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LEI-106 is a dual ABHD6 and DAGL-α inhibitor, with a Ki of 0.8 μM for ABHD6, and an IC50 of 18 nM and a Ki of 0.7 μM for DAGL-α. LEI-106 blocks the synthesis of 2-arachidonoylglycerol, reduces the level of endothelial cell-derived 2-arachidonoylglycerol, without altering the levels of cannabinoids and diacylglycerol. LEI-106 is applicable to research related to diet-induced obesity and metabolic syndrome[1].

LEI-106 (compound 15) potently inhibits human DAGL-α activity in a cell-free HEK293 membrane system, with an IC50 of 18 nM in colorimetric assays and a Ki of 0.7 μM against the natural substrate [1].
LEI-106 (20 μM; 20 min) potently inhibits the endogenous DAGL-α activity in mouse meningeal homogenate, with an IC50 of 124 nM, and also acts as an inhibitor of ABHD6 in this system [1].
LEI-106 (processed for 30 minutes) potently inhibits human ABHD6 activity in cell-free HEK293T membranes, with a Ki value of 0.8 μM for the natural substrate 2-AG [1].
LEI-106 (1.3 mM; 15 min) significantly reduced 2-AG levels in bEnd.3 mouse brain endothelial cells without altering AEA levels [2].
LEI-106 (650 μM-1.3 mM; 15 min) significantly enhances PKC activity in bEnd.3 mouse brain endothelial cells [2].
LEI-106 (650 μM-1.3 mM; 15 min) induces VE-cadherin fragmentation in mouse brain endothelial cells bEnd.3, and a concentration of 1.3 mM further reduces the levels of full-length VE-cadherin, claudin-5, and ZO-1; Rho kinase inhibition alleviates VE-cadherin fragmentation, whereas calpain or PKC inhibition has no such effect [2].
LEI-106 (650-1.3 mM; 2 min) significantly increased intracellular calcium levels in bEnd.3 mouse brain endothelial cells [2].
LEI-106 (650 μM; 15 min) significantly alters the phosphorylated proteome of bEnd.3 murine brain endothelial cells, involving changes in mRNA processing, cytoskeleton assembly, and Rho GTPase signaling pathways [2].

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