<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7(1)</volume><submitter>Schafer PH</submitter><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Spebrutinib (CC-292) is an orally administered, covalent, small-molecule inhibitor of Bruton's tyrosine kinase (BTK), part of the B-cell and Fc receptor signaling pathways. This study evaluated spebrutinib pharmacology and mechanism of action over a 4-week treatment period in patients with active rheumatoid arthritis (RA).&lt;h4>Methods&lt;/h4>Primary human B cells, T cells, natural killer cells, macrophages, dendritic cells, basophils, and osteoclasts were treated with spebrutinib in vitro. Clinical pharmacodynamics were studied in 47 patients with active RA on background methotrexate therapy randomized to oral spebrutinib 375 mg/day or placebo.&lt;h4>Results&lt;/h4>In vitro, spebrutinib inhibited B-cell proliferation more potently than T-cell proliferation and reduced both lymph</pubmed_abstract><journal>Rheumatology and therapy</journal><pagination>101-119</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7021855</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Spebrutinib (CC-292) Affects Markers of B Cell Activation, Chemotaxis, and Osteoclasts in Patients with Rheumatoid Arthritis: Results from a Mechanistic Study.</pubmed_title><pmcid>PMC7021855</pmcid><pubmed_authors>Schafer PH</pubmed_authors><pubmed_authors>Hur EM</pubmed_authors><pubmed_authors>Li L</pubmed_authors><pubmed_authors>Ringheim GE</pubmed_authors><pubmed_authors>Korish S</pubmed_authors><pubmed_authors>Adams M</pubmed_authors><pubmed_authors>Hough DR</pubmed_authors><pubmed_authors>Azaryan A</pubmed_authors><pubmed_authors>Sutherland D</pubmed_authors><pubmed_authors>Capone L</pubmed_authors><pubmed_authors>Ma J</pubmed_authors><pubmed_authors>Kivitz AJ</pubmed_authors><pubmed_authors>Kosek J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Spebrutinib (CC-292) Affects Markers of B Cell Activation, Chemotaxis, and Osteoclasts in Patients with Rheumatoid Arthritis: Results from a Mechanistic Study.</name><description>&lt;h4>Introduction&lt;/h4>Spebrutinib (CC-292) is an orally administered, covalent, small-molecule inhibitor of Bruton's tyrosine kinase (BTK), part of the B-cell and Fc receptor signaling pathways. This study evaluated spebrutinib pharmacology and mechanism of action over a 4-week treatment period in patients with active rheumatoid arthritis (RA).&lt;h4>Methods&lt;/h4>Primary human B cells, T cells, natural killer cells, macrophages, dendritic cells, basophils, and osteoclasts were treated with spebrutinib in vitro. Clinical pharmacodynamics were studied in 47 patients with active RA on background methotrexate therapy randomized to oral spebrutinib 375 mg/day or placebo.&lt;h4>Results&lt;/h4>In vitro, spebrutinib inhibited B-cell proliferation more potently than T-cell proliferation and reduced both lymph</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Mar</publication><modification>2026-05-08T06:18:57.725Z</modification><creation>2026-04-07T23:39:30.473Z</creation></dates><accession>S-EPMC7021855</accession><cross_references><pubmed>31721017</pubmed><doi>10.1007/s40744-019-00182-7</doi></cross_references></HashMap>