SL-327是一种选择性的MEK1和MEK2抑制剂，IC50值分别为0.18和0.22 μM。

MEK1和MEK2（ERK）是一种激酶，可使丝裂原活化蛋白激酶（MAPK）磷酸化。胞外信号调节激酶（ERK）的活性对联想学习任务的获得至关重要。

在成年雄性CD-1小鼠中，SL-327可抑制可卡因诱导的细胞核中Pp-ERK免疫染色。SL-327预处理可抑制细胞核中c-Fos的表达，并抑制所有杏仁核（称作LA、BLA、BMP、Ce和MePD）中ERK的活化[1]。在吗啡预处理的大鼠中，SL-327可提高（58%）吗啡诱导的精神运动致敏（SW3），完全阻止SW3中p-PEA-15、p-FADD和p-Akt1上调[2]。在成年雄性DBA/2J小鼠中，SL-327显著地减少40%的运动皮层和背侧纹状体中pERK的水平[3]。在大鼠模型中，SL-327抑制MAPK/ERK级联反应，阻止LTP依赖的基因诱导及CREB和Elk-1磷酸化，导致LTP迅速衰减[4]。

参考文献：
[1].  Radwanska K, Caboche J, Kaczmarek L. Extracellular signal-regulated kinases (ERKs) modulate cocaine-induced gene expression in the mouse amygdala. Eur J Neurosci, 2005, 22(4): 939-948.
[2].  Ramos-Miguel A, Esteban S, García-Sevilla JA. The time course of unconditioned morphine-induced psychomotor sensitization mirrors the phosphorylation of FADD and MEK/ERK in rat striatum: role of PEA-15 as a FADD-ERK binding partner in striatal plasticity. Eur Neuropsychopharmacol, 2010, 20(1): 49-64.
[3].  Groblewski PA, Franken FH, Cunningham CL. Inhibition of extracellular signal-regulated kinase (ERK) activity with SL327 does not prevent acquisition, expression, and extinction of ethanol-seeking behavior in mice. Behav Brain Res, 2011, 217(2): 399-407.
[4].  Davis S, Vanhoutte P, Pages C, et al. The MAPK/ERK cascade targets both Elk-1 and cAMP response element-binding protein to control long-term potentiation-dependent gene expression in the dentate gyrus in vivo. J Neurosci, 2000, 20(12): 4563-4572.