not the same substance.
Zonulin appears in discussions regarding the regulation of intestinal barrier permeability, while larazotide is a synthetic peptide being studied for its effects on the processes associated with it.
Similarly, larazotide should not be confused with gluten, collagen peptides, or generally referred to as gut-supporting supplements.
The common occurrence of several names in articles concerning the intestinal barrier does not mean that they have identical structure or function.
How is larazotide classified?
Chemically, larazotide is a synthetic oligopeptide, more precisely an octapeptide.
It is not a large protein or an undefined biological extract.
Its studied pharmacological function involves modulating the tight junctions between epithelial cells and the processes that regulate the function of the epithelial barrier [6].
What does the term „strict connection modulator” mean?
Tight junctions, described in the literature as tight junctions, are involved in controlling the flow of substances between adjacent epithelial cells.
The term „strict mode modulator” describes the proposed mechanism of action of larazotide.
However, this is not a general category that confirms clinical effectiveness.
A change in permeability in a laboratory experiment does not automatically mean an improvement in the patient's health.
To demonstrate clinical benefit, appropriate studies should be conducted regarding the specific disease, tissue and formulation.
Why was larazidone studied as an oral substance?
The development program for larazotide focused primarily on the potential local effects in the gastrointestinal tract.
This differs from studies on metabolic peptides, whose action is related to systemic exposure.
A peptide substance administered orally does not need to reach high concentrations in the blood if the mechanism under investigation involves local action in the intestine.
However, the place of operation cannot be assumed solely based on the delivery route.
It requires experimental confirmation [7].
Molecular structure of larazotide – amino acid sequence
Larazotide is a peptide composed of eight amino acid residues.
His published sequence is:
Gly–Gly–Val–Leu–Val–Gln–Pro–Gly (GGVLVQPG)
This sequence was presented, among other things, in a study concerning keratocyte barrier disorders [8].
The individual abbreviations mean:
- Gly – glycine;
- Val – valine;
- Leu – leucine;
- Gln – glutamine;
- Pro – proline.
The sequence of amino acids is an important element of molecular identity.
However, this does not mean that the sequence itself is sufficient to fully characterize the finished preparation.
Why is the amino acid sequence important?
The sequence allows to distinguish larazotide from other short peptides.
It also serves as a reference point when identifying substances in analytical documentation.
However, two materials described by the same sequence may differ in chemical composition, contaminant content, degradation products, and physical properties.
Therefore, the identification of the structure does not replace a full assessment of quality.
Is the larotrectinib powder equivalent to the clinically studied product?
This cannot be assumed automatically.
The ready oral pharmaceutical formulation includes not only the active substance.
The amount of peptide, excipients, release characteristics and stability are also important.
The powder form of the material and the preparation used in a controlled clinical trial may differ in properties despite the identical name of the peptide.
Does the correct sequence confirm the purity of the sample?
No.
The sample may contain the target peptide and residues of synthesis, degradation products, or other impurities.
Identity, purity, the amount of substance and the properties of the formulation are separate parameters.
Clinical studies do not replace the analytical documentation regarding a specific sample.
When interpreting the publication, it is therefore necessary to check not only the name of the substance but also the investigational preparation, the route of administration, the population, and the evaluated results.
Larazotide in scientific studies – laboratory, animal and clinical evidence
Studies of larazotide include various experimental models and clinical populations.
The most transparent way to interpret literature is to separately analyze laboratory and animal results, as well as studies involving humans.
Cellular experiments may indicate potential mechanisms related to tight junctions.
Animal studies allow us to observe the response of the entire organism.
Randomized clinical trials, on the other hand, allow the assessment of symptoms and other parameters relevant to patients.
Combining these results without distinguishing between the level of evidence can lead to overblown conclusions.
Laboratory and animal studies on larazotide
In experimental studies, the effect of larazotide on the organization of tight junctions, proteins associated with the epithelial barrier, actin cytoskeleton, and permeability of epithelial cells was analyzed.
Some experiments involved the controlled exposure of cells to inflammatory factors or other stimuli that disrupt the barrier function.
Such models allow for the detailed study of specific mechanisms.
However, they do not reproduce the complexity of chronic human diseases.
What results were obtained in epithelial models?
In certain experimental conditions, the effect of larotadine on the preservation of structures associated with tight junctions was observed.
The studies indicated, among other things, the retention or reactivation of elements of the epithelial barrier [1,6].
These results support the hypothesis regarding the modulation of permeability.
However, they do not independently confirm a reduction in the symptoms of the disease or a long-term improvement in health status in humans.
What did the studies on mice show?
The experiments used transgenic mouse models, among others, to assess the responses related to gliaden.
Researchers analyzed the structures of intercellular connections and changes related to permeability.
In certain conditions, the behavior of strict connection organizations was observed [1].
However, this does not mean that larazotide prevents all the consequences of gluten exposure in people with celiac disease.
The differences between animal models and human autoimmune disease require caution.
Has larazotide also been studied in the context of the skin barrier?
Yes.
The study published in 2025 analyzed keratocyte barrier disorders associated with histamine activity [8].
The study expanded the scope of experimental observations beyond intestinal models.
However, it does not constitute evidence that oral larazotide treats eczema or that a cosmetic product containing this substance shows proven clinical efficacy.
Such conclusions would require appropriate studies involving humans.
Clinical studies of larotrectinib in celiac disease
Celiac disease is one of the most important areas of clinical research on larazidone.
However, the individual studies concerned different clinical situations.
In some of the experiments, the participants were exposed to gluten under controlled conditions.
In others, people who continued to experience symptoms despite following a gluten-free diet were evaluated.
The result obtained under one of these conditions does not automatically mean protection against gluten or effectiveness in all people with celiac disease.
Study from 2012 – 86 participants
In a randomized study published in 2012, 86 people participated [9].
The study involved controlled exposure to gluten.
One of the parameters evaluated was intestinal permeability, determined by the ratio of lactulose to mannitol.
What results were obtained?
The permeability measurements showed significant variability.
No statistically significant difference was found between the groups studied with respect to this parameter.
At the same time, in some groups with lower tested doses, beneficial signs regarding symptoms were observed.
The results should therefore be described as mixed.
It is not possible to present improvement in certain symptoms as evidence that the main permeability measurement confirmed effectiveness.
Study involving 184 people
Another randomized study involved 184 participants [7].
The response was again analyzed under controlled gluten exposure conditions.
What were the most important observations?
Beneficial changes were observed in some of the results regarding symptoms and antibodies.
However, no statistically significant difference was found in the ratio of lactulose to mannitol.
This means that the results regarding the different endpoints were not uniformly positive.
A change in symptoms does not automatically confirm an improvement in any laboratory measure of intestinal barrier function.
A 2015 study – 342 adults with celiac disease
The study published in 2015 involved 342 adults who continued to report symptoms despite following a gluten-free diet [2].
The researchers evaluated the effect of larazotide on symptoms in this specific population.
What results were obtained?
The lowest of the tested doses met the criteria for the primary endpoint of symptoms.
The two higher doses did not show a similar advantage over placebo.
This result is significant because it does not confirm the simple assumption that more substance always provides greater effectiveness.
It also does not serve as a basis for determining the dosage on your own.
Did the study confirm the cure of celiac disease?
No.
The study involved people on a gluten-free diet.
Improving certain symptoms under these conditions does not mean the autoimmune disease is cured.
It also does not confirm that the consumption of gluten becomes safe.
Phase 3 study – NCT03569007
The next stage of the clinical program included a Phase 3 study registered under the number NCT03569007 [3].
According to the data cited in the source material, the study was completed ahead of schedule by the sponsor.
The register indicated 307 actual participants.
The results of the study were not made available in the analyzed post.
What does the end of the Phase 3 study mean?
This means that the study was not completed according to the original plan.
It cannot be presented as a completed study confirming its effectiveness.
At the same time, the „terminated” status itself does not explain all the reasons for the decision or automatically invalidate previous laboratory and clinical observations.
Full results and documentation regarding the completion of the study would be needed for a detailed assessment of the needs.
Larazotide in other areas of clinical research
Interest in larazotide has also expanded to include selected inflammatory diseases and conditions occurring after infections.
Such studies are based in part on hypotheses regarding the regulation of the epithelial barrier.
However, this does not mean that different diseases have identical causes or respond to the same intervention.
Any potential application requires separate studies.
Study in children with a multi-organ inflammatory syndrome
In 2025, a randomized, double-blind, placebo-controlled study on larotidine used as a complementary intervention in children hospitalized with a multi-organ inflammatory syndrome associated with COVID-19 was published [4].
12 children participated in the study.
What results were observed?
The researchers described a faster improvement in gastrointestinal symptoms and a faster removal of the viral antigen.
No adverse events attributed to larazidone have been reported.
These results are interesting, but they should be treated as preliminary.
The number of 12 participants is too small to draw broad conclusions about pediatric safety or efficacy in other pediatric diseases.
Why was the recruitment process terminated?
The study registry NCT05022303 indicated that recruitment was terminated due to a decrease in the number of cases of the disease [10].
This reason should not be substituted for an unconfirmed statement about security problems.
When interpreting the status of clinical trials, the information actually provided is important.
Larazotide and long COVID – study NCT05747534
A separate clinical study concerned larotrectinib acetate in people with post-COVID syndrome.
The study was registered under the number NCT05747534 [5].
According to the data cited in the source material, its status was determined as completed, and the number of participants was 107.
However, the results were not made available in the analyzed registration entry.
Does the end of the study mean confirmed effectiveness?
No.
The status „completed” means the end of the study as understood by the registry.
It is not synonymous with a positive clinical result.
It is also not possible to transfer the results of a small study in children with multiple inflammatory conditions to people with long COVID.
These are different populations and separate research questions.
How does larazotide work? Mechanisms studied in experiments
The main area of mechanistic research concerns the regulation of the epithelial barrier and tight junctions.
The epithelial barrier is not a completely closed wall.
It is a selective biological system that controls the movement of certain substances between cells.
Its functioning remains linked to immune and inflammatory processes.
What role do tight connections play?
Tight junctions help regulate transport between neighboring epithelial cells.
Studies on larazotide analyzed the behavior of proteins associated with these connections and the actin cytoskeleton under the influence of inflammatory or gluten-related stimuli.
In certain experimental arrangements, the behavior or organization of structures of tight junctions was observed [1,6].
However, this does not mean that the same effect occurs in every disease or tissue.
Is larazotide a zonulin antagonist?
The term „zonulin antagonist” appears in the literature regarding larazotide, including in a study of the multi-organ inflammatory syndrome [4].
This term refers to the substance of the proposed route for regulating permeability.
However, it should not be interpreted as evidence that all disorders commonly referred to as „leaky gut” have a single mechanism or respond to the same intervention.
How do scientists measure the permeability of a barrier?
Depending on the research model, different methods are used.
For example:
- The electrical resistance of the cell layer allows the evaluation of certain barrier properties;
- the movement of the marker enables the examination of permeability under defined conditions;
- the ratio of lactulose to mannitol is used in certain studies of intestinal permeability;
- the assessment of the symptoms allows the analysis of the experiences reported by the patients;
- antibody and histological tests provide information about other aspects of the disease.
These parameters are not interchangeable.
Improving one result does not automatically mean that all the other results will improve.
Does larazotide break down gluten?
This is not a mechanism confirmed in the studies discussed.
The studies primarily concern the regulation of epithelial connections and responses related to permeability.
They do not describe larazotide as a gluten-degrading enzyme.
Modulating the specific response of the barrier is a different mechanism than the chemical or enzymatic breakdown of gluten proteins.
Does larazotide allow gluten to be consumed safely by people with celiac disease?
This has not been demonstrated.
Results obtained during controlled exposure or in people following a gluten-free diet do not confirm the safety of unrestricted consumption of gluten.
Celiac disease is an autoimmune disease.
Observing a specific molecular mechanism does not mean eliminating its cause or all of its clinical consequences.
Limitations of scientific evidence regarding larazotide
Biological mechanism and clinical effectiveness
One of the most important interpretational problems is the difference between a biologically plausible mechanism and a reproducible clinical improvement.
The literature on larotadine clearly illustrates this distinction.
In some studies, beneficial changes in symptoms were observed, although the selected permeability parameter did not show a statistically significant improvement.
Therefore, these results cannot be automatically attributed.
Unusual results of research in celiac disease
The results of the clinical studies differed depending on the endpoint and the group analyzed.
Early permeability measurements were difficult to interpret.
Some results regarding the symptoms were positive.
However, the later Phase 3 program did not provide a completed, publicly presented confirmation of efficacy [2,3,9].
It is therefore not appropriate to describe the entire research program as uniformly positive.
Differences between populations
Adults with celiac disease, children hospitalized with a multisystem inflammatory disease, and people with long COVID constitute different clinical populations.
They differ in the mechanisms of the disease, its course, and the treatment used.
The common interest in the permeability of the epithelium does not mean a similar response to larazotide.
Small trials and limited observation time
Small studies can indicate interesting directions for further analysis.
However, they do not provide sufficient power to detect all rare adverse reactions.
The short observation time also limits the ability to assess the durability of the effects.
The absence of a reported problem in a small sample does not mean confirmed long-term safety.
Incomplete reporting of some studies
In the case of some of the registered studies, the results were not made available in the analyzed registration records.
This makes it difficult to fully assess the clinical program.
Missing data should not be substituted with assumptions regarding efficacy or safety.
Differences between research preparations and commercial products
Clinical studies refer to specific formulations used under controlled conditions.
They do not confirm the quality of independent materials sold under the name larazotide or larazotide acetate.
The identification of the peptide sequence does not replace the evaluation of stability, purity, quantity of the substance, release properties, and other pharmaceutical parameters.
What conclusions can be drawn at the present time?
Available studies indicate that larazotide exhibits activity related to the regulation of the epithelial barrier in certain experimental models.
Studies in humans provide mixed results, depending on the disease, population, and the parameter being evaluated.
They do not justify presenting larazotide as a universal intestinal repair agent, a substitute for established treatment in celiac disease or a confirmed therapy for all diseases associated with mucosal permeability.
Frequently asked questions about larazotide
1. Does larazotide mean a specific substance?
Yes. Larazotide is a specific peptide composed of eight amino acid residues. The octanoate form of larazotide represents its acetate form, while the finished pharmaceutical product also includes additional formulation elements. The GGVLVQPG sequence helps confirm the molecular identity, but does not verify the quality of the specific preparation [8]. Pharmaceutical equivalence also depends on the chemical form and properties of the product under study.
2. What do the available studies on larazidone confirm?
Studies confirm the experimental effect of larotidine on selected processes related to the epithelial barrier and favorable results in some clinical trials. At the same time, some results were ambiguous or did not show a significant difference between groups [2,6]. Evidence regarding celiac disease varies depending on the endpoint and the group being studied. They do not confirm the universal effectiveness of larotidine in all intestinal disorders.
3. Is larazotide a protein or a peptide?
Larazotide is a short peptide, more precisely an octapeptide. Its eight amino acid residues distinguish it from large proteins and undefined peptide mixtures [8]. However, the chemical classification is not evidence of medical efficacy. Larazotide should also not be confused with dietary proteins, collagen, or other substances promoted in the context of gut health.
4. What does „octane” mean in the name of larotadine acetate?
The term „octane” refers to the salt form, not to the additional peptide sequence. The name larazotide acetate appears in many clinical publications and is important when comparing the tested materials [2]. However, the chemical form does not automatically mean identical release of the substance, quality, or efficacy of the finished preparations. These properties require a separate characterization.
5. Is larazotide a proven treatment for celiac disease?
No. Available studies do not confirm that larazidone treats the cause of celiac disease or removes the autoimmune disease. The most important symptom study included people who continued to follow a gluten-free diet, and the later phase 3 program was completed ahead of schedule [2,3]. Improvement in certain symptoms does not prove that unrestricted gluten consumption is safe. Experimental larazidone studies do not replace established treatment for celiac disease.
6. Have all larotidine studies reached the main endpoints?
No. The results differed between the studies and the parameters evaluated. In the early controlled gluten exposure study, no significant difference was found in the main permeability measure, although some results regarding symptoms were favorable [9]. The study may show improvement in one parameter without confirmation of efficacy in another. Therefore, the entire clinical program should not be presented as uniformly positive.
7. Did higher doses of larotrectinib provide better results?
No. In a 2015 study, a favorable outcome for the primary endpoint was obtained in the group receiving the lowest of the tested doses, whereas the two higher groups did not show the same advantage over placebo [2]. This shows that the response to the substance does not have to increase linearly with its amount. This is the result of a specific study, and not a basis for choosing the dosage independently.
8. Does reducing symptoms mean healing of the intestinal lining?
No. The reduction of symptoms and confirmed tissue healing are separate clinical outcomes. To demonstrate structural changes, appropriate histological or other direct measurements are required. Improvement in well-being may be of importance to the patient, but does not automatically indicate epithelial repair. Symptoms, inflammation, and tissue changes should be evaluated separately.
9. Does larazotide break down gluten?
Such a mechanism has not been demonstrated. Research on larazotide focuses primarily on epithelial junctions and processes related to permeability of the intestinal barrier [1]. This is not the same as enzymatic digestion of gluten. Confusing these mechanisms could suggest a protection that has not been confirmed. Modulating the epithelial barrier response does not mean neutralizing gluten.
10. Does the end of the Phase 3 study mean that larazidone does not show any biological activity?
No. The completion of a study before the planned deadline describes the status of a specific clinical trial. The decision of the sponsor to terminate the study is indicated in the NCT03569007 registry [3]. This does not invalidate previous laboratory observations or resolve the results of all other studies. However, it means that the project cannot be presented as a completed study confirming efficacy.
11. Has larazotide been studied in children?
Yes. In a small randomized study, larazotide was evaluated as a complementary intervention in 12 children hospitalized with a multi-organ inflammatory syndrome associated with COVID-19 [4]. Preliminary positive results were observed, but the number of participants was very small. This does not allow for confirmation of broad pediatric safety or efficacy in other pediatric diseases. Larger studies are needed.
12. Does the study of a multi-organ inflammatory syndrome confirm the effectiveness of larazotide in long COVID?
No. Multisystem inflammatory disease in children and long COVID are different clinical problems. A separate study regarding long COVID was marked as completed in the registry, but the results were not made available in the analyzed post [5]. Therefore, observations from one population cannot be transferred to another. Even if both diseases are associated with specific inflammatory processes, their response to intervention requires direct evaluation.
13. Do laboratory tests of the skin confirm the effectiveness of larotadine in the treatment of eczema?
No. The keratocyte assay allows the analysis of specific mechanisms of the skin barrier, but does not provide evidence of the efficacy of eczema treatment in humans [8]. It also does not resolve the issues of the appropriate formulation, tolerability, or durability of clinical effects. To confirm such use, studies involving patients and the appropriate formulation would be necessary.
14. Does oral administration of larotadine mean that the peptide must pass into the blood in its unchanged form?
Not always. If the mechanism under investigation involves local effects in the gut, high systemic exposure may not be necessary. The development of larazotide has focused on the biology of the epithelial barrier [7]. However, this does not mean that oral administration alone confirms local action or safety. The actual site of action and exposure require appropriate experimental data.
15. Can a product sold online as larazotide rely on clinical trial results as proof of equivalence?
No. The product name alone does not confirm that it contains material corresponding to the clinically studied preparation. The significance lies in the sequence, chemical form, amount of substance, quality, stability, and release characteristics. Testing of a specific formulation does not automatically confirm the properties of an independent powder or capsule. Equivalency would require appropriate evidence regarding the specific product.
16. Does the lack of reported adverse reactions confirm the safety of larotadine during pregnancy?
No. Pregnancy safety cannot be determined based on studies that did not include appropriate assessment of pregnant women and pregnancy outcomes. Small or short-term studies also have limited ability to detect rare adverse events. The absence of a reported problem merely means that it was not observed in the specific data. It is not evidence of safety in the unstudied population.
17. What further research is most needed for larazotide?
Larger, appropriately controlled and fully reported clinical trials for each proposed indication would be of greatest value. They should include clinically relevant endpoints, an appropriate observation time, and a detailed safety assessment. Public disclosure of the results of completed studies would also be important. The biologically plausible mechanism provides justification for further experiments, but stronger conclusions require repeatable results in patients.
Applications
Larazotide is a chemically defined, synthetic octapeptide whose potential effect on the regulation of the epithelial barrier has been studied in laboratory experiments, animal models, and clinical trials.
The available results indicate activity associated with tight connections and favorable results regarding some symptoms in specific populations.
At the same time, the studies also showed ambiguous or statistically insignificant results regarding some of the endpoint measures.
The Phase 3 program in celiac disease was completed ahead of schedule and did not provide completed efficacy confirmation in the analyzed registry.
More recent studies regarding the multisystem inflammatory syndrome and long COVID require separate interpretation.
Therefore, larazotide cannot be presented as a universal remedy to repair the intestinal barrier or as a proven treatment for all diseases associated with permeability of the epithelium.
The most justified interpretation is to differentiate the results according to the disease, formulation, population, and the parameters actually being evaluated.
Educational, medical and regulatory reservations
The article is of purely scientific and informational nature and does not constitute medical advice, diagnosis, or recommendations for the purchase or use of larazotide. The studies discussed do not confirm its effectiveness as a universal treatment for intestinal barrier disorders, celiac disease, long COVID, eczema, or other diseases. Laboratory and animal results should not be automatically transferred to humans, and products marketed under the name larazoid should not be considered equivalent to clinically studied products without appropriate verification. People with celiac disease should not treat experimental results as evidence of the safety of gluten consumption or as a basis for abandoning established treatment procedures. The regulatory status of a substance may change over time, therefore decisions regarding treatment require up-to-date official information and consultation with qualified medical personnel.
References
- Gopalakrishnan, S., Durai, M., Kitchens, K., Tamiz, A. P., Somerville, R., Ginski, M., Paterson, B. M., Murray, J. A., Verdu, E. F., Alkan, S. S., & Pandey, N. B. (2012). Larazotide acetate regulates epithelial tight junctions in vitro and in vivo. Peptides, 35(1), 86–94. https://doi.org/10.1016/j.peptides.2012.02.015
- Leffler, D. A., Kelly, C. P., Green, P. H., Fedorak, R. N., DiMarino, A., Perrow, W., Rasmussen, H., Wang, C., Bercik, P., Bachir, N. M., & Murray, J. A. (2015). Larazotide acetate for persistent symptoms of celiac disease despite a gluten-free diet: a randomized controlled trial. Gastroenterology, 148(7), 1311–9.e6. https://doi.org/10.1053/j.gastro.2015.02.008
- 9 Meters Biopharma, Inc. (2022). Study to Evaluate the Efficacy and Safety of Larazotide Acetate for the Relief of CeD Symptoms (NCT03569007) [Clinical trial registration]. ClinicalTrials.gov. Retrieved October 23, 2026, from https://clinicaltrials.gov/study/NCT03569007
- Yonker, L. M., Kane, A. S., Swank, Z., Papadakis, L., Kenyon, V., Han, S., Lima, R., Guthrie, L. B., Alvarez-Carcamo, B., Lahoud-Rahme, M., Balaguru, D., Carroll, R. W., Lok, J., El Saleeby, C., Walt, D. R., & Fasano, A. (2025). Viral spike antigen clearance and augmented recovery in children with post-COVID multisystem inflammatory syndrome treated with larazotide. Science Translational Medicine, 17(809), eadu4284. https://doi.org/10.1126/scitranslmed.adu4284
- Massachusetts General Hospital. (2026). AT1001 for the Treatment of Long COVID (NCT05747534) [Clinical trial registration]. ClinicalTrials.gov. Retrieved October 23, 2026, from https://clinicaltrials.gov/study/NCT05747534
- Gopalakrishnan, S., Tripathi, A., Tamiz, A. P., Alkan, S. S., & Pandey, N. B. (2012). Larazotide acetate promotes tight junction assembly in epithelial cells. Peptides, 35(1), 95–101. https://doi.org/10.1016/j.peptides.2012.02.016
- Kelly, C. P., Green, P. H., Murray, J. A., Dimarino, A., Colatrella, A., Leffler, D. A., Alexander, T., Arsenescu, R., Leon, F., Jiang, J. G., Arterburn, L. A., Paterson, B. M., Fedorak, R. N., & Larazotide Acetate Celiac Disease Study Group. (2013). Larazotide acetate in patients with coeliac disease undergoing a gluten challenge: a randomized placebo-controlled study. Alimentary Pharmacology & Therapeutics, 37(2), 252–262. https://doi.org/10.1111/apt.12147
- Glinka, D. M., & MacGregor, G. G. (2025). The PAR2 Antagonist Larazotide Can Mitigate Acute Histamine-Stimulated Epithelial Barrier Disruption in Keratinocytes: A Potential Adjunct Treatment for Atopic Dermatitis. JID Innovations, 5(4), 100369. https://doi.org/10.1016/j.xjidi.2025.100369
- Leffler, D. A., Kelly, C. P., Abdallah, H. Z., Colatrella, A. M., Harris, L. A., Leon, F., Arterburn, L. A., Paterson, B. M., Lan, Z. H., & Murray, J. A. (2012). A randomized, double-blind study of larazotide acetate to prevent the activation of celiac disease during gluten challenge. The American Journal of Gastroenterology, 107(10), 1554–1562. https://doi.org/10.1038/ajg.2012.211
- Massachusetts General Hospital. (2024). AT1001 for the Treatment of COVID-19-Related MIS-C (NCT05022303) [Clinical trial registration]. ClinicalTrials.gov. Retrieved October 23, 2026, from https://clinicaltrials.gov/study/NCT05022303