{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T11:25:38Z","timestamp":1788175538962,"version":"build-2803163510"},"reference-count":20,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T00:00:00Z","timestamp":1745452800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Navrogen Inc"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,6,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The monoclonal antibody rituximab functions through complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) and is used to treat non-Hodgkin\u2019s lymphoma. Elevated serum CA125\/MUC16 levels, present in some follicular lymphoma patients, have been shown to correlate with reduced efficacy of rituximab. Previous studies revealed that CA125\/MUC16 binds to rituximab, diminishing its CDC and ADCC. A rituximab variant, NAV-006, was engineered to counteract CA125\/MUC16\u2019s immunosuppressive effects. NAV-006 demonstrated enhanced CDC and ADCC activities and was unaffected by CA125\/MUC16. In the present study, NAV-006 showed improved in vivo antitumor activity compared to rituximab in a human lymphoma model with reconstituted CA125\/MUC16. Additionally, CA125\/MUC16 bound to newer antibody-based lymphoma treatment agents, including obinutuzumab and tafasitamab, suppressing their immune effector functions. Bispecific antibodies mosunetuzumab and glofitamab also exhibited reduced cytotoxicity in the presence of CA125\/MUC16. These findings suggest that NAV-006 could improve therapeutic efficacy in B-cell lymphomas, particularly in patients with elevated CA125\/MUC16 levels.<\/jats:p>","DOI":"10.1093\/abt\/tbaf008","type":"journal-article","created":{"date-parts":[[2025,4,18]],"date-time":"2025-04-18T07:36:08Z","timestamp":1744961768000},"page":"171-176","source":"Crossref","is-referenced-by-count":1,"title":["Bypassing the immunosuppressive effects of CA125\/MUC16 via re-engineered rituximab (NAV-006) to improve its antitumor activity\n                    <i>in vivo<\/i>"],"prefix":"10.1093","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6559-2914","authenticated-orcid":false,"given":"Luigi","family":"Grasso","sequence":"first","affiliation":[{"name":"R&D Department, Navrogen Inc. , Cheyney, PA 19319 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bradford J","family":"Kline","sequence":"additional","affiliation":[{"name":"R&D Department, Navrogen Inc. , Cheyney, PA 19319 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas C","family":"Nicolaides","sequence":"additional","affiliation":[{"name":"R&D Department, Navrogen Inc. , Cheyney, PA 19319 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2025,4,24]]},"reference":[{"key":"2026050905022174900_ref1","volume-title":"Surveillance, Epidemiology, and End Results (SEER) Program","author":"National Cancer Institute, Bethesda MD","year":"2021"},{"key":"2026050905022174900_ref2","doi-asserted-by":"publisher","first-page":"949","DOI":"10.1182\/blood-2002-02-0469","article-title":"In vitro mechanisms of action of rituximab on primary non-Hodgkin 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