Pharmacological Evaluation of TAK-828F, a Novel Orally Available RORγt Inverse Agonist, on Murine Colitis Model
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N. Tsuchimori | Y. Ishimura | Y. Tsukimi | Akira Shibata | Keiko Igaki | M. Yamasaki | Y. Komoike | Keiko Uga | Yoshiki Nakamura
[1] Biching Sang,et al. Biochemical Properties of TAK-828F, a Potent and Selective Retinoid-Related Orphan Receptor Gamma t Inverse Agonist , 2018, Pharmacology.
[2] D. Soler,et al. MLN3126, an antagonist of the chemokine receptor CCR9, ameliorates inflammation in a T cell mediated mouse colitis model , 2018, International immunopharmacology.
[3] M. Sagara,et al. Pharmacological inhibitory profile of TAK‐828F, a potent and selective orally available ROR&ggr;t inverse agonist , 2018, Biochemical pharmacology.
[4] Biching Sang,et al. Discovery of [ cis-3-({(5 R)-5-[(7-Fluoro-1,1-dimethyl-2,3-dihydro-1 H-inden-5-yl)carbamoyl]-2-methoxy-7,8-dihydro-1,6-naphthyridin-6(5 H)-yl}carbonyl)cyclobutyl]acetic Acid (TAK-828F) as a Potent, Selective, and Orally Available Novel Retinoic Acid Receptor-Related Orphan Receptor γt Inverse Agonis , 2018, Journal of medicinal chemistry.
[5] A. Kaser,et al. Induction therapy with the selective interleukin-23 inhibitor risankizumab in patients with moderate-to-severe Crohn's disease: a randomised, double-blind, placebo-controlled phase 2 study , 2017, The Lancet.
[6] D. McAuley,et al. Innate Lymphoid Cells Are the Predominant Source of IL-17A during the Early Pathogenesis of Acute Respiratory Distress Syndrome. , 2016, American journal of respiratory and critical care medicine.
[7] J. Kelsen,et al. Transient inhibition of ROR-γt therapeutically limits intestinal inflammation by reducing TH17 cells and preserving group 3 innate lymphoid cells , 2016, Nature Medicine.
[8] G. Kaplan,et al. The global burden of IBD: from 2015 to 2025 , 2015, Nature Reviews Gastroenterology &Hepatology.
[9] Adam R. Johnson,et al. Discovery of 1-{4-[3-fluoro-4-((3s,6r)-3-methyl-1,1-dioxo-6-phenyl-[1,2]thiazinan-2-ylmethyl)-phenyl]-piperazin-1-yl}-ethanone (GNE-3500): a potent, selective, and orally bioavailable retinoic acid receptor-related orphan receptor C (RORc or RORγ) inverse agonist. , 2015, Journal of medicinal chemistry.
[10] Zhanju Liu,et al. Serum Levels of Lipopolysaccharide and 1,3-β-D-Glucan Refer to the Severity in Patients with Crohn's Disease , 2015, Mediators of inflammation.
[11] T. Schoeb,et al. Th17 cells give rise to Th1 cells that are required for the pathogenesis of colitis , 2015, Proceedings of the National Academy of Sciences.
[12] Sung Hee Lee,et al. Intestinal Permeability Regulation by Tight Junction: Implication on Inflammatory Bowel Diseases , 2015, Intestinal research.
[13] J. Preiß,et al. Anti-IL-12/23p40 antibodies for induction of remission in Crohn's disease. , 2015, The Cochrane database of systematic reviews.
[14] M. Seidl,et al. Comprehensive Intestinal T Helper Cell Profiling Reveals Specific Accumulation of IFN-&ggr;+IL-17+Coproducing CD4+ T Cells in Active Inflammatory Bowel Disease , 2014, Inflammatory bowel diseases.
[15] Xiuqin Cheng,et al. Elevated levels of Th17 cells and Th17-related cytokines are associated with disease activity in patients with inflammatory bowel disease , 2014, Inflammation Research.
[16] Mark S. Sundrud,et al. Small-molecule RORγt antagonists inhibit T helper 17 cell transcriptional network by divergent mechanisms. , 2014, Immunity.
[17] J. Gálvez. Role of Th17 Cells in the Pathogenesis of Human IBD , 2014, ISRN inflammation.
[18] Mark S. Sundrud,et al. Pharmacologic Inhibition of RORγt Regulates Th17 Signature Gene Expression and Suppresses Cutaneous Inflammation In Vivo , 2014, The Journal of Immunology.
[19] H. Tilg,et al. Targeting T and B Lymphocytes in Inflammatory Bowel Diseases: Lessons from Clinical Trials , 2013, Digestive Diseases.
[20] A. M’Koma,et al. Inflammatory Bowel Disease: An Expanding Global Health Problem , 2013, Clinical medicine insights. Gastroenterology.
[21] D. Littman,et al. Small molecule inhibitors of RORγt: Targeting Th17 cells and other applications , 2012, European journal of immunology.
[22] J. Shimizu,et al. Excessive CD4+ T cells co‐expressing interleukin‐17 and interferon‐γ in patients with Behçet's disease , 2012, Clinical and experimental immunology.
[23] M. Roncarolo,et al. The Cellular and Molecular Mechanisms of Immuno-Suppression by Human Type 1 Regulatory T Cells , 2011, Front. Immun..
[24] H. Ogata,et al. Regulatory T cells suppress development of colitis, blocking differentiation of T-helper 17 into alternative T-helper 1 cells. , 2011, Gastroenterology.
[25] S. Hanauer. The expanding role of biologic therapy for IBD , 2010, Nature Reviews Gastroenterology &Hepatology.
[26] D. Rampton,et al. DIFFERENTIAL REGULATION OF INTERLEUKIN-17 AND INTERFERON- PRODUCTION IN INFLAMMATORY BOWEL DISEASE , 2011 .
[27] P. Duquette,et al. Preferential recruitment of interferon‐γ–expressing TH17 cells in multiple sclerosis , 2009, Annals of neurology.
[28] M. Veldhoen,et al. Interleukin-17-producing gammadelta T cells selectively expand in response to pathogen products and environmental signals. , 2009, Immunity.
[29] K. Takeda,et al. TGF-beta is necessary for induction of IL-23R and Th17 differentiation by IL-6 and IL-23. , 2009, Biochemical and biophysical research communications.
[30] C. Elson,et al. Late developmental plasticity in the T helper 17 lineage. , 2009, Immunity.
[31] B. Becher,et al. RORgamma-expressing Th17 cells induce murine chronic intestinal inflammation via redundant effects of IL-17A and IL-17F. , 2009, Gastroenterology.
[32] W. Paul,et al. CD4 T cells: fates, functions, and faults. , 2008, Blood.
[33] H. Weiner,et al. Control of Treg and TH17 cell differentiation by the aryl hydrocarbon receptor , 2008, Nature.
[34] A. Rachitskaya,et al. Cutting Edge: NKT Cells Constitutively Express IL-23 Receptor and RORγt and Rapidly Produce IL-17 upon Receptor Ligation in an IL-6-Independent Fashion1 , 2008, The Journal of Immunology.
[35] D. Littman,et al. The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells. , 2006, Cell.
[36] J. Pearson,et al. The MUC2 gene product: a human intestinal mucin. , 1998, The international journal of biochemistry & cell biology.
[37] Hervé Groux,et al. A CD4+T-cell subset inhibits antigen-specific T-cell responses and prevents colitis , 1997, Nature.
[38] F. Annunziato,et al. Type 1 T-helper cell predominance and interleukin-12 expression in the gut of patients with Crohn's disease. , 1997, The American journal of pathology.
[39] M. Neurath,et al. Disparate CD4+ lamina propria (LP) lymphokine secretion profiles in inflammatory bowel disease. Crohn's disease LP cells manifest increased secretion of IFN-gamma, whereas ulcerative colitis LP cells manifest increased secretion of IL-5. , 1996, Journal of immunology.