OP0116 Effects of Blisibimod, a Subcutaneous Inhibitor of B Cell Activating Factor, in Patients with SLE
Identifieur interne : 000F38 ( Istex/Corpus ); précédent : 000F37; suivant : 000F39OP0116 Effects of Blisibimod, a Subcutaneous Inhibitor of B Cell Activating Factor, in Patients with SLE
Auteurs : R. Furie ; M. Scheinberg ; G. Leon ; E. B. Ramiterre ; M. Thomas ; A. D. Chu ; C. Hislop ; R. S. Martin ; M. A. PetriSource :
- Annals of the Rheumatic Diseases [ 0003-4967 ] ; 2013-06.
Abstract
Background Blisibimod, a potent inhibitor of B cell activating factor (BAFF), was evaluated in a Phase 2b clinical trial in patients with SLE. Objectives To determine the effect of subcutaneous blisibimod on SLE disease activity, including rate of response to the SLE responder index (SRI). Methods 547 serologically-active SLE patients with baseline SELENA-SLEDAI ≥6 were randomized to receive blisibimod (100mg weekly (QW), 200mg QW, or 200mg Q4W) or placebo in matchin dosing regimens. The primary endpoint was a comparison at Week 24 of the percentage of subjects in the pooled blisibimod and placebo groups who achieved an SRI-5 response (SRI with ≥5 point improvement in SELENA–SLEDAI). Results The primary endpoint was not met due to the lack of efficacy in the two lower doses. However, SRI-5 response was higher in subjects receiving blisibimod 200mg QW compared with placebo (p=0.02 at Week 20). SRI improvements compared with placebo were higher still in subjects who attained SELENA–SLEDAI improvements of ≥8, and in patients with severe disease (SELENA–SLEDAI≥10 and receiving corticosteroids, n=278, figure 1 ). Despite declining patient numbers, response to blisibimod remained higher than placebo beyond Week 24 while N>30 subjects per cohort. Numerically higher response was also observed with blisibimod in all components of the SRI. Blisibimod was safe and well-tolerated at all dose levels with no meaningful imbalances in serious adverse events or infections compared with placebo. Image/graphConclusions These are the first evidence that SLE disease activity may be improved with subcutaneous injections of a novel biologic therapy. Disclosure of Interest R. Furie Consultant for: Anthera Pharmaceuticals, M. Scheinberg: None Declared, G. Leon: None Declared, E. Ramiterre: None Declared, M. Thomas: None Declared, A. Chu: None Declared, C. Hislop Employee of: Anthera Pharmaceuticals, R. Martin: None Declared, M. Petri Employee of: Anthera Pharmaceuticals
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DOI: 10.1136/annrheumdis-2013-eular.321
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Leon</name><affiliation><mods:affiliation>Rheumatology Gynecology & Reproduction Institute, Lima, Peru</mods:affiliation></affiliation></author><author><name sortKey="Ramiterre, E B" sort="Ramiterre, E B" uniqKey="Ramiterre E" first="E. B." last="Ramiterre">E. B. Ramiterre</name><affiliation><mods:affiliation>Brokenshire Memorial Hospital, Davao City, Philippines</mods:affiliation></affiliation></author><author><name sortKey="Thomas, M" sort="Thomas, M" uniqKey="Thomas M" first="M." last="Thomas">M. Thomas</name><affiliation><mods:affiliation>Health and Research Centre, Trivandrum, Kerala, India</mods:affiliation></affiliation></author><author><name sortKey="Chu, A D" sort="Chu, A D" uniqKey="Chu A" first="A. D." last="Chu">A. D. Chu</name><affiliation><mods:affiliation>Anthera Pharmaceuticals</mods:affiliation></affiliation></author><author><name sortKey="Hislop, C" sort="Hislop, C" uniqKey="Hislop C" first="C." last="Hislop">C. 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Furie</name><affiliation><mods:affiliation>North Shore–Long Island Jewish Health System, Lake Success New York, United States</mods:affiliation></affiliation></author><author><name sortKey="Scheinberg, M" sort="Scheinberg, M" uniqKey="Scheinberg M" first="M." last="Scheinberg">M. Scheinberg</name><affiliation><mods:affiliation>Rheumatology Hospital Abreu Sodre Pesquisa Clínica, São Paulo, Brazil</mods:affiliation></affiliation></author><author><name sortKey="Leon, G" sort="Leon, G" uniqKey="Leon G" first="G." last="Leon">G. Leon</name><affiliation><mods:affiliation>Rheumatology Gynecology & Reproduction Institute, Lima, Peru</mods:affiliation></affiliation></author><author><name sortKey="Ramiterre, E B" sort="Ramiterre, E B" uniqKey="Ramiterre E" first="E. B." last="Ramiterre">E. B. Ramiterre</name><affiliation><mods:affiliation>Brokenshire Memorial Hospital, Davao City, Philippines</mods:affiliation></affiliation></author><author><name sortKey="Thomas, M" sort="Thomas, M" uniqKey="Thomas M" first="M." last="Thomas">M. Thomas</name><affiliation><mods:affiliation>Health and Research Centre, Trivandrum, Kerala, India</mods:affiliation></affiliation></author><author><name sortKey="Chu, A D" sort="Chu, A D" uniqKey="Chu A" first="A. D." last="Chu">A. D. Chu</name><affiliation><mods:affiliation>Anthera Pharmaceuticals</mods:affiliation></affiliation></author><author><name sortKey="Hislop, C" sort="Hislop, C" uniqKey="Hislop C" first="C." last="Hislop">C. Hislop</name><affiliation><mods:affiliation>Anthera Pharmaceuticals, Inc, Hayward</mods:affiliation></affiliation></author><author><name sortKey="Martin, R S" sort="Martin, R S" uniqKey="Martin R" first="R. S." last="Martin">R. S. Martin</name><affiliation><mods:affiliation>Anthera Pharmaceuticals, Inc, Hayward</mods:affiliation></affiliation></author><author><name sortKey="Petri, M A" sort="Petri, M A" uniqKey="Petri M" first="M. A." last="Petri">M. A. Petri</name><affiliation><mods:affiliation>Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, United States</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of the Rheumatic Diseases</title><title level="j" type="abbrev">Ann Rheum Dis</title><idno type="ISSN">0003-4967</idno><idno type="eISSN">1468-2060</idno><imprint><publisher>BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><date type="published" when="2013-06">2013-06</date><biblScope unit="volume">72</biblScope><biblScope unit="issue">Suppl 3</biblScope><biblScope unit="page" from="A90">A90</biblScope></imprint><idno type="ISSN">0003-4967</idno></series><idno type="istex">F84B96C3EE876A6D7F43D3F2DFF816080FD163F5</idno><idno type="DOI">10.1136/annrheumdis-2013-eular.321</idno><idno type="href">annrheumdis-72-A90-3.pdf</idno><idno type="ArticleID">annrheumdis-2013-eular.321</idno><idno type="local">annrheumdis;72/Suppl_3/A90-c</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0003-4967</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Background Blisibimod, a potent inhibitor of B cell activating factor (BAFF), was evaluated in a Phase 2b clinical trial in patients with SLE. Objectives To determine the effect of subcutaneous blisibimod on SLE disease activity, including rate of response to the SLE responder index (SRI). Methods 547 serologically-active SLE patients with baseline SELENA-SLEDAI ≥6 were randomized to receive blisibimod (100mg weekly (QW), 200mg QW, or 200mg Q4W) or placebo in matchin dosing regimens. The primary endpoint was a comparison at Week 24 of the percentage of subjects in the pooled blisibimod and placebo groups who achieved an SRI-5 response (SRI with ≥5 point improvement in SELENA–SLEDAI). Results The primary endpoint was not met due to the lack of efficacy in the two lower doses. However, SRI-5 response was higher in subjects receiving blisibimod 200mg QW compared with placebo (p=0.02 at Week 20). SRI improvements compared with placebo were higher still in subjects who attained SELENA–SLEDAI improvements of ≥8, and in patients with severe disease (SELENA–SLEDAI≥10 and receiving corticosteroids, n=278, figure 1 ). Despite declining patient numbers, response to blisibimod remained higher than placebo beyond Week 24 while N>30 subjects per cohort. Numerically higher response was also observed with blisibimod in all components of the SRI. Blisibimod was safe and well-tolerated at all dose levels with no meaningful imbalances in serious adverse events or infections compared with placebo. Image/graphConclusions These are the first evidence that SLE disease activity may be improved with subcutaneous injections of a novel biologic therapy. Disclosure of Interest R. Furie Consultant for: Anthera Pharmaceuticals, M. Scheinberg: None Declared, G. Leon: None Declared, E. Ramiterre: None Declared, M. Thomas: None Declared, A. Chu: None Declared, C. Hislop Employee of: Anthera Pharmaceuticals, R. Martin: None Declared, M. Petri Employee of: Anthera Pharmaceuticals</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>R. Furie</name><affiliations><json:string>North Shore–Long Island Jewish Health System, Lake Success New York, United States</json:string></affiliations></json:item><json:item><name>M. Scheinberg</name><affiliations><json:string>Rheumatology Hospital Abreu Sodre Pesquisa Clínica, São Paulo, Brazil</json:string></affiliations></json:item><json:item><name>G. Leon</name><affiliations><json:string>Rheumatology Gynecology & Reproduction Institute, Lima, Peru</json:string></affiliations></json:item><json:item><name>E. B. Ramiterre</name><affiliations><json:string>Brokenshire Memorial Hospital, Davao City, Philippines</json:string></affiliations></json:item><json:item><name>M. Thomas</name><affiliations><json:string>Health and Research Centre, Trivandrum, Kerala, India</json:string></affiliations></json:item><json:item><name>A. D. Chu</name><affiliations><json:string>Anthera Pharmaceuticals</json:string></affiliations></json:item><json:item><name>C. Hislop</name><affiliations><json:string>Anthera Pharmaceuticals, Inc, Hayward</json:string></affiliations></json:item><json:item><name>R. S. Martin</name><affiliations><json:string>Anthera Pharmaceuticals, Inc, Hayward</json:string></affiliations></json:item><json:item><name>M. A. Petri</name><affiliations><json:string>Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, United States</json:string></affiliations></json:item></author><articleId><json:string>annrheumdis-2013-eular.321</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>abstract</json:string></originalGenre><abstract>Background Blisibimod, a potent inhibitor of B cell activating factor (BAFF), was evaluated in a Phase 2b clinical trial in patients with SLE. Objectives To determine the effect of subcutaneous blisibimod on SLE disease activity, including rate of response to the SLE responder index (SRI). Methods 547 serologically-active SLE patients with baseline SELENA-SLEDAI ≥6 were randomized to receive blisibimod (100mg weekly (QW), 200mg QW, or 200mg Q4W) or placebo in matchin dosing regimens. The primary endpoint was a comparison at Week 24 of the percentage of subjects in the pooled blisibimod and placebo groups who achieved an SRI-5 response (SRI with ≥5 point improvement in SELENA–SLEDAI). Results The primary endpoint was not met due to the lack of efficacy in the two lower doses. However, SRI-5 response was higher in subjects receiving blisibimod 200mg QW compared with placebo (p=0.02 at Week 20). SRI improvements compared with placebo were higher still in subjects who attained SELENA–SLEDAI improvements of ≥8, and in patients with severe disease (SELENA–SLEDAI≥10 and receiving corticosteroids, n=278, figure 1 ). Despite declining patient numbers, response to blisibimod remained higher than placebo beyond Week 24 while N>30 subjects per cohort. Numerically higher response was also observed with blisibimod in all components of the SRI. Blisibimod was safe and well-tolerated at all dose levels with no meaningful imbalances in serious adverse events or infections compared with placebo. Image/graphConclusions These are the first evidence that SLE disease activity may be improved with subcutaneous injections of a novel biologic therapy. Disclosure of Interest R. Furie Consultant for: Anthera Pharmaceuticals, M. Scheinberg: None Declared, G. Leon: None Declared, E. Ramiterre: None Declared, M. Thomas: None Declared, A. Chu: None Declared, C. Hislop Employee of: Anthera Pharmaceuticals, R. Martin: None Declared, M. 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For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</p></availability><date>2013</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">OP0116 Effects of Blisibimod, a Subcutaneous Inhibitor of B Cell Activating Factor, in Patients with SLE</title><author xml:id="author-1"><persName><forename type="first">R.</forename><surname>Furie</surname></persName><affiliation>North Shore–Long Island Jewish Health System, Lake Success New York, United States</affiliation></author><author xml:id="author-2"><persName><forename type="first">M.</forename><surname>Scheinberg</surname></persName><affiliation>Rheumatology Hospital Abreu Sodre Pesquisa Clínica, São Paulo, Brazil</affiliation></author><author xml:id="author-3"><persName><forename type="first">G.</forename><surname>Leon</surname></persName><affiliation>Rheumatology Gynecology & Reproduction Institute, Lima, Peru</affiliation></author><author xml:id="author-4"><persName><forename type="first">E. B.</forename><surname>Ramiterre</surname></persName><affiliation>Brokenshire Memorial Hospital, Davao City, Philippines</affiliation></author><author xml:id="author-5"><persName><forename type="first">M.</forename><surname>Thomas</surname></persName><affiliation>Health and Research Centre, Trivandrum, Kerala, India</affiliation></author><author xml:id="author-6"><persName><forename type="first">A. D.</forename><surname>Chu</surname></persName><affiliation>Anthera Pharmaceuticals</affiliation></author><author xml:id="author-7"><persName><forename type="first">C.</forename><surname>Hislop</surname></persName><affiliation>Anthera Pharmaceuticals, Inc, Hayward</affiliation></author><author xml:id="author-8"><persName><forename type="first">R. S.</forename><surname>Martin</surname></persName><affiliation>Anthera Pharmaceuticals, Inc, Hayward</affiliation></author><author xml:id="author-9"><persName><forename type="first">M. A.</forename><surname>Petri</surname></persName><affiliation>Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, United States</affiliation></author></analytic><monogr><title level="j">Annals of the Rheumatic Diseases</title><title level="j" type="abbrev">Ann Rheum Dis</title><idno type="pISSN">0003-4967</idno><idno type="eISSN">1468-2060</idno><imprint><publisher>BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><date type="published" when="2013-06"></date><biblScope unit="volume">72</biblScope><biblScope unit="issue">Suppl 3</biblScope><biblScope unit="page" from="A90">A90</biblScope></imprint></monogr><idno type="istex">F84B96C3EE876A6D7F43D3F2DFF816080FD163F5</idno><idno type="DOI">10.1136/annrheumdis-2013-eular.321</idno><idno type="href">annrheumdis-72-A90-3.pdf</idno><idno type="ArticleID">annrheumdis-2013-eular.321</idno><idno type="local">annrheumdis;72/Suppl_3/A90-c</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2013</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Background Blisibimod, a potent inhibitor of B cell activating factor (BAFF), was evaluated in a Phase 2b clinical trial in patients with SLE. Objectives To determine the effect of subcutaneous blisibimod on SLE disease activity, including rate of response to the SLE responder index (SRI). Methods 547 serologically-active SLE patients with baseline SELENA-SLEDAI ≥6 were randomized to receive blisibimod (100mg weekly (QW), 200mg QW, or 200mg Q4W) or placebo in matchin dosing regimens. The primary endpoint was a comparison at Week 24 of the percentage of subjects in the pooled blisibimod and placebo groups who achieved an SRI-5 response (SRI with ≥5 point improvement in SELENA–SLEDAI). Results The primary endpoint was not met due to the lack of efficacy in the two lower doses. However, SRI-5 response was higher in subjects receiving blisibimod 200mg QW compared with placebo (p=0.02 at Week 20). SRI improvements compared with placebo were higher still in subjects who attained SELENA–SLEDAI improvements of ≥8, and in patients with severe disease (SELENA–SLEDAI≥10 and receiving corticosteroids, n=278, figure 1 ). Despite declining patient numbers, response to blisibimod remained higher than placebo beyond Week 24 while N>30 subjects per cohort. Numerically higher response was also observed with blisibimod in all components of the SRI. Blisibimod was safe and well-tolerated at all dose levels with no meaningful imbalances in serious adverse events or infections compared with placebo. Image/graphConclusions These are the first evidence that SLE disease activity may be improved with subcutaneous injections of a novel biologic therapy. Disclosure of Interest R. Furie Consultant for: Anthera Pharmaceuticals, M. Scheinberg: None Declared, G. Leon: None Declared, E. Ramiterre: None Declared, M. Thomas: None Declared, A. Chu: None Declared, C. Hislop Employee of: Anthera Pharmaceuticals, R. Martin: None Declared, M. 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B.</given-names></name><xref ref-type="aff" rid="AF01164"><sup>4</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Thomas</surname><given-names>M.</given-names></name><xref ref-type="aff" rid="AF01165"><sup>5</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Chu</surname><given-names>A. D.</given-names></name><xref ref-type="aff" rid="AF01166"><sup>6</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Hislop</surname><given-names>C.</given-names></name><xref ref-type="aff" rid="AF01167"><sup>7</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Martin</surname><given-names>R. S.</given-names></name><xref ref-type="aff" rid="AF01167"><sup>7</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Petri</surname><given-names>M. A.</given-names></name><xref ref-type="aff" rid="AF01168"><sup>8</sup></xref></contrib></contrib-group><aff id="AF01161"><sup>1</sup>North Shore–Long Island Jewish Health System, Lake Success New York, United States</aff><aff id="AF01162"><sup>2</sup>Rheumatology Hospital Abreu Sodre Pesquisa Clínica, São Paulo, Brazil</aff><aff id="AF01163"><sup>3</sup>Rheumatology Gynecology & Reproduction Institute, Lima, Peru</aff><aff id="AF01164"><sup>4</sup>Brokenshire Memorial Hospital, Davao City, Philippines</aff><aff id="AF01165"><sup>5</sup>Health and Research Centre, Trivandrum, Kerala, India</aff><aff id="AF01166"><sup>6</sup>Anthera Pharmaceuticals</aff><aff id="AF01167"><sup>7</sup>Anthera Pharmaceuticals, Inc, Hayward</aff><aff id="AF01168"><sup>8</sup>Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, United States</aff><pub-date pub-type="ppub"><month>06</month><year>2013</year></pub-date><volume>72</volume><volume-id pub-id-type="other">72</volume-id><volume-id pub-id-type="other">72</volume-id><issue>Suppl 3</issue><issue-id pub-id-type="other">annrheumdis;72/Suppl_3</issue-id><issue-id pub-id-type="other" content-type="supplement">Suppl_3</issue-id><issue-id pub-id-type="other">72/Suppl_3</issue-id><issue-title>Annual European Congress of Rheumatology EULAR abstracts 2013, 12–15 June 2013, Spain</issue-title><fpage seq="3">A90</fpage><permissions><copyright-statement>© 2013, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</copyright-statement><copyright-year>2013</copyright-year></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="annrheumdis-72-A90-3.pdf"></self-uri><abstract><sec><title>Background</title><p>Blisibimod, a potent inhibitor of B cell activating factor (BAFF), was evaluated in a Phase 2b clinical trial in patients with SLE.</p></sec><sec><title>Objectives</title><p>To determine the effect of subcutaneous blisibimod on SLE disease activity, including rate of response to the SLE responder index (SRI).</p></sec><sec><title>Methods</title><p>547 serologically-active SLE patients with baseline SELENA-SLEDAI ≥6 were randomized to receive blisibimod (100mg weekly (QW), 200mg QW, or 200mg Q4W) or placebo in matchin dosing regimens. The primary endpoint was a comparison at Week 24 of the percentage of subjects in the pooled blisibimod and placebo groups who achieved an SRI-5 response (SRI with ≥5 point improvement in SELENA–SLEDAI).</p></sec><sec><title>Results</title><p>The primary endpoint was not met due to the lack of efficacy in the two lower doses. However, SRI-5 response was higher in subjects receiving blisibimod 200mg QW compared with placebo (p=0.02 at Week 20). SRI improvements compared with placebo were higher still in subjects who attained SELENA–SLEDAI improvements of ≥8, and in patients with severe disease (SELENA–SLEDAI≥10 and receiving corticosteroids, n=278, <xref ref-type="fig" rid="F1">figure 1</xref> ). Despite declining patient numbers, response to blisibimod remained higher than placebo beyond Week 24 while N>30 subjects per cohort. Numerically higher response was also observed with blisibimod in all components of the SRI. Blisibimod was safe and well-tolerated at all dose levels with no meaningful imbalances in serious adverse events or infections compared with placebo.</p></sec><sec><title>Image/graph</title><fig id="F1" position="float"><graphic xlink:href="annrheumdis-72-A90-3-F1.jpg" alt-version="no" position="float" xlink:type="simple"></graphic></fig></sec><sec><title>Conclusions</title><p>These are the first evidence that SLE disease activity may be improved with subcutaneous injections of a novel biologic therapy.</p></sec><sec><title>Disclosure of Interest</title><p>R. Furie Consultant for: Anthera Pharmaceuticals, M. Scheinberg: None Declared, G. Leon: None Declared, E. Ramiterre: None Declared, M. Thomas: None Declared, A. Chu: None Declared, C. Hislop Employee of: Anthera Pharmaceuticals, R. Martin: None Declared, M. Petri Employee of: Anthera Pharmaceuticals</p></sec></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>OP0116 Effects of Blisibimod, a Subcutaneous Inhibitor of B Cell Activating Factor, in Patients with SLE</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>OP0116 Effects of Blisibimod, a Subcutaneous Inhibitor of B Cell Activating Factor, in Patients with SLE</title></titleInfo><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Furie</namePart><affiliation>North Shore–Long Island Jewish Health System, Lake Success New York, United States</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Scheinberg</namePart><affiliation>Rheumatology Hospital Abreu Sodre Pesquisa Clínica, São Paulo, Brazil</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Leon</namePart><affiliation>Rheumatology Gynecology & Reproduction Institute, Lima, Peru</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E. B.</namePart><namePart type="family">Ramiterre</namePart><affiliation>Brokenshire Memorial Hospital, Davao City, Philippines</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Thomas</namePart><affiliation>Health and Research Centre, Trivandrum, Kerala, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. D.</namePart><namePart type="family">Chu</namePart><affiliation>Anthera Pharmaceuticals</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Hislop</namePart><affiliation>Anthera Pharmaceuticals, Inc, Hayward</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R. S.</namePart><namePart type="family">Martin</namePart><affiliation>Anthera Pharmaceuticals, Inc, Hayward</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. A.</namePart><namePart type="family">Petri</namePart><affiliation>Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, United States</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="abstract" displayLabel="abstract"></genre><originInfo><publisher>BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><dateIssued encoding="w3cdtf">2013-06</dateIssued><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Background Blisibimod, a potent inhibitor of B cell activating factor (BAFF), was evaluated in a Phase 2b clinical trial in patients with SLE. Objectives To determine the effect of subcutaneous blisibimod on SLE disease activity, including rate of response to the SLE responder index (SRI). Methods 547 serologically-active SLE patients with baseline SELENA-SLEDAI ≥6 were randomized to receive blisibimod (100mg weekly (QW), 200mg QW, or 200mg Q4W) or placebo in matchin dosing regimens. The primary endpoint was a comparison at Week 24 of the percentage of subjects in the pooled blisibimod and placebo groups who achieved an SRI-5 response (SRI with ≥5 point improvement in SELENA–SLEDAI). Results The primary endpoint was not met due to the lack of efficacy in the two lower doses. However, SRI-5 response was higher in subjects receiving blisibimod 200mg QW compared with placebo (p=0.02 at Week 20). SRI improvements compared with placebo were higher still in subjects who attained SELENA–SLEDAI improvements of ≥8, and in patients with severe disease (SELENA–SLEDAI≥10 and receiving corticosteroids, n=278, figure 1 ). Despite declining patient numbers, response to blisibimod remained higher than placebo beyond Week 24 while N>30 subjects per cohort. Numerically higher response was also observed with blisibimod in all components of the SRI. Blisibimod was safe and well-tolerated at all dose levels with no meaningful imbalances in serious adverse events or infections compared with placebo. Image/graphConclusions These are the first evidence that SLE disease activity may be improved with subcutaneous injections of a novel biologic therapy. Disclosure of Interest R. Furie Consultant for: Anthera Pharmaceuticals, M. Scheinberg: None Declared, G. Leon: None Declared, E. Ramiterre: None Declared, M. Thomas: None Declared, A. Chu: None Declared, C. Hislop Employee of: Anthera Pharmaceuticals, R. Martin: None Declared, M. Petri Employee of: Anthera Pharmaceuticals</abstract><relatedItem type="host"><titleInfo><title>Annals of the Rheumatic Diseases</title></titleInfo><titleInfo type="abbreviated"><title>Ann Rheum Dis</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0003-4967</identifier><identifier type="eISSN">1468-2060</identifier><identifier type="PublisherID">ard</identifier><identifier type="PublisherID-hwp">annrheumdis</identifier><identifier type="PublisherID-nlm-ta">Ann Rheum Dis</identifier><part><date>2013</date><detail type="title"><title>Annual European Congress of Rheumatology EULAR abstracts 2013, 12–15 June 2013, Spain</title></detail><detail type="volume"><caption>vol.</caption><number>72</number></detail><detail type="issue"><caption>no.</caption><number>Suppl 3</number></detail><extent unit="pages"><start>A90</start></extent></part></relatedItem><identifier type="istex">F84B96C3EE876A6D7F43D3F2DFF816080FD163F5</identifier><identifier type="DOI">10.1136/annrheumdis-2013-eular.321</identifier><identifier type="href">annrheumdis-72-A90-3.pdf</identifier><identifier type="ArticleID">annrheumdis-2013-eular.321</identifier><identifier type="local">annrheumdis;72/Suppl_3/A90-c</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2013, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</accessCondition><recordInfo><recordContentSource>BMJ</recordContentSource></recordInfo></mods></metadata><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/F84B96C3EE876A6D7F43D3F2DFF816080FD163F5/annexes/jpeg</uri></json:item></annexes><enrichments><json:item><type>multicat</type><uri>https://api.istex.fr/document/F84B96C3EE876A6D7F43D3F2DFF816080FD163F5/enrichments/multicat</uri></json:item><json:item><type>refBibs</type><uri>https://api.istex.fr/document/F84B96C3EE876A6D7F43D3F2DFF816080FD163F5/enrichments/refBibs</uri></json:item></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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