KI-TOX-A3

KI-TOX-A3 (0.156-10 μM) potently inhibits the TOX-KAT7 protein-protein interaction in cell-free ELISA assays, with an IC₅₀ of 0.51 μM^[1].
KI-TOX-A3 (100 μM) binds directly to purified full-length TOX protein in cell-free ITC assays, with a K_d value of 1.05 μM^[1].
KI-TOX-A3 (0.15-10 μM) binds directly to biotinylated full-length recombinant human TOX protein in cell-free SPR assays, with a K_d of 0.92 μM^[1].
KI-TOX-A3 (20-40 μM) selectively competes for binding to TOX protein in Molt-4 cell lysates^[1].
KI-TOX-A3 (0-10 μM) dose-dependently restores TOX protein-inhibited KAT7-mediated H3K14 acetylation in cell-free in vitro assays^[1].
KI-TOX-A3 (5-10 μM; 24 h) inhibits the protein-protein interaction between TOX and KAT7 in Molt-4 T-ALL cells^[1].
KI-TOX-A3 (96 h) exerts selective cytotoxicity against TOX-dependent T-ALL and CTCL cell lines, with IC₅₀ values ranging from 2.0 μM to 6.3 μM after 96 h of treatment, whereas it shows much lower toxicity against TOX-independent cell lines^[1].
KI-TOX-A3 (10 μM) induces S-phase cell cycle arrest in Jurkat T-ALL cells^[1].
KI-TOX-A3 (5-10 μM; 4-12 h) induces proteasome-dependent degradation of TOX protein in Molt-4 T-ALL cells^[1].
KI-TOX-A3 (0.625-10 μM; 2-12 h) dose-dependently reduces TOX mRNA levels in Jurkat T-ALL cells^[1].
KI-TOX-A3 (2.5-10 μM; 24 h) reduces the expression of exhaustion markers TIM-3 and LAG-3, promotes the expression of effector cytokines, upregulates PD-1 expression in exhausted primary human CD8⁺ T cells, restores the cytotoxic activity of exhausted primary human CD8⁺ T cells against CD19⁺ Ramos cells, and restores the acetylation level of H3K14 in exhausted primary human CD8⁺ T cells to a level comparable to that of non-exhausted T cells^[1].

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