A novel modality of BAFF-specific inhibitor AMG623 peptibody reduces B-cell number and improves outcomes in murine models of autoimmune disease
AMG623, also known as A-623, is an antagonist of B-cell activating factor (BAFF). The present study was to evaluate the effects of AMG623 on murine models of autoimmune diseases. AMG623 was generated through phage library. Inhibitory activities of AMG623 against human and murine BAFF were measured b...
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Veröffentlicht in: | Clinical and experimental rheumatology 2012-03, Vol.30 (2), p.197-201 |
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creator | HSU, H KHARE, S. D XIONG, F BOONE, T ZACK, D. J LEE, F MINER, K HU, Y.-L STOLINA, M HAWKINS, N CHEN, Q HO, S. J MIN, H |
description | AMG623, also known as A-623, is an antagonist of B-cell activating factor (BAFF). The present study was to evaluate the effects of AMG623 on murine models of autoimmune diseases.
AMG623 was generated through phage library. Inhibitory activities of AMG623 against human and murine BAFF were measured by biacore binding and BAFF-mediated B-cell proliferation assay. Pharmacological effects of AMG623 were studied in BALB/c mice, collagen-induced arthritis model (CIA) and in the NZBxNZW F1 lupus model.
AMG623 binds to both soluble and cell surface BAFF. AMG623 blocks both human murine BAFF binding to the receptors. Treatment of AMG623 resulted in B-cell number reduction, and improvement of arthritis and lupus development in mice.
AMG623 is a novel modality of BAFF antagonist. AMG623 is a potential therapeutic agent for the treatment of SLE, rheumatoid arthritis, and other B-cell-mediated autoimmune diseases. |
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AMG623 was generated through phage library. Inhibitory activities of AMG623 against human and murine BAFF were measured by biacore binding and BAFF-mediated B-cell proliferation assay. Pharmacological effects of AMG623 were studied in BALB/c mice, collagen-induced arthritis model (CIA) and in the NZBxNZW F1 lupus model.
AMG623 binds to both soluble and cell surface BAFF. AMG623 blocks both human murine BAFF binding to the receptors. Treatment of AMG623 resulted in B-cell number reduction, and improvement of arthritis and lupus development in mice.
AMG623 is a novel modality of BAFF antagonist. AMG623 is a potential therapeutic agent for the treatment of SLE, rheumatoid arthritis, and other B-cell-mediated autoimmune diseases.</description><identifier>ISSN: 0392-856X</identifier><identifier>EISSN: 1593-098X</identifier><identifier>PMID: 22325420</identifier><language>eng</language><publisher>Pisa: Clinical and Experimental Rheumatology</publisher><subject>Animals ; Arthritis, Experimental - drug therapy ; Arthritis, Experimental - immunology ; B-Cell Activating Factor - antagonists & inhibitors ; B-Cell Activating Factor - genetics ; B-Cell Activating Factor - metabolism ; B-Cell Activation Factor Receptor - metabolism ; B-Lymphocytes - drug effects ; B-Lymphocytes - immunology ; Biological and medical sciences ; Cell Proliferation - drug effects ; Diseases of the osteoarticular system ; Female ; HEK293 Cells ; Humans ; Immunologic Factors - pharmacology ; Lupus Erythematosus, Systemic - drug therapy ; Lupus Erythematosus, Systemic - immunology ; Lymphocyte Activation - drug effects ; Male ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Mice, Inbred DBA ; Recombinant Fusion Proteins - pharmacology ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; Time Factors ; Transfection</subject><ispartof>Clinical and experimental rheumatology, 2012-03, Vol.30 (2), p.197-201</ispartof><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25935247$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22325420$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HSU, H</creatorcontrib><creatorcontrib>KHARE, S. D</creatorcontrib><creatorcontrib>XIONG, F</creatorcontrib><creatorcontrib>BOONE, T</creatorcontrib><creatorcontrib>ZACK, D. J</creatorcontrib><creatorcontrib>LEE, F</creatorcontrib><creatorcontrib>MINER, K</creatorcontrib><creatorcontrib>HU, Y.-L</creatorcontrib><creatorcontrib>STOLINA, M</creatorcontrib><creatorcontrib>HAWKINS, N</creatorcontrib><creatorcontrib>CHEN, Q</creatorcontrib><creatorcontrib>HO, S. J</creatorcontrib><creatorcontrib>MIN, H</creatorcontrib><title>A novel modality of BAFF-specific inhibitor AMG623 peptibody reduces B-cell number and improves outcomes in murine models of autoimmune disease</title><title>Clinical and experimental rheumatology</title><addtitle>Clin Exp Rheumatol</addtitle><description>AMG623, also known as A-623, is an antagonist of B-cell activating factor (BAFF). The present study was to evaluate the effects of AMG623 on murine models of autoimmune diseases.
AMG623 was generated through phage library. Inhibitory activities of AMG623 against human and murine BAFF were measured by biacore binding and BAFF-mediated B-cell proliferation assay. Pharmacological effects of AMG623 were studied in BALB/c mice, collagen-induced arthritis model (CIA) and in the NZBxNZW F1 lupus model.
AMG623 binds to both soluble and cell surface BAFF. AMG623 blocks both human murine BAFF binding to the receptors. Treatment of AMG623 resulted in B-cell number reduction, and improvement of arthritis and lupus development in mice.
AMG623 is a novel modality of BAFF antagonist. AMG623 is a potential therapeutic agent for the treatment of SLE, rheumatoid arthritis, and other B-cell-mediated autoimmune diseases.</description><subject>Animals</subject><subject>Arthritis, Experimental - drug therapy</subject><subject>Arthritis, Experimental - immunology</subject><subject>B-Cell Activating Factor - antagonists & inhibitors</subject><subject>B-Cell Activating Factor - genetics</subject><subject>B-Cell Activating Factor - metabolism</subject><subject>B-Cell Activation Factor Receptor - metabolism</subject><subject>B-Lymphocytes - drug effects</subject><subject>B-Lymphocytes - immunology</subject><subject>Biological and medical sciences</subject><subject>Cell Proliferation - drug effects</subject><subject>Diseases of the osteoarticular system</subject><subject>Female</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Immunologic Factors - pharmacology</subject><subject>Lupus Erythematosus, Systemic - drug therapy</subject><subject>Lupus Erythematosus, Systemic - immunology</subject><subject>Lymphocyte Activation - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred DBA</subject><subject>Recombinant Fusion Proteins - pharmacology</subject><subject>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><subject>Time Factors</subject><subject>Transfection</subject><issn>0392-856X</issn><issn>1593-098X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkd1KAzEQhRdRbK2-guRG8GYhP5t0c9kWW4WKNwq9K_mZxchms242Qp_CVzbFilczDB9z5pw5K6aES1ZiWe_OiylmkpY1F7tJcRXjB8ZUcDG_LCaUMsoriqfF9wJ14Qta5INVrRsPKDRouVivy9iDcY0zyHXvTrsxDGjxvBGUoR760elgD2gAmwxEtCwNtC3qktcwINVZ5Hw_5L0RhTSa4HPjOuTT4Do4SkEbj0IqjcF5n_LQuggqwnVx0ag2ws2pzoq39cPr6rHcvmyeVott2dOKjCUhjAMzc1VxoWmNuSYSUw2SaWGs0VLaRtQNZpo0ZI7r2oqcha2MslLKbGJW3P_uzWd-Jojj3rt4NKE6CCnuCSZYMMFrltHbE5q0B7vvB-fVcNj_hZiBuxOgolFtM6jOuPjP5Y9wWs3ZD-68fKk</recordid><startdate>20120301</startdate><enddate>20120301</enddate><creator>HSU, H</creator><creator>KHARE, S. D</creator><creator>XIONG, F</creator><creator>BOONE, T</creator><creator>ZACK, D. J</creator><creator>LEE, F</creator><creator>MINER, K</creator><creator>HU, Y.-L</creator><creator>STOLINA, M</creator><creator>HAWKINS, N</creator><creator>CHEN, Q</creator><creator>HO, S. J</creator><creator>MIN, H</creator><general>Clinical and Experimental Rheumatology</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20120301</creationdate><title>A novel modality of BAFF-specific inhibitor AMG623 peptibody reduces B-cell number and improves outcomes in murine models of autoimmune disease</title><author>HSU, H ; KHARE, S. D ; XIONG, F ; BOONE, T ; ZACK, D. J ; LEE, F ; MINER, K ; HU, Y.-L ; STOLINA, M ; HAWKINS, N ; CHEN, Q ; HO, S. J ; MIN, H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p241t-1135e3c7a456b2805b1902be93b6cdcb99df68f03b1f17088d6392d4cad999623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Arthritis, Experimental - drug therapy</topic><topic>Arthritis, Experimental - immunology</topic><topic>B-Cell Activating Factor - antagonists & inhibitors</topic><topic>B-Cell Activating Factor - genetics</topic><topic>B-Cell Activating Factor - metabolism</topic><topic>B-Cell Activation Factor Receptor - metabolism</topic><topic>B-Lymphocytes - drug effects</topic><topic>B-Lymphocytes - immunology</topic><topic>Biological and medical sciences</topic><topic>Cell Proliferation - drug effects</topic><topic>Diseases of the osteoarticular system</topic><topic>Female</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Immunologic Factors - pharmacology</topic><topic>Lupus Erythematosus, Systemic - drug therapy</topic><topic>Lupus Erythematosus, Systemic - immunology</topic><topic>Lymphocyte Activation - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred DBA</topic><topic>Recombinant Fusion Proteins - pharmacology</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</topic><topic>Time Factors</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HSU, H</creatorcontrib><creatorcontrib>KHARE, S. D</creatorcontrib><creatorcontrib>XIONG, F</creatorcontrib><creatorcontrib>BOONE, T</creatorcontrib><creatorcontrib>ZACK, D. J</creatorcontrib><creatorcontrib>LEE, F</creatorcontrib><creatorcontrib>MINER, K</creatorcontrib><creatorcontrib>HU, Y.-L</creatorcontrib><creatorcontrib>STOLINA, M</creatorcontrib><creatorcontrib>HAWKINS, N</creatorcontrib><creatorcontrib>CHEN, Q</creatorcontrib><creatorcontrib>HO, S. J</creatorcontrib><creatorcontrib>MIN, H</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and experimental rheumatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HSU, H</au><au>KHARE, S. D</au><au>XIONG, F</au><au>BOONE, T</au><au>ZACK, D. J</au><au>LEE, F</au><au>MINER, K</au><au>HU, Y.-L</au><au>STOLINA, M</au><au>HAWKINS, N</au><au>CHEN, Q</au><au>HO, S. J</au><au>MIN, H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A novel modality of BAFF-specific inhibitor AMG623 peptibody reduces B-cell number and improves outcomes in murine models of autoimmune disease</atitle><jtitle>Clinical and experimental rheumatology</jtitle><addtitle>Clin Exp Rheumatol</addtitle><date>2012-03-01</date><risdate>2012</risdate><volume>30</volume><issue>2</issue><spage>197</spage><epage>201</epage><pages>197-201</pages><issn>0392-856X</issn><eissn>1593-098X</eissn><abstract>AMG623, also known as A-623, is an antagonist of B-cell activating factor (BAFF). The present study was to evaluate the effects of AMG623 on murine models of autoimmune diseases.
AMG623 was generated through phage library. Inhibitory activities of AMG623 against human and murine BAFF were measured by biacore binding and BAFF-mediated B-cell proliferation assay. Pharmacological effects of AMG623 were studied in BALB/c mice, collagen-induced arthritis model (CIA) and in the NZBxNZW F1 lupus model.
AMG623 binds to both soluble and cell surface BAFF. AMG623 blocks both human murine BAFF binding to the receptors. Treatment of AMG623 resulted in B-cell number reduction, and improvement of arthritis and lupus development in mice.
AMG623 is a novel modality of BAFF antagonist. AMG623 is a potential therapeutic agent for the treatment of SLE, rheumatoid arthritis, and other B-cell-mediated autoimmune diseases.</abstract><cop>Pisa</cop><pub>Clinical and Experimental Rheumatology</pub><pmid>22325420</pmid><tpages>5</tpages></addata></record> |
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subjects | Animals Arthritis, Experimental - drug therapy Arthritis, Experimental - immunology B-Cell Activating Factor - antagonists & inhibitors B-Cell Activating Factor - genetics B-Cell Activating Factor - metabolism B-Cell Activation Factor Receptor - metabolism B-Lymphocytes - drug effects B-Lymphocytes - immunology Biological and medical sciences Cell Proliferation - drug effects Diseases of the osteoarticular system Female HEK293 Cells Humans Immunologic Factors - pharmacology Lupus Erythematosus, Systemic - drug therapy Lupus Erythematosus, Systemic - immunology Lymphocyte Activation - drug effects Male Medical sciences Mice Mice, Inbred BALB C Mice, Inbred DBA Recombinant Fusion Proteins - pharmacology Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Time Factors Transfection |
title | A novel modality of BAFF-specific inhibitor AMG623 peptibody reduces B-cell number and improves outcomes in murine models of autoimmune disease |
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