{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T17:11:49Z","timestamp":1786122709905,"version":"build-2736575974"},"reference-count":40,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T00:00:00Z","timestamp":1785888000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Oncol Pharm Pract"],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Glioblastoma (GBM) is an aggressive primary brain tumor with a dismal prognosis. Alterations in the Epidermal Growth Factor Receptor (EGFR) in about half of the cases, represent a key therapeutic target. Depatuxizumab mafodotin (Depatux-M) is an antibody-drug conjugate (ADC) developed to deliver a cytotoxic payload specifically to EGFR-amplified tumor cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>This systematic review aims to synthesize all available clinical evidence to evaluate the antitumor efficacy, safety profile, pharmacokinetics, and biomarker-based stratification for Depatux-M in the treatment of glioblastoma.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A systematic literature search was conducted across PubMed, Scopus, Cochrane Library and Web of Science. After screening, 11 clinical studies involving a total of 1420 patients were included for analysis. Data on efficacy, safety, biomarkers, and pharmacokinetics were extracted and synthesized.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>The review found that Depatux-M demonstrated modest antitumor activity, with objective responses and improved progression-free survival primarily observed in the molecular subgroup of patients with tumors harboring EGFR amplification and\/or the EGFRvIII mutation. Pharmacokinetic data showed linear, predictable exposure with low potential for drug-drug interactions, notably with temozolomide (TMZ). Ocular toxicities were the most common adverse events, occurring in over 90% of patients; these were often reversible and manageable. The overall safety profile was considered acceptable.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Depatuxizumab mafodotin presents a targeted treatment option with a manageable safety profile for a molecularly defined subset of glioblastoma patients. Its clinical benefit remains limited, underscoring the disease's heterogeneity and therapeutic resistance. The findings support the continued investigation of biomarker-guided ADC therapy and highlight the critical need for future clinical trials to integrate comprehensive molecular profiling for optimal patient selection.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/10781552261470027","type":"journal-article","created":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T15:05:51Z","timestamp":1785942351000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Depatuxizumab mafodotin in glioblastoma: A systematic review of efficacy, safety, pharmacokinetics and biomarker stratification"],"prefix":"10.1177","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-0379-0249","authenticated-orcid":false,"given":"Hasan","family":"Matar","sequence":"first","affiliation":[{"name":"Jordan University of Science and Technology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bassel","family":"Alrabadi","sequence":"additional","affiliation":[{"name":"Jordan University of Science and Technology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aseel","family":"Abu Ata","sequence":"additional","affiliation":[{"name":"The University of Jordan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zainab","family":"Bahdar","sequence":"additional","affiliation":[{"name":"Al-Yarmouk University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Zagiczek","sequence":"additional","affiliation":[{"name":"Pomeranian Medical University"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2026,8,5]]},"reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/neuonc\/nou223"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1470-2045(09)70025-7"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.critrevonc.2016.01.018"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1215\/15228517-2007-062"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2013.09.034"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1111\/febs.12393"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-07-1966"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.3389\/fonc.2015.00005"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1093\/neuonc\/nov013"},{"key":"e_1_3_2_11_2","article-title":"Network meta-analysis of erlotinib, gefitinib, Afatinib and icotinib in patients with advanced non-small-cell lung cancer harboring EGFR mutations","volume":"9","author":"Liang W","year":"2014","unstructured":"Liang W, Wu X, Fang W, et al. 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