Idelalisib
Selective PI3Kδ inhibitor / Potent (IC50 = 2.5nM) and selective (IC50’s: PI3Ka = 820nM, PI3Kb = 565nM, PI3Kg = 89nM) PI3Kd inhibitor.1,2 Useful clinical agent for the treatment of various blood cancers. Idelalisib attenuates regulatory T cells (Treg) but not conventional T cells (Tconv) resulting in a significant increase in tumor-infiltrating antigen-specific CD8 T cells in a murine lung cancer model.3 Conversely, systemic PI3Kd inactivation antagonized anti-CTLA-4 and anti-PD-L1 treatment.4 Others have found that Idelalisib minimally influenced rituximab- and obinutuzumab-mediated Ab-dependent cellular cytotoxicity in human lymphoma cells.5
Biochemicals & reagents
870281-82-6
1) Herman et al. (2010), Phosphatidylinositol 2-kinase-d inhibitor CAL-101 shows promising preclinical activity in chronic lymphocytic leukemia by antagonizing intrinsic and extrinsic cellular survival signals; Blood 116 2078 2) Lannutti et al. (2011), CAL-101, a p110d selective phosphatidylinositol-3-kinase inhibitor for the treatment of B-cell malignancies, inhibits PI3K signaling and cellular viability; Blood 117 591 3) Ahmad et al. (2017), Differential PI3Kd Signaling in CD4+ T-cell Subsets Enables Selective Targeting of T Regulatory Cells to Enhance Cancer Immunotherapy; Cancer Res. 77 1892 4) Lim et al. (2018), Phosphoinositide 3-kinase d inhibition promotes antitumor responses but antagonizes checkpoint inhibitors; JCI Insight 3 e120626 5) Palazzo et al. (2018), The PI3Kd-Selective Inhibitor Idelalisib Minimally Interferes with Immune Effector Function Mediated by Rituximab or Obinutuzumab and Significantly Augment B Cell Depletion In Vivo; J.Immunol. 200 2304
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TARGET: Kinase -- PATHWAY: PI3K; AKT -- DISEASE AREA: Cancer