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• W2109697114 abstract "Clinical Practice Points •Brentuximab vedotin (b-vedotin), a CD30-directed antibody-drug conjugate, has shown activity in treating CD30-positive (CD30+) neoplasms (classical Hodgkin lymphoma [CHL] and systemic anaplastic large cell lymphoma [ALCL]); however, its in vivo saturation, internalization kinetics, and pathologic findings are unknown. •We quantified antigen density on CD30+ cell lines cultured with b-vedotin and demonstrated the greatest expression of CD30 and bound b-vedotin at 24 to 48 hours, reaching a nadir by 120 hours. Similarly, serial tumor biopsies from a patient with relapsed ALCL revealed maximal CD30 expression (1.01x105 molecules/cell) at baseline. After treatment, CD30 (7.83x104 molecules/cell at 24 hours; 5.08x104 molecules/cell at 48 hours) and bound b-vedotin (2.26x103 molecules/cell at 24 hours and 1.40x103 molecules/cell at 48 hours) antigen density rapidly declined, consistent with internalization. Histologic evaluation showed a dense infiltrate of neoplastic CD30+ cells before treatment, apoptosis at 48 hours, and no neoplastic cells at day 21. •These results demonstrate the potent and rapid anti-tumor properties and support the mechanism of action of b-vedotin. Additionally, as relatively few b-vedotin molecules are required for clinical efficacy, these results suggest that this drug should be evaluated in neoplasms with relatively low expression of CD30. •Brentuximab vedotin (b-vedotin), a CD30-directed antibody-drug conjugate, has shown activity in treating CD30-positive (CD30+) neoplasms (classical Hodgkin lymphoma [CHL] and systemic anaplastic large cell lymphoma [ALCL]); however, its in vivo saturation, internalization kinetics, and pathologic findings are unknown. •We quantified antigen density on CD30+ cell lines cultured with b-vedotin and demonstrated the greatest expression of CD30 and bound b-vedotin at 24 to 48 hours, reaching a nadir by 120 hours. Similarly, serial tumor biopsies from a patient with relapsed ALCL revealed maximal CD30 expression (1.01x105 molecules/cell) at baseline. After treatment, CD30 (7.83x104 molecules/cell at 24 hours; 5.08x104 molecules/cell at 48 hours) and bound b-vedotin (2.26x103 molecules/cell at 24 hours and 1.40x103 molecules/cell at 48 hours) antigen density rapidly declined, consistent with internalization. Histologic evaluation showed a dense infiltrate of neoplastic CD30+ cells before treatment, apoptosis at 48 hours, and no neoplastic cells at day 21. •These results demonstrate the potent and rapid anti-tumor properties and support the mechanism of action of b-vedotin. Additionally, as relatively few b-vedotin molecules are required for clinical efficacy, these results suggest that this drug should be evaluated in neoplasms with relatively low expression of CD30." @default.
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• W2109697114 date "2012-08-01" @default.
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• W2109697114 title "Clinical Binding Properties, Internalization Kinetics, and Clinicopathologic Activity of Brentuximab Vedotin: An Antibody-Drug Conjugate for CD30-Positive Lymphoid Neoplasms" @default.
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• W2109697114 doi "https://doi.org/10.1016/j.clml.2012.01.012" @default.
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