<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Virtakoivu R</submitter><funding>European Union&amp;apos;s Horizon 2020 research and innovation program</funding><funding>Cancer Research UK</funding><funding>Cancer Foundation Finland sr</funding><pagination>4205-4220</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9401456</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>27(15)</volume><pubmed_abstract>&lt;h4>Purpose&lt;/h4>Macrophages are critical in driving an immunosuppressive tumor microenvironment that counteracts the efficacy of T-cell-targeting therapies. Thus, agents able to reprogram macrophages toward a proinflammatory state hold promise as novel immunotherapies for solid cancers. Inhibition of the macrophage scavenger receptor Clever-1 has shown benefit in inducing CD8&lt;sup>+&lt;/sup> T-cell-mediated antitumor responses in mouse models of cancer, which supports the clinical development of Clever-1-targeting antibodies for cancer treatment.&lt;h4>Patients and methods&lt;/h4>In this study, we analyzed the mode of action of a humanized IgG4 anti-Clever-1 antibody, FP-1305 (bexmarilimab), both &lt;i>in vitro&lt;/i> and in patients with heavily pretreated metastatic cancer (&lt;i>n&lt;/i> = 30) participating </pubmed_abstract><journal>Clinical cancer research : an official journal of the American Association for Cancer Research</journal><pubmed_title>Systemic Blockade of Clever-1 Elicits Lymphocyte Activation Alongside Checkpoint Molecule Downregulation in Patients with Solid Tumors: Results from a Phase I/II Clinical Trial.</pubmed_title><pmcid>PMC9401456</pmcid><funding_grant_id>200086</funding_grant_id><funding_grant_id>C53575/A29959</funding_grant_id><funding_grant_id>200096</funding_grant_id><funding_grant_id>960914</funding_grant_id><funding_grant_id>200081</funding_grant_id><funding_grant_id>29959</funding_grant_id><pubmed_authors>Shetty S</pubmed_authors><pubmed_authors>Robbrecht D</pubmed_authors><pubmed_authors>Hollmen M</pubmed_authors><pubmed_authors>Viitala M</pubmed_authors><pubmed_authors>Lonnberg T</pubmed_authors><pubmed_authors>de Jonge MJA</pubmed_authors><pubmed_authors>Virtakoivu R</pubmed_authors><pubmed_authors>Minchom A</pubmed_authors><pubmed_authors>Ma YT</pubmed_authors><pubmed_authors>Rannikko JH</pubmed_authors><pubmed_authors>Jaakkola P</pubmed_authors><pubmed_authors>Bono P</pubmed_authors><pubmed_authors>Koivunen J</pubmed_authors><pubmed_authors>Mandelin J</pubmed_authors><pubmed_authors>Takeda A</pubmed_authors><pubmed_authors>Jalkanen S</pubmed_authors><pubmed_authors>Skytta T</pubmed_authors><pubmed_authors>Vaura F</pubmed_authors><pubmed_authors>Pasanen A</pubmed_authors><pubmed_authors>Karvonen MK</pubmed_authors></additional><is_claimable>false</is_claimable><name>Systemic Blockade of Clever-1 Elicits Lymphocyte Activation Alongside Checkpoint Molecule Downregulation in Patients with Solid Tumors: Results from a Phase I/II Clinical Trial.</name><description>&lt;h4>Purpose&lt;/h4>Macrophages are critical in driving an immunosuppressive tumor microenvironment that counteracts the efficacy of T-cell-targeting therapies. Thus, agents able to reprogram macrophages toward a proinflammatory state hold promise as novel immunotherapies for solid cancers. Inhibition of the macrophage scavenger receptor Clever-1 has shown benefit in inducing CD8&lt;sup>+&lt;/sup> T-cell-mediated antitumor responses in mouse models of cancer, which supports the clinical development of Clever-1-targeting antibodies for cancer treatment.&lt;h4>Patients and methods&lt;/h4>In this study, we analyzed the mode of action of a humanized IgG4 anti-Clever-1 antibody, FP-1305 (bexmarilimab), both &lt;i>in vitro&lt;/i> and in patients with heavily pretreated metastatic cancer (&lt;i>n&lt;/i> = 30) participating </description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Aug</publication><modification>2026-05-10T06:44:19.657Z</modification><creation>2025-04-04T13:08:55.812Z</creation></dates><accession>S-EPMC9401456</accession><cross_references><pubmed>34078651</pubmed><doi>10.1158/1078-0432.CCR-20-4862</doi></cross_references></HashMap>