BP79

BP79 (5-20 µM; 36 h) inhibits TSLP-induced IL-13 (80% inhibition at 20 µM) and IL-4 (60% inhibition at 20 µM) secretion in HuT78 cells in a concentration-dependent manner ^[1].
BP79 (0.15-20 µM; 36 h) potently inhibits TSLP-induced IL-4 (IC₅₀ = 2.88 µM) and IL-13 (IC₅₀ = 0.97 µM) secretion in primary human CD4⁺ T cells, with ≥80% inhibition at 10 µM and 20 µM^[1].
BP79 (0.15-20 µM; 24 h) shows no significant cytotoxicity at concentrations up to 20 µM in primary human CD4+ T cells, keratinocytes, and fibroblasts, with viability remaining ≥80%^[1].
BP79 (20 µM; 1-5 days) abrogates TSLP-mediated hyperproliferation of primary human CD4⁺ T cells^[1].
BP79 (20 µM) inhibits TSLP-induced STAT6 phosphorylation in primary human CD4⁺ T cells and STAT3 phosphorylation in primary human keratinocytes^[1].
BP79 (20 µM; 24 h) inhibits TSLP-induced OX-40L expression and CCL17 secretion in primary human myeloid dendritic cells, and reduces dendritic cell-mediated IL-13 secretion from naive CD4⁺ T cells^[1].
BP79 (20 µM; 10 min) directly interacts with recombinant TSLPR, thermally stabilizing the protein up to 45 °C^[1].
BP79 (20 µM; topical; once daily for 4 days) suppresses pro-inflammatory cytokine secretion, restores skin barrier protein expression, inhibits TSLP production, and blocks CD4⁺ T-cell infiltration in a human atopic diseases multi-organ chip model, with beneficial effects on both skin and lung tissues^[1].
BP79 (10 μM) exhibits moderate binding to some kinases, but does not inhibit JAK2/JAK3/TYK2 kinases in the TSLP signaling pathway^[2].
BP79 prevents the co-localization of TSLPR and IL-7Rα in primary keratinocytes following TSLP treatment, supporting its targeting of the TSLP signaling pathway^[2].

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