Recombinant Humanized (from mouse) antibody to Human ITGA4+ITGB7. Vedolizumab (trade name vedolizumab) is a monoclonal antibody for the treatment of ulcerative colitis and Crohn's disease.It binds to integrin α4β7 (LPAM-1, lymphocyte Peyer's patch adhesion molecule 1). Blocking the α4β7 integrin results in gut-selective anti-inflammatory activity. It is marketed under the trade name vedolizumab.
Figure 1 Correlation of dynamic changes in integrin and chemokine receptor expression in patients under vedolizumab treatment.
Correlation of changes vs. baseline (T1) observed before treatment 2–8 (T2–8) in flow cytometric α4β7 expression on peripheral CD4+ and CD8+ T cells from Crohn's disease (CD) patients (A) and of changes in flow cytometric CCR2 and CCR6 expression on peripheral CD4+ T cells from ulcerative colitis (UC) patients (B) treated with vedolizumab. Left panels: representative plots from one patient showing the percentage of α4+β7+ among CD4+ and CD8+ T cells (A) and the percentage of CCR2+ and CCR6+ among CD4+ T cells (B) at baseline (T1) and before treatment 3 or 4 (T3/T4) as indicated. Right panel: pooled data from 12 (A) and 15 patients (B) depicting the changes vs. T1 observed before T2 to T8. Pearson's r and significances are indicated.
Fuchs, F., Schillinger, D., Atreya, R., Hirschmann, S., Fischer, S., Neufert, C., ... & Zundler, S. (2017). Clinical response to vedolizumab in ulcerative colitis patients is associated with changes in integrin expression profiles. Frontiers in immunology, 8, 764.
Figure 2 Correlation of dynamic changes in αEβ7 integrin expression with clinical parameters in patients under vedolizumab therapy.
(A) Correlation of changes vs. baseline (T1) observed before treatment 2–8 (T2–8) in αEβ7 expression on peripheral CD4+ UC T cells with changes in C-reactive protein levels. (B) Changes in αEβ7 expression on peripheral CD8+ UC T cells in patients with decreasing, unchanged, or increasing Mayo rectal bleeding score. Left panels: representative plots from one patient showing the expression of αEβ7 on CD4+ or CD8+ T cells before the mentioned treatments and indicating the corresponding clinical parameters below. Right panels: pooled data from 9 patients depicting the changes vs. T1 observed at T2–T8. Pearson's r and significances are indicated. (C,D) Representative images showing immunohistochemistry of gut cryosections for αEβ7 (red) and epithelial E-cadherin (green) in a non-IBD patient (CON) and a CD patient (C) as well as in a patient treated with vedolizumab (D). White arrows indicate αEβ7+ cells in contact with E-cadherin+ epithelial cells. VDZ, vedolizumab; IBD, inflammatory bowel diseases; CD, Crohn's disease; UC, ulcerative colitis.
Fuchs, F., Schillinger, D., Atreya, R., Hirschmann, S., Fischer, S., Neufert, C., ... & Zundler, S. (2017). Clinical response to vedolizumab in ulcerative colitis patients is associated with changes in integrin expression profiles. Frontiers in immunology, 8, 764.
Figure 3 Binding of vedolizumab to human peripheral blood B and memory CD4 T lymphocytes.
A, saturation binding curve of vedoliumab-alexa-647 binding to peripheral blood B lymphocytes (F) and memory CD4 T lymphocytes (E). B, dose-dependent inhibition curve of vedolizumab-alexa-647 binding to B lymphocytes (F) and memory CD4 lymphocytes (E) by unlabeled vedolizumab. Control antibody for B lymphocytes (f) and memory CD4 T lymphocytes ( ). The data represent multiple donors.
Soler, D., Chapman, T., Yang, L. L., Wyant, T., Egan, R., & Fedyk, E. R. (2009). The binding specificity and selective antagonism of vedolizumab, an anti-α4β7 integrin therapeutic antibody in development for inflammatory bowel diseases. Journal of Pharmacology and Experimental Therapeutics, 330(3), 864-875.
Figure 4 Potency and specificity of vedolizumab antagonism of 4 7 integrin adhesion to MAdCAM-1 and fibronectin, but not to VCAM-1. Effect of vedolizumab.
(F, A–D, F), a humanized mAb negative control ( A–B, F), an anti- 4- mAb (F, A–D, F), and isotype control Ig (asterisk, A–D, F) on adhesion of 4 7-expressing RPMI8866 cells to MAdCAM-1 with high (A) and low (B) affinity, to VCAM-1 with high (C and E) and low (D and E) affinity, and to fibronectin with high affinity (F). In E, data are the mean of three independent experiments with standard deviations indicated by the error bars. Relative fluorescent unit (RFU) values for cells incubated with antibody were compared with RFU values for cells not incubated with antibody with use of a two-tailed, homoscedastic Student's t test.
Soler, D., Chapman, T., Yang, L. L., Wyant, T., Egan, R., & Fedyk, E. R. (2009). The binding specificity and selective antagonism of vedolizumab, an anti-α4β7 integrin therapeutic antibody in development for inflammatory bowel diseases. Journal of Pharmacology and Experimental Therapeutics, 330(3), 864-875.
Figure 5 Histological changes in colonic biopsies of UC patients with mucosal healing after vedolizumab (VDZ) therapy (H&E stain; original magnification (OM) ×50 (detail OM ×100)).
(A) H&E stainings from a UC patient with endoscopic and histological healing at week (W)6 and W52 after VDZ therapy. W0, moderately active erosive UC (Geboes score 5.3); W6, epithelial restoration, decrease of the mononuclear cell infiltrate, no residual neutrophils (Geboes score 1.1); W52, intact mucosa, hypocellular lamina propria (Geboes score 1.1). (B) H&E stainings from a UC patient with endoscopic and histological healing at W12 after VDZ therapy. W0, dense mixed inflammatory infiltrate with crypt destruction (Geboes score 5.1); W12, patchy residual mononuclear cell infiltrate, no neutrophils (Geboes score 1.1).
Arijs, I., De Hertogh, G., Lemmens, B., Van Lommel, L., de Bruyn, M., Vanhove, W., ... & Van Assche, G. (2018). Effect of vedolizumab (anti-α4β7-integrin) therapy on histological healing and mucosal gene expression in patients with UC. Gut, 67(1), 43-52.
Figure 6 The localisation and cellular expression of MADCAM1, ITGB7 and LPHN2.
Immunohistochemistry for detection and localisation of MADCAM1 (A–C), ITGB7 (D–F) and LPHN2 (G–I) in paraffin-embedded, formalin-fixed tissue sections from colonic biopsies from control individuals (A, D, G), patients with active UC before vedolizumab (VDZ) therapy (B, E, H) and inactive patients with UC at week (W)52 after VDZ therapy (C, F, I) (original magnification (OM) ×200 (detail OM ×400)).
Arijs, I., De Hertogh, G., Lemmens, B., Van Lommel, L., de Bruyn, M., Vanhove, W., ... & Van Assche, G. (2018). Effect of vedolizumab (anti-α4β7-integrin) therapy on histological healing and mucosal gene expression in patients with UC. Gut, 67(1), 43-52.
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Afuco™ Anti-ITGA4 and ITGB7 ADCC Recombinant Antibody (Vedolizumab), ADCC EnhancedThis product is an ADCC enhanced antibody produced by our Afuco™ platform. Recombinant Humanized (from mouse) antibody to Human ITGA4+ITGB7. Vedolizumab (trade name vedolizumab) is a monoclonal antibody for the treatment of ulcerative colitis and Crohn's disease.It binds to integrin α4β7 (LPAM-1, lymphocyte Peyer's patch adhesion molecule 1). Blocking the α4β7 integrin results in gut-selective anti-inflammatory activity. It is marketed under the trade name vedolizumab.
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CAT | Product Name | Application | Type |
---|---|---|---|
TAB-H02 | Anti-Human ITGA4+ITGB7 Recombinant Antibody (Abrilumab) | IP, IF, FuncS, FC, Neut, ELISA, WB | IgG2 - kappa |
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