BP79 

BP79 is a potent TSLP receptor inhibitor. BP79 disrupts TSLP-mediated ternary complex formation, blocks TSLPR-IL7Rα co-localization, binds and stabilizes TSLPR, and inhibits phosphorylated STAT3/6. BP79 suppresses immune cell infiltration, secretion of IL-13, IL-4. BP79 can be used for the research of inflammation diseases, such as atopic dermatitis, allergic asthma, and allergic rhinitis^[1][2][3].

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.

259.09

C₁₀H₈Cl₂N₂O₂

3104965-33-2

Solid

White to off-white

NC(/C=C\C(NC1=CC(Cl)=C(C=C1)Cl)=O)=O

Room temperature in continental US; may vary elsewhere.

4°C, sealed storage, away from moisture and light

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Adhikary PP, et al. Disrupting TSLP-TSLP receptor interactions via putative small molecule inhibitors yields a novel and efficient treatment option for atopic diseases. EMBO Mol Med. 2024;16(7):1630-1656.

  [2]. Christopher Hoang. The development of small molecule inhibitors of thymic stromal lymphopoietin signaling for the treatment of atopic dermatitis. \t
  University of British Columbia. December 2023.

  [3]. Sarah Hedtrich, et al. N1-(3,4-dichlorophenyl)maleamide derivatives and the use thereof in the treatment of inflammatory disorders. WO2025213277A1. 2025-10-16.