BMS-1166 | PD-1/PD-L1 inhibitor

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BMS-1166 (1818314-88-3) blocks the cell surface interaction of PD-L1 with PD-1 alleviating the inhibitory effect of PD-L1 on T-cell receptor-mediated activation of T-lymphocytes (IC50 = 1.4 nM).1,2  It suppressed growth and invasion of glioma cells3 and induced apoptosis in conjunction with the dual PI3K/mTOR inhibitor BEZ2354. BMS-1166 reversed HEL-mediated T cell suppression in acute myeloid leukemia patients.5 It significantly decreased cell viability and enhanced chemotherapy-induced cytotoxicity in MDF-MB-231 and MCF-7 breast cancer models.6

References/Citations:

  1. Skalniak et al. (2017), Small-molecule inhibitors of PD-1/PD-L1 immune checkpoint alleviate the PD-L1-induced exhaustion of T-cells; Oncotarget 8 72167
  2. Guzik et al. (2017), Small-molecule inhibitors of Programmed Cell Death-1/Programmed Death-ligand 1 (PD-1/PD-L1) interaction via transiently-induced protein states and dimerization of PD-L1; J. Med. Chem. 60 5857
  3. Wang et al. (2024), PD-1/PD-L1 axis is involved in the interaction between microglial polarization and glioma; Int. Immunopharmacol. 133 112074
  4. Liu et al. (2024), Dual PI3K/mTOR Inhibitor BEZ235 combined with BMS-1166 Promoting Apoptosis in Colorectal Cancer; Int. J. Med. Sci. 21 1814
  5. da Cruz et al. (2025), Bone marrow tumor microenvironment profiling predicts distinct immunosuppressive phenotypes and immunotherapy potential in AML patients; Biomed. Pharmacother. 189 118287
  6. Özen et al. (2025), PD-1/PD-L1 Inhibitors and Chemotherapy Synergy: Impact of Drug Resistance and PD-L1 Expression in Breast Cancer-Immune Cell Co-Cultures; Int. J. Mol. Sci. 26 6876
1818314-88-3, BMS-1166, BMS-1166 supplier, BMS1166, PD-1 inhibitor, PD-1/PD-L1 inhibitor

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Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee

BMS-1166 (1818314-88-3) blocks the cell surface interaction of PD-L1 with PD-1 alleviating the inhibitory effect of PD-L1 on T-cell receptor-mediated activation of T-lymphocytes (IC50 = 1.4 nM).1,2  It suppressed growth and invasion of glioma cells3 and induced apoptosis in conjunction with the dual PI3K/mTOR inhibitor BEZ2354. BMS-1166 reversed HEL-mediated T cell suppression in acute myeloid leukemia patients.5 It significantly decreased cell viability and enhanced chemotherapy-induced cytotoxicity in MDF-MB-231 and MCF-7 breast cancer models.6

References/Citations:

  1. Skalniak et al. (2017), Small-molecule inhibitors of PD-1/PD-L1 immune checkpoint alleviate the PD-L1-induced exhaustion of T-cells; Oncotarget 8 72167
  2. Guzik et al. (2017), Small-molecule inhibitors of Programmed Cell Death-1/Programmed Death-ligand 1 (PD-1/PD-L1) interaction via transiently-induced protein states and dimerization of PD-L1; J. Med. Chem. 60 5857
  3. Wang et al. (2024), PD-1/PD-L1 axis is involved in the interaction between microglial polarization and glioma; Int. Immunopharmacol. 133 112074
  4. Liu et al. (2024), Dual PI3K/mTOR Inhibitor BEZ235 combined with BMS-1166 Promoting Apoptosis in Colorectal Cancer; Int. J. Med. Sci. 21 1814
  5. da Cruz et al. (2025), Bone marrow tumor microenvironment profiling predicts distinct immunosuppressive phenotypes and immunotherapy potential in AML patients; Biomed. Pharmacother. 189 118287
  6. Özen et al. (2025), PD-1/PD-L1 Inhibitors and Chemotherapy Synergy: Impact of Drug Resistance and PD-L1 Expression in Breast Cancer-Immune Cell Co-Cultures; Int. J. Mol. Sci. 26 6876