PD-L1 inhibitory peptide TFA

PD-L1 inhibitory peptide TFA binds to the natural PD-L1 interaction pocket on human PD-1 with a theoretical binding energy of -10.28 kJ^[2].
PD-L1 inhibitory peptide TFA (0.024-120 μM) binds directly to recombinant human PD-1 with dose-dependent affinity, and competitively inhibits PD-L1 binding to PD-1 in a dose-dependent manner^[2].
PD-L1 inhibitory peptide TFA (0.2984 μg/mL; 30 min pre-incubation, 6 h co-culture) blocks the PD-1/PD-L1 interaction in co-cultures of PD-L1-expressing CHO-K1 cells and PD-1-expressing Jurkat E6-1 cells with an EC₅₀ of 0.2984 μg/mL^[2].
PD-L1 inhibitory peptide TFA rescues Jurkat E6-1 cells and murine primary lymphocytes from PD-L1-induced apoptosis, reducing apoptotic signals by 25% in Jurkat cells and preserving primary lymphocyte viability without inducing T-cell death^[2].
PD-L1 inhibitory peptide TFA (24 h) promotes a dose-dependent increase in active CD3⁺/CD45⁺/CD8⁺ T-cells in co-cultures of human PBMCs and MDA-MB-231 cells^[2].
PD-L1 inhibitory peptide TFA (10 nM-11.6 μM; 24 h) at 11.6 μM rescues murine primary T-cells from apoptosis in co-culture with 4T1 cells, increases 4T1 cell death, and induces a significant, dose-dependent increase in Granzyme B production by CD3⁺/CD8⁺ T-cells^[2].
PD-L1 inhibitory peptide TFA (0.2-12.5 μg/mL; 24 h) induces dose-dependent increases in IFNγ and dose-dependent decreases in IL-12p70 and IL-10 secretion by murine primary lymphocytes co-cultured with 4T1 cells, indicating enhanced T-cell activation and reduced inhibitory signaling^[2].
PD-L1 inhibitory peptide TFA (30 μM; 30 min pre-treatment, 24 h co-culture) enhances Jurkat E6-1 cell infiltration into a 3D MDA-MB-231 tumor microenvironment, reduces Jurkat apoptosis, and induces greater MDA-MB-231 cell death than anti-PD-1 antibody treatment^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.