Chemically Modified Interleukin-6 Aptamer Inhibits Development of Collagen-Induced Arthritis in Cynomolgus Monkeys
Interleukin-6 (IL-6) is a potent mediator of inflammatory and immune responses, and a validated target for therapeutic intervention of inflammatory diseases. Previous studies have shown that SL1026, a slow off-rate modified aptamer (SOMAmer) antagonist of IL-6, neutralizes IL-6 signaling in vitro ....
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| Veröffentlicht in: | Nucleic acid therapeutics 2016-02, Vol.26 (1), p.1-19 |
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| creator | Hirota, Masao Murakami, Ikuo Ishikawa, Yuichi Suzuki, Tomoki Sumida, Shun-ichiro Ibaragi, Shigeru Kasai, Hayato Horai, Naoto Drolet, Daniel W. Gupta, Shashi Janjic, Nebojsa Schneider, Daniel J. |
| description | Interleukin-6 (IL-6) is a potent mediator of inflammatory and immune responses, and a validated target for therapeutic intervention of inflammatory diseases. Previous studies have shown that SL1026, a slow off-rate modified aptamer (SOMAmer) antagonist of IL-6, neutralizes IL-6 signaling
in vitro
. In the present study, we show that SL1026 delays the onset and reduces the severity of rheumatoid symptoms in a collagen-induced arthritis model in cynomolgus monkeys. SL1026 (1 and 10 mg/kg), administered q.i.d., delayed the progression of arthritis and the concomitant increase in serum IL-6 levels compared to the untreated control group. Furthermore, SL1026 inhibited IL-6-induced STAT3 phosphorylation
ex vivo
in T lymphocytes from human blood and IL-6-induced C-reactive protein and serum amyloid A production in human primary hepatocytes. Importantly, SOMAmer treatment did not elicit an immune response, as evidenced by the absence of anti-SOMAmer antibodies in plasma of treated monkeys. These results demonstrate that SOMAmer antagonists of IL-6 may be attractive agents for the treatment of IL-6-mediated diseases, including rheumatoid arthritis. |
| doi_str_mv | 10.1089/nat.2015.0567 |
| format | Article |
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in vitro
. In the present study, we show that SL1026 delays the onset and reduces the severity of rheumatoid symptoms in a collagen-induced arthritis model in cynomolgus monkeys. SL1026 (1 and 10 mg/kg), administered q.i.d., delayed the progression of arthritis and the concomitant increase in serum IL-6 levels compared to the untreated control group. Furthermore, SL1026 inhibited IL-6-induced STAT3 phosphorylation
ex vivo
in T lymphocytes from human blood and IL-6-induced C-reactive protein and serum amyloid A production in human primary hepatocytes. Importantly, SOMAmer treatment did not elicit an immune response, as evidenced by the absence of anti-SOMAmer antibodies in plasma of treated monkeys. These results demonstrate that SOMAmer antagonists of IL-6 may be attractive agents for the treatment of IL-6-mediated diseases, including rheumatoid arthritis.</description><identifier>ISSN: 2159-3337</identifier><identifier>EISSN: 2159-3345</identifier><identifier>DOI: 10.1089/nat.2015.0567</identifier><identifier>PMID: 26579954</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Amino Acid Sequence ; Animals ; Aptamers, Peptide - chemistry ; Arthritis, Experimental - chemically induced ; Arthritis, Experimental - prevention & control ; Cells, Cultured ; Collagen - adverse effects ; Cynomolgus ; Cytokines ; Female ; Humans ; Immune response ; Immune system ; Interleukin-6 - blood ; Interleukin-6 - chemistry ; Lymphocytes ; Macaca fascicularis ; Molecular Sequence Data ; Monkeys & apes ; Original ; Original Articles ; Pharmacology ; Phosphorylation ; Rheumatoid arthritis ; Sequence Homology, Amino Acid ; Special Issue on Aptamers ; STAT3 Transcription Factor - metabolism ; T-Lymphocytes - metabolism</subject><ispartof>Nucleic acid therapeutics, 2016-02, Vol.26 (1), p.1-19</ispartof><rights>Masao Hirota et al, 2015; Published by Mary Ann Liebert, Inc.</rights><rights>(©) © Masao Hirota et al, 2015; Published by Mary Ann Liebert, Inc.</rights><rights>Masao Hirota , 2015; Published by Mary Ann Liebert, Inc. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c492t-dd11a000c810f5390a7c8d6531579588d60053bdbb40c8159d0e57464bba9edd3</citedby><cites>FETCH-LOGICAL-c492t-dd11a000c810f5390a7c8d6531579588d60053bdbb40c8159d0e57464bba9edd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26579954$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hirota, Masao</creatorcontrib><creatorcontrib>Murakami, Ikuo</creatorcontrib><creatorcontrib>Ishikawa, Yuichi</creatorcontrib><creatorcontrib>Suzuki, Tomoki</creatorcontrib><creatorcontrib>Sumida, Shun-ichiro</creatorcontrib><creatorcontrib>Ibaragi, Shigeru</creatorcontrib><creatorcontrib>Kasai, Hayato</creatorcontrib><creatorcontrib>Horai, Naoto</creatorcontrib><creatorcontrib>Drolet, Daniel W.</creatorcontrib><creatorcontrib>Gupta, Shashi</creatorcontrib><creatorcontrib>Janjic, Nebojsa</creatorcontrib><creatorcontrib>Schneider, Daniel J.</creatorcontrib><title>Chemically Modified Interleukin-6 Aptamer Inhibits Development of Collagen-Induced Arthritis in Cynomolgus Monkeys</title><title>Nucleic acid therapeutics</title><addtitle>Nucleic Acid Ther</addtitle><description>Interleukin-6 (IL-6) is a potent mediator of inflammatory and immune responses, and a validated target for therapeutic intervention of inflammatory diseases. Previous studies have shown that SL1026, a slow off-rate modified aptamer (SOMAmer) antagonist of IL-6, neutralizes IL-6 signaling
in vitro
. In the present study, we show that SL1026 delays the onset and reduces the severity of rheumatoid symptoms in a collagen-induced arthritis model in cynomolgus monkeys. SL1026 (1 and 10 mg/kg), administered q.i.d., delayed the progression of arthritis and the concomitant increase in serum IL-6 levels compared to the untreated control group. Furthermore, SL1026 inhibited IL-6-induced STAT3 phosphorylation
ex vivo
in T lymphocytes from human blood and IL-6-induced C-reactive protein and serum amyloid A production in human primary hepatocytes. Importantly, SOMAmer treatment did not elicit an immune response, as evidenced by the absence of anti-SOMAmer antibodies in plasma of treated monkeys. These results demonstrate that SOMAmer antagonists of IL-6 may be attractive agents for the treatment of IL-6-mediated diseases, including rheumatoid arthritis.</description><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Aptamers, Peptide - chemistry</subject><subject>Arthritis, Experimental - chemically induced</subject><subject>Arthritis, Experimental - prevention & control</subject><subject>Cells, Cultured</subject><subject>Collagen - adverse effects</subject><subject>Cynomolgus</subject><subject>Cytokines</subject><subject>Female</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Interleukin-6 - blood</subject><subject>Interleukin-6 - chemistry</subject><subject>Lymphocytes</subject><subject>Macaca fascicularis</subject><subject>Molecular Sequence Data</subject><subject>Monkeys & apes</subject><subject>Original</subject><subject>Original Articles</subject><subject>Pharmacology</subject><subject>Phosphorylation</subject><subject>Rheumatoid arthritis</subject><subject>Sequence Homology, Amino Acid</subject><subject>Special Issue on Aptamers</subject><subject>STAT3 Transcription Factor - 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Academic</collection><collection>Biotechnology Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nucleic acid therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hirota, Masao</au><au>Murakami, Ikuo</au><au>Ishikawa, Yuichi</au><au>Suzuki, Tomoki</au><au>Sumida, Shun-ichiro</au><au>Ibaragi, Shigeru</au><au>Kasai, Hayato</au><au>Horai, Naoto</au><au>Drolet, Daniel W.</au><au>Gupta, Shashi</au><au>Janjic, Nebojsa</au><au>Schneider, Daniel J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chemically Modified Interleukin-6 Aptamer Inhibits Development of Collagen-Induced Arthritis in Cynomolgus Monkeys</atitle><jtitle>Nucleic acid therapeutics</jtitle><addtitle>Nucleic Acid Ther</addtitle><date>2016-02-01</date><risdate>2016</risdate><volume>26</volume><issue>1</issue><spage>1</spage><epage>19</epage><pages>1-19</pages><issn>2159-3337</issn><eissn>2159-3345</eissn><abstract>Interleukin-6 (IL-6) is a potent mediator of inflammatory and immune responses, and a validated target for therapeutic intervention of inflammatory diseases. Previous studies have shown that SL1026, a slow off-rate modified aptamer (SOMAmer) antagonist of IL-6, neutralizes IL-6 signaling
in vitro
. In the present study, we show that SL1026 delays the onset and reduces the severity of rheumatoid symptoms in a collagen-induced arthritis model in cynomolgus monkeys. SL1026 (1 and 10 mg/kg), administered q.i.d., delayed the progression of arthritis and the concomitant increase in serum IL-6 levels compared to the untreated control group. Furthermore, SL1026 inhibited IL-6-induced STAT3 phosphorylation
ex vivo
in T lymphocytes from human blood and IL-6-induced C-reactive protein and serum amyloid A production in human primary hepatocytes. Importantly, SOMAmer treatment did not elicit an immune response, as evidenced by the absence of anti-SOMAmer antibodies in plasma of treated monkeys. These results demonstrate that SOMAmer antagonists of IL-6 may be attractive agents for the treatment of IL-6-mediated diseases, including rheumatoid arthritis.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>26579954</pmid><doi>10.1089/nat.2015.0567</doi><tpages>19</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amino Acid Sequence Animals Aptamers, Peptide - chemistry Arthritis, Experimental - chemically induced Arthritis, Experimental - prevention & control Cells, Cultured Collagen - adverse effects Cynomolgus Cytokines Female Humans Immune response Immune system Interleukin-6 - blood Interleukin-6 - chemistry Lymphocytes Macaca fascicularis Molecular Sequence Data Monkeys & apes Original Original Articles Pharmacology Phosphorylation Rheumatoid arthritis Sequence Homology, Amino Acid Special Issue on Aptamers STAT3 Transcription Factor - metabolism T-Lymphocytes - metabolism |
| title | Chemically Modified Interleukin-6 Aptamer Inhibits Development of Collagen-Induced Arthritis in Cynomolgus Monkeys |
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