Tyrphostin A1 inhibits CD40L-stimulated IL-12 production in macrophage cultures and antigen-induced generation of Th1 cells.
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Tyrphostin A1 (AG9) is effective in inhibiting CD40L-stimulated IL-12 production in macrophage cultures and preventing the antigen-induced generation of Th1 cells. Its application leads to a dose-dependent reduction of IL-12 p40 levels, achieving maximum inhibition (62.5%) at a 10 μM concentration. Tyrphostin A1 also obstructs the CD40L-induced translocation of NF-κB to the nucleus and diminishes the activation of the IL-12 p40 gene. Therapeutic use of A1 in vivo results in decreased generation of myelin basic protein (MBP) specific encephalitogenic T cells and attenuates experimental allergic encephalomyelitis (EAE) in SJL/J mice, highlighting its potential for therapeutic applications in autoimmunity [1]. Compared to other tyrphostins, Tyrphostin A1 is a significantly weaker inhibitor of tyrosine kinase (TK), with an IC50 greater than 1250 μM for the epidermal growth factor receptor (EGFR) kinase, indicating its utility in distinguishing TK-mediated effects from non-specific actions of tyrphostins [2].
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