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Antithrombotic Effects of Fostamatinib in Combination with Conventional Antiplatelet Drugs
New antithrombotic medications with less effect on haemostasis are needed for the long-term treatment of acute coronary syndromes (ACS). The platelet receptor glycoprotein VI (GPVI) is critical in atherothrombosis, mediating platelet activation at atherosclerotic plaque. The inhibition of spleen tyr...
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Published in: | International journal of molecular sciences 2022-06, Vol.23 (13), p.6982 |
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description | New antithrombotic medications with less effect on haemostasis are needed for the long-term treatment of acute coronary syndromes (ACS). The platelet receptor glycoprotein VI (GPVI) is critical in atherothrombosis, mediating platelet activation at atherosclerotic plaque. The inhibition of spleen tyrosine kinase (Syk) has been shown to block GPVI-mediated platelet function. The aim of our study was to investigate if the Syk inhibitor fostamatinib could be repurposed as an antiplatelet drug, either alone or in combination with conventional antiplatelet therapy. The effect of the active metabolite of fostamatinib (R406) was assessed on platelet activation and function induced by atherosclerotic plaque and a range of agonists in the presence and absence of the commonly used antiplatelet agents aspirin and ticagrelor. The effects were determined ex vivo using blood from healthy volunteers and aspirin- and ticagrelor-treated patients with ACS. Fostamatinib was also assessed in murine models of thrombosis. R406 mildly inhibited platelet responses induced by atherosclerotic plaque homogenate, likely due to GPVI inhibition. The anti-GPVI effects of R406 were amplified by the commonly-used antiplatelet medications aspirin and ticagrelor; however, the effects of R406 were concentration-dependent and diminished in the presence of plasma proteins, which may explain why fostamatinib did not significantly inhibit thrombosis in murine models. For the first time, we demonstrate that the Syk inhibitor R406 provides mild inhibition of platelet responses induced by atherosclerotic plaque and that this is mildly amplified by aspirin and ticagrelor. |
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The platelet receptor glycoprotein VI (GPVI) is critical in atherothrombosis, mediating platelet activation at atherosclerotic plaque. The inhibition of spleen tyrosine kinase (Syk) has been shown to block GPVI-mediated platelet function. The aim of our study was to investigate if the Syk inhibitor fostamatinib could be repurposed as an antiplatelet drug, either alone or in combination with conventional antiplatelet therapy. The effect of the active metabolite of fostamatinib (R406) was assessed on platelet activation and function induced by atherosclerotic plaque and a range of agonists in the presence and absence of the commonly used antiplatelet agents aspirin and ticagrelor. The effects were determined ex vivo using blood from healthy volunteers and aspirin- and ticagrelor-treated patients with ACS. Fostamatinib was also assessed in murine models of thrombosis. R406 mildly inhibited platelet responses induced by atherosclerotic plaque homogenate, likely due to GPVI inhibition. The anti-GPVI effects of R406 were amplified by the commonly-used antiplatelet medications aspirin and ticagrelor; however, the effects of R406 were concentration-dependent and diminished in the presence of plasma proteins, which may explain why fostamatinib did not significantly inhibit thrombosis in murine models. For the first time, we demonstrate that the Syk inhibitor R406 provides mild inhibition of platelet responses induced by atherosclerotic plaque and that this is mildly amplified by aspirin and ticagrelor.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms23136982</identifier><identifier>PMID: 35805988</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acute coronary syndromes ; Aminopyridines ; Animal models ; Animals ; antiplatelet therapy ; antithrombotic therapy ; Arteriosclerosis ; Aspirin ; Atherosclerosis ; Blood clots ; Blood platelets ; Collagen ; Fibrinolytic Agents - pharmacology ; Fibrinolytic Agents - therapeutic use ; fostamatinib ; Glycoprotein VI ; Humans ; Metabolites ; Mice ; Morpholines ; Oxazines - pharmacology ; Phosphorylation ; Plaque, Atherosclerotic ; Plasma proteins ; Platelet Aggregation Inhibitors - pharmacology ; Platelet Aggregation Inhibitors - therapeutic use ; Protein-tyrosine kinase ; Pyridines - pharmacology ; Pyrimidines ; R406 ; Spleen ; Syk ; Syk protein ; Thrombosis ; Thrombosis - drug therapy ; Ticagrelor - pharmacology ; Tyrosine ; tyrosine kinase</subject><ispartof>International journal of molecular sciences, 2022-06, Vol.23 (13), p.6982</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-426be9be3ade75f7e6d95443a958acc1969dd203a36730e23cef4cbb4e0164973</citedby><cites>FETCH-LOGICAL-c478t-426be9be3ade75f7e6d95443a958acc1969dd203a36730e23cef4cbb4e0164973</cites><orcidid>0000-0002-2860-5509 ; 0000-0002-4843-2975 ; 0000-0002-8892-5192</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2686103037?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2686103037?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,38516,43895,44590,53791,53793,74412,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35805988$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Harbi, Maan H</creatorcontrib><creatorcontrib>Smith, Christopher W</creatorcontrib><creatorcontrib>Alenazy, Fawaz O</creatorcontrib><creatorcontrib>Nicolson, Phillip L R</creatorcontrib><creatorcontrib>Tiwari, Alok</creatorcontrib><creatorcontrib>Watson, Steve P</creatorcontrib><creatorcontrib>Thomas, Mark R</creatorcontrib><title>Antithrombotic Effects of Fostamatinib in Combination with Conventional Antiplatelet Drugs</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>New antithrombotic medications with less effect on haemostasis are needed for the long-term treatment of acute coronary syndromes (ACS). The platelet receptor glycoprotein VI (GPVI) is critical in atherothrombosis, mediating platelet activation at atherosclerotic plaque. The inhibition of spleen tyrosine kinase (Syk) has been shown to block GPVI-mediated platelet function. The aim of our study was to investigate if the Syk inhibitor fostamatinib could be repurposed as an antiplatelet drug, either alone or in combination with conventional antiplatelet therapy. The effect of the active metabolite of fostamatinib (R406) was assessed on platelet activation and function induced by atherosclerotic plaque and a range of agonists in the presence and absence of the commonly used antiplatelet agents aspirin and ticagrelor. The effects were determined ex vivo using blood from healthy volunteers and aspirin- and ticagrelor-treated patients with ACS. Fostamatinib was also assessed in murine models of thrombosis. R406 mildly inhibited platelet responses induced by atherosclerotic plaque homogenate, likely due to GPVI inhibition. The anti-GPVI effects of R406 were amplified by the commonly-used antiplatelet medications aspirin and ticagrelor; however, the effects of R406 were concentration-dependent and diminished in the presence of plasma proteins, which may explain why fostamatinib did not significantly inhibit thrombosis in murine models. For the first time, we demonstrate that the Syk inhibitor R406 provides mild inhibition of platelet responses induced by atherosclerotic plaque and that this is mildly amplified by aspirin and ticagrelor.</description><subject>Acute coronary syndromes</subject><subject>Aminopyridines</subject><subject>Animal models</subject><subject>Animals</subject><subject>antiplatelet therapy</subject><subject>antithrombotic therapy</subject><subject>Arteriosclerosis</subject><subject>Aspirin</subject><subject>Atherosclerosis</subject><subject>Blood clots</subject><subject>Blood platelets</subject><subject>Collagen</subject><subject>Fibrinolytic Agents - pharmacology</subject><subject>Fibrinolytic Agents - therapeutic use</subject><subject>fostamatinib</subject><subject>Glycoprotein VI</subject><subject>Humans</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Morpholines</subject><subject>Oxazines - pharmacology</subject><subject>Phosphorylation</subject><subject>Plaque, Atherosclerotic</subject><subject>Plasma proteins</subject><subject>Platelet Aggregation Inhibitors - pharmacology</subject><subject>Platelet Aggregation Inhibitors - therapeutic use</subject><subject>Protein-tyrosine kinase</subject><subject>Pyridines - pharmacology</subject><subject>Pyrimidines</subject><subject>R406</subject><subject>Spleen</subject><subject>Syk</subject><subject>Syk protein</subject><subject>Thrombosis</subject><subject>Thrombosis - drug therapy</subject><subject>Ticagrelor - pharmacology</subject><subject>Tyrosine</subject><subject>tyrosine kinase</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>COVID</sourceid><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkktv1DAQgC0EomXhxhlF4sKhC37FjwtStW2hUiUucOFi2c5k61USL7ZTxL_H6ZZqy8me8edPM_Yg9Jbgj4xp_CnsxkwZYUIr-gydEk7pGmMhnx_tT9CrnHcYU0Zb_RKdsFbhVit1in6eTyWU2xRHF0vwzWXfgy-5iX1zFXOxoy1hCq4JU7OpTJhqHKfmd71TE9MdTEtsh2bx7AdbYIDSXKR5m1-jF70dMrx5WFfox9Xl983X9c23L9eb85u151KVNafCgXbAbAey7SWITrecM6tbZb0nWuiuo5hZJiTDQJmHnnvnOGAiuJZsha4P3i7andmnMNr0x0QbzH0ipq2xqfY2gOHEEc-wcNwTDoyqXvaEWiWwU7ptu-r6fHDtZzdC52t7yQ5PpE9PpnBrtvHOaCrEUuAKfXgQpPhrhlzMGLKHYbATxDkbKpSUlEutKvr-P3QX51Tf8p4SBDPMFuHZgfIp5pygfyyGYLMMgDkegIq_O27gEf734-wvLBOtIg</recordid><startdate>20220623</startdate><enddate>20220623</enddate><creator>Harbi, Maan H</creator><creator>Smith, Christopher W</creator><creator>Alenazy, Fawaz O</creator><creator>Nicolson, Phillip L R</creator><creator>Tiwari, Alok</creator><creator>Watson, Steve P</creator><creator>Thomas, Mark R</creator><general>MDPI AG</general><general>MDPI</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>COVID</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-2860-5509</orcidid><orcidid>https://orcid.org/0000-0002-4843-2975</orcidid><orcidid>https://orcid.org/0000-0002-8892-5192</orcidid></search><sort><creationdate>20220623</creationdate><title>Antithrombotic Effects of Fostamatinib in Combination with Conventional Antiplatelet Drugs</title><author>Harbi, Maan H ; Smith, Christopher W ; Alenazy, Fawaz O ; Nicolson, Phillip L R ; Tiwari, Alok ; Watson, Steve P ; Thomas, Mark R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-426be9be3ade75f7e6d95443a958acc1969dd203a36730e23cef4cbb4e0164973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Acute coronary syndromes</topic><topic>Aminopyridines</topic><topic>Animal models</topic><topic>Animals</topic><topic>antiplatelet therapy</topic><topic>antithrombotic therapy</topic><topic>Arteriosclerosis</topic><topic>Aspirin</topic><topic>Atherosclerosis</topic><topic>Blood clots</topic><topic>Blood platelets</topic><topic>Collagen</topic><topic>Fibrinolytic Agents - pharmacology</topic><topic>Fibrinolytic Agents - therapeutic use</topic><topic>fostamatinib</topic><topic>Glycoprotein VI</topic><topic>Humans</topic><topic>Metabolites</topic><topic>Mice</topic><topic>Morpholines</topic><topic>Oxazines - pharmacology</topic><topic>Phosphorylation</topic><topic>Plaque, Atherosclerotic</topic><topic>Plasma proteins</topic><topic>Platelet Aggregation Inhibitors - pharmacology</topic><topic>Platelet Aggregation Inhibitors - therapeutic use</topic><topic>Protein-tyrosine kinase</topic><topic>Pyridines - pharmacology</topic><topic>Pyrimidines</topic><topic>R406</topic><topic>Spleen</topic><topic>Syk</topic><topic>Syk protein</topic><topic>Thrombosis</topic><topic>Thrombosis - drug therapy</topic><topic>Ticagrelor - pharmacology</topic><topic>Tyrosine</topic><topic>tyrosine kinase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Harbi, Maan H</creatorcontrib><creatorcontrib>Smith, Christopher W</creatorcontrib><creatorcontrib>Alenazy, Fawaz O</creatorcontrib><creatorcontrib>Nicolson, Phillip L R</creatorcontrib><creatorcontrib>Tiwari, Alok</creatorcontrib><creatorcontrib>Watson, Steve P</creatorcontrib><creatorcontrib>Thomas, Mark R</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Harbi, Maan H</au><au>Smith, Christopher W</au><au>Alenazy, Fawaz O</au><au>Nicolson, Phillip L R</au><au>Tiwari, Alok</au><au>Watson, Steve P</au><au>Thomas, Mark R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antithrombotic Effects of Fostamatinib in Combination with Conventional Antiplatelet Drugs</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2022-06-23</date><risdate>2022</risdate><volume>23</volume><issue>13</issue><spage>6982</spage><pages>6982-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>New antithrombotic medications with less effect on haemostasis are needed for the long-term treatment of acute coronary syndromes (ACS). The platelet receptor glycoprotein VI (GPVI) is critical in atherothrombosis, mediating platelet activation at atherosclerotic plaque. The inhibition of spleen tyrosine kinase (Syk) has been shown to block GPVI-mediated platelet function. The aim of our study was to investigate if the Syk inhibitor fostamatinib could be repurposed as an antiplatelet drug, either alone or in combination with conventional antiplatelet therapy. The effect of the active metabolite of fostamatinib (R406) was assessed on platelet activation and function induced by atherosclerotic plaque and a range of agonists in the presence and absence of the commonly used antiplatelet agents aspirin and ticagrelor. The effects were determined ex vivo using blood from healthy volunteers and aspirin- and ticagrelor-treated patients with ACS. Fostamatinib was also assessed in murine models of thrombosis. R406 mildly inhibited platelet responses induced by atherosclerotic plaque homogenate, likely due to GPVI inhibition. The anti-GPVI effects of R406 were amplified by the commonly-used antiplatelet medications aspirin and ticagrelor; however, the effects of R406 were concentration-dependent and diminished in the presence of plasma proteins, which may explain why fostamatinib did not significantly inhibit thrombosis in murine models. For the first time, we demonstrate that the Syk inhibitor R406 provides mild inhibition of platelet responses induced by atherosclerotic plaque and that this is mildly amplified by aspirin and ticagrelor.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>35805988</pmid><doi>10.3390/ijms23136982</doi><orcidid>https://orcid.org/0000-0002-2860-5509</orcidid><orcidid>https://orcid.org/0000-0002-4843-2975</orcidid><orcidid>https://orcid.org/0000-0002-8892-5192</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Acute coronary syndromes Aminopyridines Animal models Animals antiplatelet therapy antithrombotic therapy Arteriosclerosis Aspirin Atherosclerosis Blood clots Blood platelets Collagen Fibrinolytic Agents - pharmacology Fibrinolytic Agents - therapeutic use fostamatinib Glycoprotein VI Humans Metabolites Mice Morpholines Oxazines - pharmacology Phosphorylation Plaque, Atherosclerotic Plasma proteins Platelet Aggregation Inhibitors - pharmacology Platelet Aggregation Inhibitors - therapeutic use Protein-tyrosine kinase Pyridines - pharmacology Pyrimidines R406 Spleen Syk Syk protein Thrombosis Thrombosis - drug therapy Ticagrelor - pharmacology Tyrosine tyrosine kinase |
title | Antithrombotic Effects of Fostamatinib in Combination with Conventional Antiplatelet Drugs |
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