Integrin antagonists as potential therapeutic options for the treatment of Crohn’s disease

Reference

• Molodecky NA, Soon IS, Rabi DM, et al increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review. Gastroenterology. 2012;142(1):4654 e42; quiz e30.
   Google Scholar
• Hanauer SB. Inflammatory bowel disease: epidemiology, pathogenesis, and therapeutic opportunities. Inflamm Bowel Dis. 2006;12(Suppl 1):S3S9.
   Google Scholar
• Loftus EV Jr. Clinical epidemiology of inflammatory bowel disease: incidence, prevalence, and environmental influences. Gastroenterology. 2004;126(6):1504–1517.
   PubMed Web of Science ®Google Scholar
• Xavier RJ, Podolsky DK. Unravelling the pathogenesis of inflammatory bowel disease. Nature. 2007;448(7152):427–434.
   PubMed Web of Science ®Google Scholar
• Satsangi J, Jewell DP, Rosenberg WM, et al. Genetics of inflammatory bowel disease. Gut. 1994;35(5):696–700.
   PubMed Web of Science ®Google Scholar
• Floyd DN, Langham S, Severac HC, et al. The economic and quality-of-life burden of Crohn’s disease in Europe and the United States, 2000 to 2013: a systematic review. Dig Dis Sci. 2015;60(2):299–312.
   PubMed Web of Science ®Google Scholar
• Schirbel A, Fiocchi C. Inflammatory bowel disease: established and evolving considerations on its etiopathogenesis and therapy. J Dig Dis. 2010;11(5):266–276.
   PubMed Web of Science ®Google Scholar
• Packey CD, Sartor RB. Interplay of commensal and pathogenic bacteria, genetic mutations, and immunoregulatory defects in the pathogenesis of inflammatory bowel diseases. J Intern Med. 2008;263(6):597–606.
   PubMed Web of Science ®Google Scholar
• Birrenbach T, Bocker U. Inflammatory bowel disease and smoking: a review of epidemiology, pathophysiology, and therapeutic implications. Inflamm Bowel Dis. 2004;10(6):848–859.
   PubMed Web of Science ®Google Scholar
• McGovern D, Kugathasan S, Cho JH. Genetics of inflammatory bowel diseases. Gastroenterology. 2015;149:11631176.e2.
   PubMedGoogle Scholar
• Soler D, Chapman T, Yang -L-L, et al. The binding specificity and selective antagonism of vedolizumab, an anti-alpha4beta7 integrin therapeutic antibody in development for inflammatory bowel diseases. J Pharmacol Exp Ther. 2009;330(3):864–875.
   PubMed Web of Science ®Google Scholar
• Bernell O, Lapidus A, Hellers G. Risk factors for surgery and recurrence in 907 patients with primary ileocaecal Crohn’s disease. Br J Surg. 2000;87(12):1697–1701.
   PubMed Web of Science ®Google Scholar
• Leung Y, Panaccione R. Anti-adhesion molecule strategies for Crohn disease. BioDrugs. 2008;22(4):259–264.
   PubMed Web of Science ®Google Scholar
• Ben-Horin S, Chowers Y. Review article: loss of response to anti-TNF treatments in Crohn’s disease. Aliment Pharmacol Ther. 2011;33(9):987–995.
   PubMed Web of Science ®Google Scholar
• McLean LP, Shea-Donohue T, Cross RK. Vedolizumab for the treatment of ulcerative colitis and Crohn’s disease. Immunotherapy. 2012;4(9):883–898.
   PubMed Web of Science ®Google Scholar
• Barreiro O, Sanchez-Madrid F. Molecular basis of leukocyte-endothelium interactions during the inflammatory response. Rev Esp Cardiol. 2009;62(5):552–562.
   PubMed Web of Science ®Google Scholar
• Fiorino G, Correale C, Fries W, et al. Leukocyte traffic control: a novel therapeutic strategy for inflammatory bowel disease. Expert Rev Clin Immunol. 2010;6(4):567–572.
   PubMed Web of Science ®Google Scholar
• Pan WJ, Hsu H, Rees WA, et al. Pharmacology of AMG 181, a human anti-alpha4 beta7 antibody that specifically alters trafficking of gut-homing T cells. Br J Pharmacol. 2013;169(1):51–68.
   PubMed Web of Science ®Google Scholar
• Targan SR, Feagan BG, Fedorak RN, et al. Natalizumab for the treatment of active Crohn’s disease: results of the ENCORE Trial. Gastroenterology. 2007;132(5):1672–1683.
   PubMed Web of Science ®Google Scholar
• Sandborn WJ, Colombel JF, Enns R, et al. Natalizumab induction and maintenance therapy for Crohn’s disease. N Engl J Med. 2005;353(18):1912–1925.
   PubMed Web of Science ®Google Scholar
• Hunt D, Giovannoni G. Natalizumab-associated progressive multifocal leucoencephalopathy: a practical approach to risk profiling and monitoring. Pract Neurol. 2012;12(1):25–35.
   PubMedGoogle Scholar
• Biogen Idec, Inc. TYSABRI(R), prescribing information. Cambridge (MA): Biogen Idec; 2012.
   Google Scholar
• Chandar AK, Singh S, Murad MH, et al. Efficacy and safety of natalizumab and vedolizumab for the management of Crohn’s disease: a systematic review and meta-analysis. Inflamm Bowel Dis. 2015;21(7):1695–1708.
   PubMed Web of Science ®Google Scholar
• Briskin M, Winsor-Hines D, Shyjan A, et al. Human mucosal addressin cell adhesion molecule-1 is preferentially expressed in intestinal tract and associated lymphoid tissue. Am J Pathol. 1997;151(1):97–110.
   PubMed Web of Science ®Google Scholar
• Milch C, Wyant T, Xu J, et al. Vedolizumab does not reduce the CD4+:CD8+ ratio in the CSF of healthy volunteers. In: 19th United European Gastroenterology Week. Stockholm; 2011.
   Google Scholar
• Fedyk E, Csizmadia V, Shyu W, et al. The gastrointestinal-selective biologic vedolizumab does not impair immune surveillance of the central nervous system in non-human primates. Inflamm Bowel Dis. 2011;17(Supplement 1):S4S5.
   Google Scholar
• Sandborn WJ, Feagan BG, Rutgeerts P, et al. Vedolizumab as induction and maintenance therapy for Crohn’s disease. N Engl J Med. 2013;369(8):711–721.
   PubMed Web of Science ®Google Scholar
• Feagan BG, Rutgeerts P, Sands BE, et al. Vedolizumab as induction and maintenance therapy for ulcerative colitis. N Engl J Med. 2013;369(8):699–710.
   PubMed Web of Science ®Google Scholar
• United States Food and Drug Administration. FDA approves Entyvio to treat ulcerative colitis and Crohn’s disease. Silver Spring (MD): FDA; 2014.
   Google Scholar
• Sands BE, Feagan BG, Rutgeerts P, et al. Effects of vedolizumab induction therapy for patients with Crohn’s disease in whom tumor necrosis factor antagonist treatment failed. Gastroenterology. 2014;147(3):618627 e613.
   Google Scholar
• Rutgeerts PJ, Fedorak RN, Hommes DW, et al. A randomised phase I study of etrolizumab (rhuMAb beta7) in moderate to severe ulcerative colitis. Gut. 2013;62(8):1122–1130.
   PubMed Web of Science ®Google Scholar
• Cepek KL, Parker CM, Madara JL, et al. Integrin alpha E beta 7 mediates adhesion of T lymphocytes to epithelial cells. J Immunol. 1993;150(8 Pt 1):3459–3470.
   PubMed Web of Science ®Google Scholar
• Karecla PI, Bowden SJ, Green SJ, et al. Recognition of E-cadherin on epithelial cells by the mucosal T cell integrin alpha M290 beta 7 (alpha E beta 7). Eur J Immunol. 1995;25(3):852–856.
   PubMed Web of Science ®Google Scholar
• Schon MP, Arya A, Murphy EA, et al. Mucosal T lymphocyte numbers are selectively reduced in integrin alpha E (CD103)-deficient mice. J Immunol. 1999;162(11):6641–6649.
   PubMed Web of Science ®Google Scholar
• Elewaut D, Van Damme N, De Keyser F, et al. Altered expression of alpha E beta 7 integrin on intra-epithelial and lamina propria lymphocytes in patients with Crohn’s disease. Acta Gastroenterol Belg. 1998;61(3):288–294.
   PubMed Web of Science ®Google Scholar
• Oshitani N, Watanabe K, Maeda K, et al. Differential expression of homing receptor CD103 on lamina propria lymphocytes and association of CD103 with epithelial adhesion molecules in inflammatory bowel disease. Int J Mol Med. 2003;12(5):715–719.
   PubMed Web of Science ®Google Scholar
• Ludviksson BR, Strober W, Nishikomori R, et al. Administration of mAb against alpha E beta 7 prevents and ameliorates immunization-induced colitis in IL-2-/- mice. J Immunol. 1999;162(8):4975–4982.
   PubMed Web of Science ®Google Scholar
• Stefanich EG, Danilenko DM, Wang H, et al. A humanized monoclonal antibody targeting the beta7 integrin selectively blocks intestinal homing of T lymphocytes. Br J Pharmacol. 2011;162(8):1855–1870.
   PubMed Web of Science ®Google Scholar
• Danilenko DM, Wang H. The yin and yang of immunomodulatory biologics: assessing the delicate balance between benefit and risk. Toxicol Pathol. 2012;40(2):272–287.
   PubMed Web of Science ®Google Scholar
• Vermeire S, O’Byrne S, Keir M, et al. Etrolizumab as induction therapy for ulcerative colitis: a randomised, controlled, phase 2 trial. Lancet. 2014;384(9940):309–318.
   PubMed Web of Science ®Google Scholar
• Takazoe M, Watanabe M, Kawaguchi T, et al. Oral alpha-4 integrin inhibitor (AJM300) in patients with active Crohn’s disease — a randomized, double-blind, placebo-controlled trial. Gastroenterology. 2009;136(5):A–181.
   Google Scholar
• Yoshimura N, Watanabe M, Motoya S, et al. Safety and efficacy of AJM300, an oral antagonist of α4 integrin, in induction therapy for patients with active ulcerative colitis. Gastroenterology. 2015;149(7):1775–1783.e2. doi:10.1053/j.gastro.2015.08.044
   Web of Science ®Google Scholar
• Pan WJ, Kock K, Rees WA, et al. Clinical pharmacology of AMG 181, a gut-specific human anti-alpha4beta7 monoclonal antibody, for treating inflammatory bowel diseases. Br J Clin Pharmacol. 2014;78(6):1315–1333.
   PubMed Web of Science ®Google Scholar
• Vermeire S, Ghosh S, Panes J, et al. The mucosal addressin cell adhesion molecule antibody PF-00547,659 in ulcerative colitis: a randomised study. Gut. 2011;60(8):1068–1075.
   PubMed Web of Science ®Google Scholar
• Sandborn WJ, Lee SD, Tarabar D, et al. Anti-MAdCAM-1 antibody (PF-00547659) for active refractory Crohn’s disease: results of the OPERA study. Gastroenterology. 2015;148(4):S–162.
   Web of Science ®Google Scholar
• Yacyshyn B, Chey WY, Wedel MK, et al. A randomized, double-masked, placebo-controlled study of alicaforsen, an antisense inhibitor of intercellular adhesion molecule 1, for the treatment of subjects with active Crohn’s disease. Clin Gastroenterol Hepatol. 2007;5(2):215–220.
   PubMed Web of Science ®Google Scholar
• National Institutes of Health. Open-label extension and safety study for patients with Crohn’s disease previously enrolled in the etrolizumab phase III study GA29144. National Institutes of Health; 2015.
   Google Scholar
• National Institutes of Health. Open-label extension and safety study for patients with ulcerative colitis previously enrolled in etrolizumab phase III studies. National Institutes of Health; 2015.
   Google Scholar
• National Institutes of Health. A study comparing the efficacy and safety of etrolizumab with adalimumab and placebo in patients with moderate to severe ulcerative colitis in patients naive to TNF inhibitors (Study #1). National Institutes of Health; 2015.
   Google Scholar
• National Institutes of Health. A study comparing the efficacy and safety of etrolizumab with adalimumab and placebo in patients with moderate to severe ulcerative colitis in patients naive to TNF inhibitors (Study #2). National Institutes of Health; 2015.
   Google Scholar
• National Institutes of Health. A study comparing the efficacy and safety of etrolizumab to infliximab in patients with moderate to severe ulcerative colitis who are naive to TNF inhibitors. National Institutes of Health; 2015.
   Google Scholar
• National Institutes of Health. A study of the efficacy and safety of etrolizumab treatment in maintenance of disease remission in ulcerative colitis patients who are naive to TNF inhibitors. National Institutes of Health; 2015.
   Google Scholar
• National Institutes of Health. A study of the efficacy and safety of etrolizumab in ulcerative colitis patients who are refractory to or intolerant of TNF inhibitors. National Institutes of Health; 2015.
   Google Scholar
• Sugiura T, Kageyama S, Andou A, et al. Oral treatment with a novel small molecule alpha 4 integrin antagonist, AJM300, prevents the development of experimental colitis in mice. J Crohns Colitis. 2013;7(11):e533e542.
   Google Scholar
• National Institutes of Health. AMG 181 in subjects with moderate to severe Crohn’s disease. National Institutes of Health; 2015.
   Google Scholar
• National Institutes of Health. Study to test whether PF-00547659 is safe and improves disease symptoms in patients with Crohn’s disease (OPERA). National Institutes of Health; 2015.
   Google Scholar
• Oppenheimer-Marks N, Davis LS, Bogue DT, et al. Differential utilization of ICAM-1 and VCAM-1 during the adhesion and transendothelial migration of human T lymphocytes. J Immunol. 1991;147(9):2913–2921.
   PubMed Web of Science ®Google Scholar
• Van Seventer GA, Shimizu Y, Horgan KJ, et al. Remote T cell co-stimulation via LFA-1/ICAM-1 and CD2/LFA-3: demonstration with immobilized ligand/mAb and implication in monocyte-mediated co-stimulation. Eur J Immunol. 1991;21(7):1711–1718.
   PubMed Web of Science ®Google Scholar
• Makgoba MW, Sanders ME, Ginther Luce GE, et al. Functional evidence that intercellular adhesion molecule-1 (ICAM-1) is a ligand for LFA-1-dependent adhesion in T cell-mediated cytotoxicity. Eur J Immunol. 1988;18(4):637–640.
   PubMed Web of Science ®Google Scholar
• National Institutes of Health. Randomized study of topical alicaforsen enema in antibiotic refractory pouchitis. National Institutes of Health; 2015.
   Google Scholar
• Bandzar S, Gupta S, Platt MO. Crohn’s disease: a review of treatment options and current research. Cell Immunol. 2013;286(12):45–52.
   PubMedGoogle Scholar
• Sandborn WJ, Feagan BG, Reinisch W, et al. Mo1217 effects of continued vedolizumab therapy for Crohn’s disease in week 6 induction therapy nonresponders. Gastroenterology. 2014;146(5):S–588.
   Google Scholar
• Shelton E, Allegretti JR, Stevens B, et al. Efficacy of vedolizumab as induction therapy in refractory IBD patients: a multicenter cohort. Inflamm Bowel Dis. 2015;21(12):2879–2885.
   PubMed Web of Science ®Google Scholar