Larazotide acetate
Also Known As
AT1001 | Octapeptide
What is Larazotide?
Larazotide acetate is an oral peptide derived from zonula occludens that acts as a tight junction regulator and zonulin antagonist. It binds to receptors of apical intestinal cells and antagonises zonulin, preventing the opening of the epithelial intestinal tight junctions caused by gluten/gliadin, glyphosate, pro-inflammatory cytokines, zonulin bacterial antigens such as lipopolysaccharide (LPS) and bacterial dysbiosis.
Zonulin is a main target of Larazotide acetate; the zonulin protein opens tight junctions and causes intestinal hyper-permeability (leakiness) and increases the passage of stressors into circulation and the lamina propria; eliciting an immune response and inflammation.
Subsequent tissue damage, immune dysfunction, blood-brain barrier breakdown, neuroinflammation, increased liver detoxification burden and allergic/histamine responses result when the first line barrier breaks down.
Larazotide acetate has been shown in the 2012 study by Gopalakrishnan et al to “inhibit gliadin-induced macrophage accumulation in the intestine and preserve normal TJ structure, as well as inhibited the increase in TJ permeability elicited by basolaterally applied cytokines”.
Larazotide acetate is being touted as a promising “non-dietary treatment for coeliac disease”. It has passed, and is also currently being researched in multiple clinical trials, with a growing body of evidence showing promise in the scientific literature for those with coeliac disease and other bowel diseases.
Larazotide Mechanisms of Action:
Larazotide is an inhibitor of paracellular permeability and a zonlin antagonist.
In celiac disease, one pathway that allows fragments of gliadin protein to get past the intestinal epithelium and subsequently trigger an immune response begins with binding of indigestible gliadin fragments to the chemokine CXC motif receptor 3 (CXCR3) on the luminal side of the intestinal epithelium (see this page).
This leads to the induction of myeloid differentiation factor 88 (MYD88) and the release of zonulin into the lumen.
Zonulin then binds to epidermal growth factor receptor (EGFR) and protease-activated receptor 2 (PAR2) in the intestinal epithelium.
This complex then initiates a signalling pathway that eventually results in tight junction disassembly and increased intestinal permeability.
Larazotide acetate intervenes in the middle of this pathway by blocking zonulin receptors, thereby preventing tight junction disassembly and associated increase in intestinal permeability.
Larazotide Studies:
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
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
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 randomised placebo-controlled study. Alimentary pharmacology & therapeutics, 37(2), 252–262. https://doi.org/10.1111/apt.12147
Khaleghi, S., Ju, J. M., Lamba, A., & Murray, J. A. (2016). The potential utility of tight junction regulation in celiac disease: focus on larazotide acetate. Therapeutic advances in gastroenterology, 9(1), 37–49. https://doi.org/10.1177/1756283X15616576
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
Serena, G., Kelly, C. P., & Fasano, A. (2019). Nondietary Therapies for Celiac Disease. Gastroenterology clinics of North America, 48(1), 145–163. https://doi.org/10.1016/j.gtc.2018.09.011
Valitutti, F., & Fasano, A. (2019). Breaking Down Barriers: How Understanding Celiac Disease Pathogenesis Informed the Development of Novel Treatments. Digestive diseases and sciences, 64(7), 1748–1758. https://doi.org/10.1007/s10620-019-05646-y
Yoosuf, S., & Makharia, G. K. (2019). Evolving Therapy for Celiac Disease. Frontiers in Pediatrics, 7, 193. https://doi.org/10.3389/fped.2019.00193
Larazotide Clinical Trials
NCT00492960 Study to Assess the Efficacy of Larazotide Acetate for the Treatment of Celiac Disease Phase 2 – Completed
NCT00620451 Randomized, Double-Blind, Placebo-Controlled Study of Larazotide Acetate in Subjects With Active Celiac Disease. Phase 2 – Completed
NCT00889473 Study of the Efficacy of Larazotide Acetate to Treat Celiac Disease Phase 2 – Completed.
NCT01396213 A Double-blind Placebo-controlled Study to Evaluate Larazotide Acetate for the Treatment of Celiac Disease. Phase 2 – Completed.
NCT00362856 Safety and Tolerability Study of Larazotide Acetate in Celiac Disease Subjects – Underway.