VAF347 is a cell permeable and highly affinity aryl hydrocarbon receptor (AhR) agonist and induces AhR signaling. VAF347 inhibits the development of CD14 + CD11b + monocytes from granulo-monocytic (GM stage) precursors. VAF347 has anti-inflammatory effects In Vitro VAF347 (0.01-20 μM; 48-72 hours; HL-60 cells) treatment enhances retinoic acid-induced cell cycle arrest. VAF347 (20 μM; 48 hours; HL-60 cells) treatment augments retinoic acid-induced expression of AhR, Lyn, Vav1, and c-Cbl as well as p47phox. Several interactions of partners in the signalsome appear to be enhanced: Fgr interaction with c-Cbl, CD38, and with pS259c-Raf and AhR interaction with c-Cbl and Lyn. VAF347 inhibits IL-4 + GM-CSF induced IL-6 production in MM1 cells with an IC 50 of ~5 nM. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Cycle AnalysisCell Line: HL-60 cells Concentration: 10 nM, 100 nM, 1 μM, 10 μM, 20 μM Incubation Time: 48 hours or 72 hours Result: Enhanced retinoic acid-induced cell cycle arrest in G1/0. Western Blot AnalysisCell Line: HL-60 cells Concentration: 20 μM Incubation Time: 48 hours Result: Augmented retinoic acid-induced expression of AhR, Lyn, Vav1, and c-Cbl as well as p47phox. In Vivo In wild-type mice, VAF347 treatment leads to a strong reduction of total serum IgE levels compared with vehicle-treated animals. IL-5 levels in the bronchoalveolar fluid are inhibited to a comparable degree. AhR-deficient mice are resistant to the VAF347's ability to block allergic lung inflammation in vivo. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Form:Solid IC50& Target:Aryl hydrocarbon receptor