Figure 1.
Figure 1. The PI3Kδ inhibitor TGR-1202 is active in lymphoma models. (A) The structural formulae of TGR-1202 (TG) and idelalisib with the active quinazolinone moieties circled. (B) Cell-free in vitro kinase assay of PI3Kδ in the presence of TGR-1202. (C) Cell-based assay measuring inhibition of S473 p-AKT in leukemia and lymphoma cell lines treated for 4 hours. (D) Response of the subcutaneous xenograft model of T-ALL to 3 treatments, including vehicle control and TGR-1202 (150 mg/kg) over 25 days. The xenograft was derived from the MOLT-4 cell line in NOD/SCID mice. P values were <.001 between the treatment and control groups on day 25. (E) LY7, Z-138, and H9 cells were treated by idelalisib and TGR-1202 for 24 hours (LY7) and 48 hours (Z-138 and H9) then viability was measured by Cell Titer Glo.

The PI3Kδ inhibitor TGR-1202 is active in lymphomamodels. (A) The structural formulae of TGR-1202 (TG) and idelalisib with the active quinazolinone moieties circled. (B) Cell-free in vitro kinase assay of PI3Kδ in the presence of TGR-1202. (C) Cell-based assay measuring inhibition of S473 p-AKT in leukemia and lymphoma cell lines treated for 4 hours. (D) Response of the subcutaneous xenograft model of T-ALL to 3 treatments, including vehicle control and TGR-1202 (150 mg/kg) over 25 days. The xenograft was derived from the MOLT-4 cell line in NOD/SCID mice. P values were <.001 between the treatment and control groups on day 25. (E) LY7, Z-138, and H9 cells were treated by idelalisib and TGR-1202 for 24 hours (LY7) and 48 hours (Z-138 and H9) then viability was measured by Cell Titer Glo.

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