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809 A bispecific antibody targeting CCR8 & CTLA-4: Potent anti-tumor efficacy with better safety by preferentially eliminating tumor-infiltrating regulatory T cells
BackgroundRegulatory T (Treg) cells play a critical role in maintaining homeostasis and self-tolerance. In tumor immunology, Tregs hamper anti-tumor immune responses and thus promotes tumor development and progression.1 Many Treg-targeting therapies are currently under clinical investigation. Howeve...
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Published in: | Journal for immunotherapy of cancer 2023-11, Vol.11 (Suppl 1), p.A907-A907 |
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description | BackgroundRegulatory T (Treg) cells play a critical role in maintaining homeostasis and self-tolerance. In tumor immunology, Tregs hamper anti-tumor immune responses and thus promotes tumor development and progression.1 Many Treg-targeting therapies are currently under clinical investigation. However, due to difficulty in selectively targeting tumor-infiltrating Treg cells, many of these agents have shown limited efficacy and/or treatment-limiting systemic toxicity. CCR8, a chemokine receptor, has recently been identified to mainly be expressed on tumor associated Tregs but other effector T cell populations also express CCR8, raising the uncertainty of universally depleting CCR8-positive cells.2 To increase the specificity of targeting tumor Tregs, CTLA-4 was selected as a target pair with CCR8 for the generation of an IgG-like bispecific antibody.MethodsAnti-CCR8 x CTLA-4 bispecifics were generated in a 1+1 format and screened from multiple anti-CCR8 and anti-CTLA-4 binding arms with a wide range of affinities. CCR8 and CTLA-4 single-positive cells and CCR8/CTLA-4 double-positive cells were generated to screen for bispecifics with preferential binding and killing towards double-positive cells over single-positive cells in vitro. Lead candidates were generated to evaluate anti-tumor efficacy as a proof-of-concept study in human-CCR8/CTLA-4 double knock-in mice, inoculated with CT-26 tumor cells. An anti-CCR8 x CTLA-4 surrogate antibody was also generated to evaluate immunotoxicity in human-CLTA-4 knock-in mice.ResultsOur lead anti-CCR8 x CTLA-4 bispecific showed strong binding to CCR8/CTLA-4 double-positive cells but weak to minimal binding to either CCR8 or CTLA-4 single-positive cells. This binding profile translated to strong ADCC activity towards double-positive cells but much weaker activity towards CCR8 or CLTA4 single-positive cells. Accordingly, anti-CCR8 x CTLA-4 bispecifics showed superior anti-tumor efficacy in vivo, with similar or better tumor growth inhibition compared to the corresponding monospecific agents. Importantly, the bispecifics showed limited depletion of surface CLTA4 and weak blocking activity against CTLA-4 single-positive cells, which have been proposed to be contributing factors of immunotoxicity in the clinic when targeting CTLA-4. In agreement with this concept, a CCR8 x CTLA-4 surrogate bispecific did not induce immunotoxicity in a mouse model in combination with anti-PD1.ConclusionsWe have successfully generated an anti-CC |
doi_str_mv | 10.1136/jitc-2023-SITC2023.0809 |
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fullrecord | <record><control><sourceid>proquest_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_5df9ef5fbac9433badca5ee537f90762</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_5df9ef5fbac9433badca5ee537f90762</doaj_id><sourcerecordid>2888527989</sourcerecordid><originalsourceid>FETCH-LOGICAL-b1879-16e8113cd70adb810a20510c28990e47f695cf59df1d4546c717b2b66064187e3</originalsourceid><addsrcrecordid>eNpFkd2K1DAYhosguKx7DQYEz7Lmp2kTz4ai7sCAi47HIUm_jCmdZkwzSM_2xFvxwrwS0xnFo4SP531JvqeqXlFyTylv3g4hO8wI4_jLdt-tl3siiXpW3TAiKKY1a15Ud_M8EEIo4VxKeVP9KsTvp58bZMN8Ahd8cMhMOdjYLyibdIAcpgPqus8SvUHdfrfB9Tv0GDNM-QLifD7GhMCXpHEL-hHyN2QhZ0hoNh7yguyCTgk8pJIJZhwXBGM4hslcqi95HCYfxpyuowSH82hyTAvaIwfjOL-snnszznD397ytvn54v-8e8O7Tx2232WFLZaswbUCWXbi-Jaa3khKzfp04JpUiULe-UcJ5oXpP-1rUjWtpa5ltGtLUpQD4bbW99vbRDPqUwtGkRUcT9GUQ00GblIMbQYveK_DCW-NUzbk1vTMCQPDWK9I2rHS9vnadUvx-hjnrIZ7TVJ6vWdm9YK2SqlD8Stnj8B-gRK9O9epUryr1P6d6dcr_AFBGmi8</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2888527989</pqid></control><display><type>article</type><title>809 A bispecific antibody targeting CCR8 & CTLA-4: Potent anti-tumor efficacy with better safety by preferentially eliminating tumor-infiltrating regulatory T cells</title><source>BMJ Open Access Journals</source><source>Access via ProQuest (Open Access)</source><source>PubMed Central</source><creator>Chen, Liandi ; Zhai, Tianhang ; Huang, Weifeng ; Miao, Xiaoniu ; Dai, Shuang ; Peng, Shaogang ; Wang, Chao ; Tsun, Andy ; Luo, Yi</creator><creatorcontrib>Chen, Liandi ; Zhai, Tianhang ; Huang, Weifeng ; Miao, Xiaoniu ; Dai, Shuang ; Peng, Shaogang ; Wang, Chao ; Tsun, Andy ; Luo, Yi</creatorcontrib><description>BackgroundRegulatory T (Treg) cells play a critical role in maintaining homeostasis and self-tolerance. In tumor immunology, Tregs hamper anti-tumor immune responses and thus promotes tumor development and progression.1 Many Treg-targeting therapies are currently under clinical investigation. However, due to difficulty in selectively targeting tumor-infiltrating Treg cells, many of these agents have shown limited efficacy and/or treatment-limiting systemic toxicity. CCR8, a chemokine receptor, has recently been identified to mainly be expressed on tumor associated Tregs but other effector T cell populations also express CCR8, raising the uncertainty of universally depleting CCR8-positive cells.2 To increase the specificity of targeting tumor Tregs, CTLA-4 was selected as a target pair with CCR8 for the generation of an IgG-like bispecific antibody.MethodsAnti-CCR8 x CTLA-4 bispecifics were generated in a 1+1 format and screened from multiple anti-CCR8 and anti-CTLA-4 binding arms with a wide range of affinities. CCR8 and CTLA-4 single-positive cells and CCR8/CTLA-4 double-positive cells were generated to screen for bispecifics with preferential binding and killing towards double-positive cells over single-positive cells in vitro. Lead candidates were generated to evaluate anti-tumor efficacy as a proof-of-concept study in human-CCR8/CTLA-4 double knock-in mice, inoculated with CT-26 tumor cells. An anti-CCR8 x CTLA-4 surrogate antibody was also generated to evaluate immunotoxicity in human-CLTA-4 knock-in mice.ResultsOur lead anti-CCR8 x CTLA-4 bispecific showed strong binding to CCR8/CTLA-4 double-positive cells but weak to minimal binding to either CCR8 or CTLA-4 single-positive cells. This binding profile translated to strong ADCC activity towards double-positive cells but much weaker activity towards CCR8 or CLTA4 single-positive cells. Accordingly, anti-CCR8 x CTLA-4 bispecifics showed superior anti-tumor efficacy in vivo, with similar or better tumor growth inhibition compared to the corresponding monospecific agents. Importantly, the bispecifics showed limited depletion of surface CLTA4 and weak blocking activity against CTLA-4 single-positive cells, which have been proposed to be contributing factors of immunotoxicity in the clinic when targeting CTLA-4. In agreement with this concept, a CCR8 x CTLA-4 surrogate bispecific did not induce immunotoxicity in a mouse model in combination with anti-PD1.ConclusionsWe have successfully generated an anti-CCR8 x CTLA-4 bispecific that preferentially eliminates CCR8/CTLA-4 double-positive tumor-infiltrating Treg cells with minimized interference towards single-positive cells. This achieves superior anti-tumor activity than the corresponding monospecific agents, with lower immunotoxicity, and may thus function as a safer, more specific, and highly effective tumor-infiltrating Treg-depleting agent.AcknowledgementsWe would like to acknowledge our collaborator Adimab for generating the anti-CCR8 mAbs on the Adimab Platform.ReferencesOhue Y, H Nishikawa, Regulatory T (Treg) cells in cancer: Can Treg cells be a new therapeutic target? Cancer Sci, 2019;110(7):2080–2089.Yi G, et al. Identification and functional analysis of heterogeneous FOXP3(+) Treg cell subpopulations in human pancreatic ductal adenocarcinoma. Sci Bull (Beijing), 2018;63(15):972–981.Ethics ApprovalAll mice were maintained under specified pathogen-free conditions, and all studies were approved by the Animal Care and Use Committee of HUST-Suzhou Institute for Brainsmatics.</description><identifier>EISSN: 2051-1426</identifier><identifier>DOI: 10.1136/jitc-2023-SITC2023.0809</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd</publisher><subject>Antibodies ; Immunotherapy ; Regular and Young Investigator Award Abstracts</subject><ispartof>Journal for immunotherapy of cancer, 2023-11, Vol.11 (Suppl 1), p.A907-A907</ispartof><rights>Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</rights><rights>2023 Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. http://creativecommons.org/licenses/by-nc/4.0/ This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/ . Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://jitc.bmj.com/content/11/Suppl_1/A907.full.pdf$$EPDF$$P50$$Gbmj$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://jitc.bmj.com/content/11/Suppl_1/A907.full$$EHTML$$P50$$Gbmj$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,27924,27925,37012,55350,77660,77686</link.rule.ids></links><search><creatorcontrib>Chen, Liandi</creatorcontrib><creatorcontrib>Zhai, Tianhang</creatorcontrib><creatorcontrib>Huang, Weifeng</creatorcontrib><creatorcontrib>Miao, Xiaoniu</creatorcontrib><creatorcontrib>Dai, Shuang</creatorcontrib><creatorcontrib>Peng, Shaogang</creatorcontrib><creatorcontrib>Wang, Chao</creatorcontrib><creatorcontrib>Tsun, Andy</creatorcontrib><creatorcontrib>Luo, Yi</creatorcontrib><title>809 A bispecific antibody targeting CCR8 & CTLA-4: Potent anti-tumor efficacy with better safety by preferentially eliminating tumor-infiltrating regulatory T cells</title><title>Journal for immunotherapy of cancer</title><addtitle>J Immunother Cancer</addtitle><description>BackgroundRegulatory T (Treg) cells play a critical role in maintaining homeostasis and self-tolerance. In tumor immunology, Tregs hamper anti-tumor immune responses and thus promotes tumor development and progression.1 Many Treg-targeting therapies are currently under clinical investigation. However, due to difficulty in selectively targeting tumor-infiltrating Treg cells, many of these agents have shown limited efficacy and/or treatment-limiting systemic toxicity. CCR8, a chemokine receptor, has recently been identified to mainly be expressed on tumor associated Tregs but other effector T cell populations also express CCR8, raising the uncertainty of universally depleting CCR8-positive cells.2 To increase the specificity of targeting tumor Tregs, CTLA-4 was selected as a target pair with CCR8 for the generation of an IgG-like bispecific antibody.MethodsAnti-CCR8 x CTLA-4 bispecifics were generated in a 1+1 format and screened from multiple anti-CCR8 and anti-CTLA-4 binding arms with a wide range of affinities. CCR8 and CTLA-4 single-positive cells and CCR8/CTLA-4 double-positive cells were generated to screen for bispecifics with preferential binding and killing towards double-positive cells over single-positive cells in vitro. Lead candidates were generated to evaluate anti-tumor efficacy as a proof-of-concept study in human-CCR8/CTLA-4 double knock-in mice, inoculated with CT-26 tumor cells. An anti-CCR8 x CTLA-4 surrogate antibody was also generated to evaluate immunotoxicity in human-CLTA-4 knock-in mice.ResultsOur lead anti-CCR8 x CTLA-4 bispecific showed strong binding to CCR8/CTLA-4 double-positive cells but weak to minimal binding to either CCR8 or CTLA-4 single-positive cells. This binding profile translated to strong ADCC activity towards double-positive cells but much weaker activity towards CCR8 or CLTA4 single-positive cells. Accordingly, anti-CCR8 x CTLA-4 bispecifics showed superior anti-tumor efficacy in vivo, with similar or better tumor growth inhibition compared to the corresponding monospecific agents. Importantly, the bispecifics showed limited depletion of surface CLTA4 and weak blocking activity against CTLA-4 single-positive cells, which have been proposed to be contributing factors of immunotoxicity in the clinic when targeting CTLA-4. In agreement with this concept, a CCR8 x CTLA-4 surrogate bispecific did not induce immunotoxicity in a mouse model in combination with anti-PD1.ConclusionsWe have successfully generated an anti-CCR8 x CTLA-4 bispecific that preferentially eliminates CCR8/CTLA-4 double-positive tumor-infiltrating Treg cells with minimized interference towards single-positive cells. This achieves superior anti-tumor activity than the corresponding monospecific agents, with lower immunotoxicity, and may thus function as a safer, more specific, and highly effective tumor-infiltrating Treg-depleting agent.AcknowledgementsWe would like to acknowledge our collaborator Adimab for generating the anti-CCR8 mAbs on the Adimab Platform.ReferencesOhue Y, H Nishikawa, Regulatory T (Treg) cells in cancer: Can Treg cells be a new therapeutic target? Cancer Sci, 2019;110(7):2080–2089.Yi G, et al. Identification and functional analysis of heterogeneous FOXP3(+) Treg cell subpopulations in human pancreatic ductal adenocarcinoma. Sci Bull (Beijing), 2018;63(15):972–981.Ethics ApprovalAll mice were maintained under specified pathogen-free conditions, and all studies were approved by the Animal Care and Use Committee of HUST-Suzhou Institute for Brainsmatics.</description><subject>Antibodies</subject><subject>Immunotherapy</subject><subject>Regular and Young Investigator Award Abstracts</subject><issn>2051-1426</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>9YT</sourceid><sourceid>DOA</sourceid><recordid>eNpFkd2K1DAYhosguKx7DQYEz7Lmp2kTz4ai7sCAi47HIUm_jCmdZkwzSM_2xFvxwrwS0xnFo4SP531JvqeqXlFyTylv3g4hO8wI4_jLdt-tl3siiXpW3TAiKKY1a15Ud_M8EEIo4VxKeVP9KsTvp58bZMN8Ahd8cMhMOdjYLyibdIAcpgPqus8SvUHdfrfB9Tv0GDNM-QLifD7GhMCXpHEL-hHyN2QhZ0hoNh7yguyCTgk8pJIJZhwXBGM4hslcqi95HCYfxpyuowSH82hyTAvaIwfjOL-snnszznD397ytvn54v-8e8O7Tx2232WFLZaswbUCWXbi-Jaa3khKzfp04JpUiULe-UcJ5oXpP-1rUjWtpa5ltGtLUpQD4bbW99vbRDPqUwtGkRUcT9GUQ00GblIMbQYveK_DCW-NUzbk1vTMCQPDWK9I2rHS9vnadUvx-hjnrIZ7TVJ6vWdm9YK2SqlD8Stnj8B-gRK9O9epUryr1P6d6dcr_AFBGmi8</recordid><startdate>20231101</startdate><enddate>20231101</enddate><creator>Chen, Liandi</creator><creator>Zhai, Tianhang</creator><creator>Huang, Weifeng</creator><creator>Miao, Xiaoniu</creator><creator>Dai, Shuang</creator><creator>Peng, Shaogang</creator><creator>Wang, Chao</creator><creator>Tsun, Andy</creator><creator>Luo, Yi</creator><general>BMJ Publishing Group Ltd</general><general>BMJ Publishing Group LTD</general><general>BMJ Publishing Group</general><scope>9YT</scope><scope>ACMMV</scope><scope>K9.</scope><scope>DOA</scope></search><sort><creationdate>20231101</creationdate><title>809 A bispecific antibody targeting CCR8 & CTLA-4: Potent anti-tumor efficacy with better safety by preferentially eliminating tumor-infiltrating regulatory T cells</title><author>Chen, Liandi ; Zhai, Tianhang ; Huang, Weifeng ; Miao, Xiaoniu ; Dai, Shuang ; Peng, Shaogang ; Wang, Chao ; Tsun, Andy ; Luo, Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b1879-16e8113cd70adb810a20510c28990e47f695cf59df1d4546c717b2b66064187e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Antibodies</topic><topic>Immunotherapy</topic><topic>Regular and Young Investigator Award Abstracts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Liandi</creatorcontrib><creatorcontrib>Zhai, Tianhang</creatorcontrib><creatorcontrib>Huang, Weifeng</creatorcontrib><creatorcontrib>Miao, Xiaoniu</creatorcontrib><creatorcontrib>Dai, Shuang</creatorcontrib><creatorcontrib>Peng, Shaogang</creatorcontrib><creatorcontrib>Wang, Chao</creatorcontrib><creatorcontrib>Tsun, Andy</creatorcontrib><creatorcontrib>Luo, Yi</creatorcontrib><collection>BMJ Open Access Journals</collection><collection>BMJ Journals:Open Access</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Journal for immunotherapy of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Liandi</au><au>Zhai, Tianhang</au><au>Huang, Weifeng</au><au>Miao, Xiaoniu</au><au>Dai, Shuang</au><au>Peng, Shaogang</au><au>Wang, Chao</au><au>Tsun, Andy</au><au>Luo, Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>809 A bispecific antibody targeting CCR8 & CTLA-4: Potent anti-tumor efficacy with better safety by preferentially eliminating tumor-infiltrating regulatory T cells</atitle><jtitle>Journal for immunotherapy of cancer</jtitle><stitle>J Immunother Cancer</stitle><date>2023-11-01</date><risdate>2023</risdate><volume>11</volume><issue>Suppl 1</issue><spage>A907</spage><epage>A907</epage><pages>A907-A907</pages><eissn>2051-1426</eissn><abstract>BackgroundRegulatory T (Treg) cells play a critical role in maintaining homeostasis and self-tolerance. In tumor immunology, Tregs hamper anti-tumor immune responses and thus promotes tumor development and progression.1 Many Treg-targeting therapies are currently under clinical investigation. However, due to difficulty in selectively targeting tumor-infiltrating Treg cells, many of these agents have shown limited efficacy and/or treatment-limiting systemic toxicity. CCR8, a chemokine receptor, has recently been identified to mainly be expressed on tumor associated Tregs but other effector T cell populations also express CCR8, raising the uncertainty of universally depleting CCR8-positive cells.2 To increase the specificity of targeting tumor Tregs, CTLA-4 was selected as a target pair with CCR8 for the generation of an IgG-like bispecific antibody.MethodsAnti-CCR8 x CTLA-4 bispecifics were generated in a 1+1 format and screened from multiple anti-CCR8 and anti-CTLA-4 binding arms with a wide range of affinities. CCR8 and CTLA-4 single-positive cells and CCR8/CTLA-4 double-positive cells were generated to screen for bispecifics with preferential binding and killing towards double-positive cells over single-positive cells in vitro. Lead candidates were generated to evaluate anti-tumor efficacy as a proof-of-concept study in human-CCR8/CTLA-4 double knock-in mice, inoculated with CT-26 tumor cells. An anti-CCR8 x CTLA-4 surrogate antibody was also generated to evaluate immunotoxicity in human-CLTA-4 knock-in mice.ResultsOur lead anti-CCR8 x CTLA-4 bispecific showed strong binding to CCR8/CTLA-4 double-positive cells but weak to minimal binding to either CCR8 or CTLA-4 single-positive cells. This binding profile translated to strong ADCC activity towards double-positive cells but much weaker activity towards CCR8 or CLTA4 single-positive cells. Accordingly, anti-CCR8 x CTLA-4 bispecifics showed superior anti-tumor efficacy in vivo, with similar or better tumor growth inhibition compared to the corresponding monospecific agents. Importantly, the bispecifics showed limited depletion of surface CLTA4 and weak blocking activity against CTLA-4 single-positive cells, which have been proposed to be contributing factors of immunotoxicity in the clinic when targeting CTLA-4. In agreement with this concept, a CCR8 x CTLA-4 surrogate bispecific did not induce immunotoxicity in a mouse model in combination with anti-PD1.ConclusionsWe have successfully generated an anti-CCR8 x CTLA-4 bispecific that preferentially eliminates CCR8/CTLA-4 double-positive tumor-infiltrating Treg cells with minimized interference towards single-positive cells. This achieves superior anti-tumor activity than the corresponding monospecific agents, with lower immunotoxicity, and may thus function as a safer, more specific, and highly effective tumor-infiltrating Treg-depleting agent.AcknowledgementsWe would like to acknowledge our collaborator Adimab for generating the anti-CCR8 mAbs on the Adimab Platform.ReferencesOhue Y, H Nishikawa, Regulatory T (Treg) cells in cancer: Can Treg cells be a new therapeutic target? Cancer Sci, 2019;110(7):2080–2089.Yi G, et al. Identification and functional analysis of heterogeneous FOXP3(+) Treg cell subpopulations in human pancreatic ductal adenocarcinoma. Sci Bull (Beijing), 2018;63(15):972–981.Ethics ApprovalAll mice were maintained under specified pathogen-free conditions, and all studies were approved by the Animal Care and Use Committee of HUST-Suzhou Institute for Brainsmatics.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd</pub><doi>10.1136/jitc-2023-SITC2023.0809</doi><oa>free_for_read</oa></addata></record> |
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title | 809 A bispecific antibody targeting CCR8 & CTLA-4: Potent anti-tumor efficacy with better safety by preferentially eliminating tumor-infiltrating regulatory T cells |
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