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 effect
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Product Description
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.
