{"meta":{"totalResults":2,"from":0},"results":[{"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"},{"aliases":[{"type":"USBrandName","name":"Tecentriq Hybreza"},{"type":"Synonym","name":"atezolizumab and recombinant human hyaluronidase-tqjs"},{"type":"Synonym","name":"atezolizumab and recombinant human hyaluronidase"},{"type":"Synonym","name":"atezolizumab + rHuPH20"},{"type":"Synonym","name":"atezolizumab and hyaluronidase"},{"type":"Synonym","name":"atezolizumab with rHuPH20"},{"type":"Synonym","name":"atezolizumab-rHuPH20"},{"type":"Synonym","name":"atezolizumab/rHuPH20 co-formulation"},{"type":"Synonym","name":"recombinant human hyaluronidase mixed with atezolizumab"},{"type":"Synonym","name":"Tecentriq/rHuPH20"}],"definition":{"html":"A co-formulation composed of atezolizumab, a humanized, Fc optimized, monoclonal antibody directed against the protein ligand PD-L1 (programmed cell death-1 ligand 1; CD274), and a recombinant form of human hyaluronidase (rHuPH20), with potential immune checkpoint inhibitory and antineoplastic activities. Upon subcutaneous administration of atezolizumab and hyaluronidase, atezolizumab targets and 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). Hyaluronidase hydrolyzes and degrades the glycosaminoglycan hyaluronic acid (HA), thereby decreasing interstitial viscosity and enhancing penetration of atezolizumab through the interstitial space. This facilitates the delivery of atezolizumab to PD-L1-expressing tumor cells.","text":"A co-formulation composed of atezolizumab, a humanized, Fc optimized, monoclonal antibody directed against the protein ligand PD-L1 (programmed cell death-1 ligand 1; CD274), and a recombinant form of human hyaluronidase (rHuPH20), with potential immune checkpoint inhibitory and antineoplastic activities. Upon subcutaneous administration of atezolizumab and hyaluronidase, atezolizumab targets and 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). Hyaluronidase hydrolyzes and degrades the glycosaminoglycan hyaluronic acid (HA), thereby decreasing interstitial viscosity and enhancing penetration of atezolizumab through the interstitial space. This facilitates the delivery of atezolizumab to PD-L1-expressing tumor cells."},"drugInfoSummaryLink":{"uri":"https://www.cancer.gov/about-cancer/treatment/drugs/atezolizumab-and-hyaluronidase-tqjs","text":"Atezolizumab and Hyaluronidase-tqjs"},"nciConceptId":"C186549","nciConceptName":"Atezolizumab and Recombinant Human Hyaluronidase","termId":809887,"name":"atezolizumab and hyaluronidase-tqjs","firstLetter":"a","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"atezolizumab-and-recombinant-human-hyaluronidase"}],"links":null}