N-Arylsulfonyl Indolines as Retinoic Acid Receptor-Related Orphan Receptor γ (RORγ) Agonists
The nuclear retinoic acid receptor‐related orphan receptor γ (RORγ; NR1F3) is a key regulator of inflammatory gene programs involved in T helper 17 (TH17) cell proliferation. As such, synthetic small‐molecule repressors (inverse agonists) targeting RORγ have been extensively studied for their potent...
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| Veröffentlicht in: | ChemMedChem 2016-12, Vol.11 (23), p.2607-2620 |
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| creator | Doebelin, Christelle Patouret, Rémi Garcia-Ordonez, Ruben D. Chang, Mi Ra Dharmarajan, Venkatasubramanian Kuruvilla, Dana S. Novick, Scott J. Lin, Li Cameron, Michael D. Griffin, Patrick R. Kamenecka, Theodore M. |
| description | The nuclear retinoic acid receptor‐related orphan receptor γ (RORγ; NR1F3) is a key regulator of inflammatory gene programs involved in T helper 17 (TH17) cell proliferation. As such, synthetic small‐molecule repressors (inverse agonists) targeting RORγ have been extensively studied for their potential as therapeutic agents for various autoimmune diseases. Alternatively, enhancing TH17 cell proliferation through activation (agonism) of RORγ may boost an immune response, thereby offering a potentially new approach in cancer immunotherapy. Herein we describe the development of N‐arylsulfonyl indolines as RORγ agonists. Structure–activity studies reveal a critical linker region in these molecules as the major determinant for agonism. Hydrogen/deuterium exchange coupled to mass spectrometry (HDX‐MS) analysis of RORγ–ligand complexes help rationalize the observed results.
Pharmacology switches from inverse agonist to agonist: Immunotherapy is an exciting new approach in oncology. RORγ agonists have the potential to enhance immune responses through modulation of TH17 cell proliferation. Starting from an N‐arylsulfonamide indoline RORγ inverse agonist, we were able to identify the key area where small modifications lead to RORγ agonists. A binding mode hypothesis, supported by HDX‐MS analysis, is also proposed. |
| doi_str_mv | 10.1002/cmdc.201600491 |
| format | Article |
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Pharmacology switches from inverse agonist to agonist: Immunotherapy is an exciting new approach in oncology. RORγ agonists have the potential to enhance immune responses through modulation of TH17 cell proliferation. Starting from an N‐arylsulfonamide indoline RORγ inverse agonist, we were able to identify the key area where small modifications lead to RORγ agonists. A binding mode hypothesis, supported by HDX‐MS analysis, is also proposed.</description><identifier>ISSN: 1860-7179</identifier><identifier>EISSN: 1860-7187</identifier><identifier>DOI: 10.1002/cmdc.201600491</identifier><identifier>PMID: 27879053</identifier><language>eng</language><publisher>Germany: Blackwell Publishing Ltd</publisher><subject>Autoimmune diseases ; Binding Sites ; Cancer immunotherapy ; Cell activation ; Cell growth ; Cell proliferation ; Chemical compounds ; Coordination compounds ; Deuterium ; Drug Inverse Agonism ; HEK293 Cells ; Helper cells ; Heterocyclic compounds ; Humans ; Hydrogen-deuterium exchange ; Immune response ; Immune system ; Immunotherapy ; Indoles - chemical synthesis ; Indoles - chemistry ; Indoles - metabolism ; Inflammation ; Interleukin-17 - genetics ; Interleukin-17 - metabolism ; Inverse agonists ; Lymphocytes T ; Mass spectrometry ; Mass spectroscopy ; Molecular Docking Simulation ; N-arylsulfonyl indolines ; nuclear receptors ; Pharmacology ; Promoter Regions, Genetic ; Protein Binding ; Protein Structure, Tertiary ; Receptors ; Receptors, Retinoic Acid - agonists ; Receptors, Retinoic Acid - metabolism ; Repressors ; Retinoic acid ; Retinoic Acid Receptor gamma ; RORγ agonists ; Structure-Activity Relationship ; Th17 Cells - cytology ; Th17 Cells - immunology ; Th17 Cells - metabolism</subject><ispartof>ChemMedChem, 2016-12, Vol.11 (23), p.2607-2620</ispartof><rights>2016 Wiley‐VCH Verlag GmbH & Co. KGaA, Weinheim</rights><rights>2016 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4841-481ac0f27ceb267097b08a2889d100ddecd2d4cd41ebff57dbac12ba885d56bf3</citedby><cites>FETCH-LOGICAL-c4841-481ac0f27ceb267097b08a2889d100ddecd2d4cd41ebff57dbac12ba885d56bf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fcmdc.201600491$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fcmdc.201600491$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27879053$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Doebelin, Christelle</creatorcontrib><creatorcontrib>Patouret, Rémi</creatorcontrib><creatorcontrib>Garcia-Ordonez, Ruben D.</creatorcontrib><creatorcontrib>Chang, Mi Ra</creatorcontrib><creatorcontrib>Dharmarajan, Venkatasubramanian</creatorcontrib><creatorcontrib>Kuruvilla, Dana S.</creatorcontrib><creatorcontrib>Novick, Scott J.</creatorcontrib><creatorcontrib>Lin, Li</creatorcontrib><creatorcontrib>Cameron, Michael D.</creatorcontrib><creatorcontrib>Griffin, Patrick R.</creatorcontrib><creatorcontrib>Kamenecka, Theodore M.</creatorcontrib><title>N-Arylsulfonyl Indolines as Retinoic Acid Receptor-Related Orphan Receptor γ (RORγ) Agonists</title><title>ChemMedChem</title><addtitle>ChemMedChem</addtitle><description>The nuclear retinoic acid receptor‐related orphan receptor γ (RORγ; NR1F3) is a key regulator of inflammatory gene programs involved in T helper 17 (TH17) cell proliferation. As such, synthetic small‐molecule repressors (inverse agonists) targeting RORγ have been extensively studied for their potential as therapeutic agents for various autoimmune diseases. Alternatively, enhancing TH17 cell proliferation through activation (agonism) of RORγ may boost an immune response, thereby offering a potentially new approach in cancer immunotherapy. Herein we describe the development of N‐arylsulfonyl indolines as RORγ agonists. Structure–activity studies reveal a critical linker region in these molecules as the major determinant for agonism. Hydrogen/deuterium exchange coupled to mass spectrometry (HDX‐MS) analysis of RORγ–ligand complexes help rationalize the observed results.
Pharmacology switches from inverse agonist to agonist: Immunotherapy is an exciting new approach in oncology. RORγ agonists have the potential to enhance immune responses through modulation of TH17 cell proliferation. Starting from an N‐arylsulfonamide indoline RORγ inverse agonist, we were able to identify the key area where small modifications lead to RORγ agonists. A binding mode hypothesis, supported by HDX‐MS analysis, is also proposed.</description><subject>Autoimmune diseases</subject><subject>Binding Sites</subject><subject>Cancer immunotherapy</subject><subject>Cell activation</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Chemical compounds</subject><subject>Coordination compounds</subject><subject>Deuterium</subject><subject>Drug Inverse Agonism</subject><subject>HEK293 Cells</subject><subject>Helper cells</subject><subject>Heterocyclic compounds</subject><subject>Humans</subject><subject>Hydrogen-deuterium exchange</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunotherapy</subject><subject>Indoles - chemical synthesis</subject><subject>Indoles - chemistry</subject><subject>Indoles - metabolism</subject><subject>Inflammation</subject><subject>Interleukin-17 - genetics</subject><subject>Interleukin-17 - metabolism</subject><subject>Inverse agonists</subject><subject>Lymphocytes T</subject><subject>Mass spectrometry</subject><subject>Mass spectroscopy</subject><subject>Molecular Docking Simulation</subject><subject>N-arylsulfonyl indolines</subject><subject>nuclear receptors</subject><subject>Pharmacology</subject><subject>Promoter Regions, Genetic</subject><subject>Protein Binding</subject><subject>Protein Structure, Tertiary</subject><subject>Receptors</subject><subject>Receptors, Retinoic Acid - agonists</subject><subject>Receptors, Retinoic Acid - metabolism</subject><subject>Repressors</subject><subject>Retinoic acid</subject><subject>Retinoic Acid Receptor gamma</subject><subject>RORγ agonists</subject><subject>Structure-Activity Relationship</subject><subject>Th17 Cells - cytology</subject><subject>Th17 Cells - immunology</subject><subject>Th17 Cells - metabolism</subject><issn>1860-7179</issn><issn>1860-7187</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM2O0zAURi0EoqXDliWKxKYs0rHdOHaWVZgpI3WmUjWjjtgYx3YgxY2LnQiyY8MT9T36EDwJrloixIaVf3S-T_ceAF4hOEEQ4ku5VXKCIUohTDL0BAwRS2FMEaNP-zvNBuCF95uAJAyx52CAKaMZJNMh-HgXz1xnfGtKW3cmuqmVNVWtfSR8tNJNVdtKRjNZqfCSetdYF6-0EY1W0dLtPou6___14-dhH41Xy9Vh_zaafbJ15Rt_AZ6Vwnj98nyOwMP11X3-Pl4s5zf5bBHLhCUoDoMJCUtMpS5wSmFGC8gEZixTYU-ltFRYJVIlSBdlSagqhES4EIwRRdKinI7A-NS7c_Zrq33Dt5WX2hhRa9t6jhghkKYE4oC--Qfd2NbVYTqOSQqDSkZZoCYnSjrrvdMl37lqK1zHEeRH9_zonvfuQ-D1ubYttlr1-B_ZAchOwLfK6O4_dTy_fZf_XR6fssGp_t5nhfvCUzqlhK_v5vxDvqB4vqb8cfobwl2hhQ</recordid><startdate>20161206</startdate><enddate>20161206</enddate><creator>Doebelin, Christelle</creator><creator>Patouret, Rémi</creator><creator>Garcia-Ordonez, Ruben D.</creator><creator>Chang, Mi Ra</creator><creator>Dharmarajan, Venkatasubramanian</creator><creator>Kuruvilla, Dana S.</creator><creator>Novick, Scott J.</creator><creator>Lin, Li</creator><creator>Cameron, Michael D.</creator><creator>Griffin, Patrick R.</creator><creator>Kamenecka, Theodore M.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20161206</creationdate><title>N-Arylsulfonyl Indolines as Retinoic Acid Receptor-Related Orphan Receptor γ (RORγ) Agonists</title><author>Doebelin, Christelle ; Patouret, Rémi ; Garcia-Ordonez, Ruben D. ; Chang, Mi Ra ; Dharmarajan, Venkatasubramanian ; Kuruvilla, Dana S. ; Novick, Scott J. ; Lin, Li ; Cameron, Michael D. ; Griffin, Patrick R. ; Kamenecka, Theodore M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4841-481ac0f27ceb267097b08a2889d100ddecd2d4cd41ebff57dbac12ba885d56bf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Autoimmune diseases</topic><topic>Binding Sites</topic><topic>Cancer immunotherapy</topic><topic>Cell activation</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Chemical compounds</topic><topic>Coordination compounds</topic><topic>Deuterium</topic><topic>Drug Inverse Agonism</topic><topic>HEK293 Cells</topic><topic>Helper cells</topic><topic>Heterocyclic compounds</topic><topic>Humans</topic><topic>Hydrogen-deuterium exchange</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunotherapy</topic><topic>Indoles - chemical synthesis</topic><topic>Indoles - chemistry</topic><topic>Indoles - metabolism</topic><topic>Inflammation</topic><topic>Interleukin-17 - genetics</topic><topic>Interleukin-17 - metabolism</topic><topic>Inverse agonists</topic><topic>Lymphocytes T</topic><topic>Mass spectrometry</topic><topic>Mass spectroscopy</topic><topic>Molecular Docking Simulation</topic><topic>N-arylsulfonyl indolines</topic><topic>nuclear receptors</topic><topic>Pharmacology</topic><topic>Promoter Regions, Genetic</topic><topic>Protein Binding</topic><topic>Protein Structure, Tertiary</topic><topic>Receptors</topic><topic>Receptors, Retinoic Acid - agonists</topic><topic>Receptors, Retinoic Acid - metabolism</topic><topic>Repressors</topic><topic>Retinoic acid</topic><topic>Retinoic Acid Receptor gamma</topic><topic>RORγ agonists</topic><topic>Structure-Activity Relationship</topic><topic>Th17 Cells - cytology</topic><topic>Th17 Cells - immunology</topic><topic>Th17 Cells - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Doebelin, Christelle</creatorcontrib><creatorcontrib>Patouret, Rémi</creatorcontrib><creatorcontrib>Garcia-Ordonez, Ruben D.</creatorcontrib><creatorcontrib>Chang, Mi Ra</creatorcontrib><creatorcontrib>Dharmarajan, Venkatasubramanian</creatorcontrib><creatorcontrib>Kuruvilla, Dana S.</creatorcontrib><creatorcontrib>Novick, Scott J.</creatorcontrib><creatorcontrib>Lin, Li</creatorcontrib><creatorcontrib>Cameron, Michael D.</creatorcontrib><creatorcontrib>Griffin, Patrick R.</creatorcontrib><creatorcontrib>Kamenecka, Theodore M.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>ChemMedChem</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Doebelin, Christelle</au><au>Patouret, Rémi</au><au>Garcia-Ordonez, Ruben D.</au><au>Chang, Mi Ra</au><au>Dharmarajan, Venkatasubramanian</au><au>Kuruvilla, Dana S.</au><au>Novick, Scott J.</au><au>Lin, Li</au><au>Cameron, Michael D.</au><au>Griffin, Patrick R.</au><au>Kamenecka, Theodore M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>N-Arylsulfonyl Indolines as Retinoic Acid Receptor-Related Orphan Receptor γ (RORγ) Agonists</atitle><jtitle>ChemMedChem</jtitle><addtitle>ChemMedChem</addtitle><date>2016-12-06</date><risdate>2016</risdate><volume>11</volume><issue>23</issue><spage>2607</spage><epage>2620</epage><pages>2607-2620</pages><issn>1860-7179</issn><eissn>1860-7187</eissn><abstract>The nuclear retinoic acid receptor‐related orphan receptor γ (RORγ; NR1F3) is a key regulator of inflammatory gene programs involved in T helper 17 (TH17) cell proliferation. As such, synthetic small‐molecule repressors (inverse agonists) targeting RORγ have been extensively studied for their potential as therapeutic agents for various autoimmune diseases. Alternatively, enhancing TH17 cell proliferation through activation (agonism) of RORγ may boost an immune response, thereby offering a potentially new approach in cancer immunotherapy. Herein we describe the development of N‐arylsulfonyl indolines as RORγ agonists. Structure–activity studies reveal a critical linker region in these molecules as the major determinant for agonism. Hydrogen/deuterium exchange coupled to mass spectrometry (HDX‐MS) analysis of RORγ–ligand complexes help rationalize the observed results.
Pharmacology switches from inverse agonist to agonist: Immunotherapy is an exciting new approach in oncology. RORγ agonists have the potential to enhance immune responses through modulation of TH17 cell proliferation. Starting from an N‐arylsulfonamide indoline RORγ inverse agonist, we were able to identify the key area where small modifications lead to RORγ agonists. A binding mode hypothesis, supported by HDX‐MS analysis, is also proposed.</abstract><cop>Germany</cop><pub>Blackwell Publishing Ltd</pub><pmid>27879053</pmid><doi>10.1002/cmdc.201600491</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Autoimmune diseases Binding Sites Cancer immunotherapy Cell activation Cell growth Cell proliferation Chemical compounds Coordination compounds Deuterium Drug Inverse Agonism HEK293 Cells Helper cells Heterocyclic compounds Humans Hydrogen-deuterium exchange Immune response Immune system Immunotherapy Indoles - chemical synthesis Indoles - chemistry Indoles - metabolism Inflammation Interleukin-17 - genetics Interleukin-17 - metabolism Inverse agonists Lymphocytes T Mass spectrometry Mass spectroscopy Molecular Docking Simulation N-arylsulfonyl indolines nuclear receptors Pharmacology Promoter Regions, Genetic Protein Binding Protein Structure, Tertiary Receptors Receptors, Retinoic Acid - agonists Receptors, Retinoic Acid - metabolism Repressors Retinoic acid Retinoic Acid Receptor gamma RORγ agonists Structure-Activity Relationship Th17 Cells - cytology Th17 Cells - immunology Th17 Cells - metabolism |
| title | N-Arylsulfonyl Indolines as Retinoic Acid Receptor-Related Orphan Receptor γ (RORγ) Agonists |
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