{"aliases":[{"type":"CodeName","name":"RG7446"},{"type":"Synonym","name":"MPDL328OA"},{"type":"CodeName","name":"MPDL-3280A"},{"type":"ChemicalStructureName","name":"immunoglobulin G1, anti-(human CD antigen cd274) (human monoclonal MPDL3280A heavy chain), disulfide with human monoclonal MPDL3280A kappa-chain, dimer"},{"type":"CodeName","name":"RO5541267"},{"type":"USBrandName","name":"Tecentriq"},{"type":"Synonym","name":"MPDL 328OA"},{"type":"CodeName","name":"MPDL 3280A"},{"type":"CodeName","name":"MPDL3280A"},{"type":"CASRegistryName","name":"1380723-44-3"}],"definition":{"html":"A humanized, Fc optimized, monoclonal antibody directed against the protein ligand PD-L1 (programmed cell death-1 ligand 1; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Atezolizumab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1; PDCD1) expressed on activated T cells, which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. In addition, by binding to PD-L1, atezolizumab also prevents binding of this ligand to B7.1 (CD80) expressed on activated T cells, which further enhances the T-cell-mediated immune response. PD-L1 is overexpressed on many human cancer cell types and on various tumor-infiltrating immune cells. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in increased immune evasion. PD-1, a transmembrane protein, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells. The Fc region of atezolizumab is modified in such a way that it does not induce either antibody-dependent cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC).","text":"A humanized, Fc optimized, monoclonal antibody directed against the protein ligand PD-L1 (programmed cell death-1 ligand 1; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Atezolizumab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1; PDCD1) expressed on activated T cells, which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. In addition, by binding to PD-L1, atezolizumab also prevents binding of this ligand to B7.1 (CD80) expressed on activated T cells, which further enhances the T-cell-mediated immune response. PD-L1 is overexpressed on many human cancer cell types and on various tumor-infiltrating immune cells. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in increased immune evasion. PD-1, a transmembrane protein, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells. The Fc region of atezolizumab is modified in such a way that it does not induce either antibody-dependent cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC)."},"drugInfoSummaryLink":{"uri":"https://www.cancer.gov/about-cancer/treatment/drugs/atezolizumab","text":"Atezolizumab"},"nciConceptId":"C106250","nciConceptName":"Atezolizumab","termId":702758,"name":"atezolizumab","firstLetter":"a","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"atezolizumab"}