{"meta":{"totalResults":1,"from":0},"results":[{"aliases":[{"type":"Synonym","name":"anti-CD30 antibody-drug conjugate SGN-35"},{"type":"Synonym","name":"anti-CD30 ADC SGN-35"},{"type":"Synonym","name":"antibody-drug conjugate SGN-35"},{"type":"CodeName","name":"SGN-35"},{"type":"USBrandName","name":"Adcetris"},{"type":"Abbreviation","name":"cAC10-vcMMAE"},{"type":"CASRegistryName","name":"914088-09-8"},{"type":"CodeName","name":"ADC SGN-35"},{"type":"Synonym","name":"anti-CD30 monoclonal antibody-MMAE SGN-35"},{"type":"Synonym","name":"anti-CD30 monoclonal antibody-monomethylauristatin E SGN-35"}],"definition":{"html":"An antibody-drug conjugate (ADC) directed against the tumor necrosis factor (TNF) receptor CD30 with potential antineoplastic activity. Brentuximab vedotin is generated by conjugating the chimeric anti-CD30 monoclonal antibody SGN-30 to the cytotoxic agent monomethyl auristatin E (MMAE) via a valine-citrulline peptide linker. Upon administration and internalization by CD30-positive tumor cells, brentuximab vedotin undergoes enzymatic cleavage, releasing MMAE into the cytosol; MMAE binds to tubulin and inhibits tubulin polymerization, which may result in G2/M phase arrest and tumor cell apoptosis. Transiently activated during lymphocyte activation, CD30 (tumor necrosis factor receptor superfamily, member 8;TNFRSF8) may be constitutively expressed in hematologic malignancies including Hodgkin lymphoma and some T-cell non-Hodgkin lymphomas. The linkage system in brentuximab vedotin is highly stable in plasma, resulting in cytotoxic specificity for CD30-positive cells.","text":"An antibody-drug conjugate (ADC) directed against the tumor necrosis factor (TNF) receptor CD30 with potential antineoplastic activity. Brentuximab vedotin is generated by conjugating the chimeric anti-CD30 monoclonal antibody SGN-30 to the cytotoxic agent monomethyl auristatin E (MMAE) via a valine-citrulline peptide linker. Upon administration and internalization by CD30-positive tumor cells, brentuximab vedotin undergoes enzymatic cleavage, releasing MMAE into the cytosol; MMAE binds to tubulin and inhibits tubulin polymerization, which may result in G2/M phase arrest and tumor cell apoptosis. Transiently activated during lymphocyte activation, CD30 (tumor necrosis factor receptor superfamily, member 8;TNFRSF8) may be constitutively expressed in hematologic malignancies including Hodgkin lymphoma and some T-cell non-Hodgkin lymphomas. The linkage system in brentuximab vedotin is highly stable in plasma, resulting in cytotoxic specificity for CD30-positive cells."},"drugInfoSummaryLink":{"uri":"https://www.cancer.gov/about-cancer/treatment/drugs/brentuximabvedotin","text":"Brentuximab Vedotin"},"nciConceptId":"C66944","nciConceptName":"Brentuximab Vedotin","termId":530758,"name":"brentuximab vedotin","firstLetter":"b","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"brentuximab-vedotin"}],"links":null}