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. 2021 Jan 26;22(3):1204. doi: 10.3390/ijms22031204

Figure 5.

Figure 5

The blocking capacity of the MAGL inhibitors JJKK-048, KML29 and the dual MAGL-FAAH inhibitor AKU-005 in the CNS and the PNS. (A) JJKK-048 (100 nM) almost completely inhibited MAGL activity at peripheral level: by 90% in TG and cervical DRG (cDRG), 85% in thoracic DRG (tDRG) and 95% in lumbar DRG (lDRG). (B) JJKK-048 (100 nM) inhibited MAGL activity by 66% in brainstem (BS), 72% in cervical spinal cord (cSC), 68% in thoracic spinal cord (tSC), 79% in lumbar spinal cord (lSC). (C) JJKK-048 (100 nM) inhibited MAGL activity by 95% in frontal cortex (FC) and 90% in temporal and occipital cortexes (TC and OC). (D) KML29 (1 μM) strongly reduced MAGL activity at peripheral level: 92% TG, 88% cDRG, 86% tDRG, 93% lDRG. (E) KML29 (1 μM) inhibitory effect on brainstem and cSC was 69%, in tSC 55% and 72% in lSC. (F) KML29 (1 μM) strongly reduced MAGL activity at cortical level: by 92% in FC, 88% in TC, 90% in OC. (G) AKU-005 (1 μM) reduced MAGL basal activity at peripheral level: 93% in TG, 91% in cDRG, 92% in tDRG and 93% in lDRG. (H) AKU-005 (1 μM) inhibited basal MAGL activity also in brainstem (77%) and spinal cord (70% cSC, 78% tSC, 95% lSC). (I) AKU-005 (1 μM) inhibitory effect on cortical MAGL activity was of 92% in FC, 91% in TC and 90% in OC. One-way ANOVA with Tukey’s multiple comparison post-hoc test was used for statistical analysis between the MAGL activities after control (DMSO) and inhibitor treatments, (* p < 0.05, ** p < 0.01, *** p < 0.001). For JJKK-048: n = 8 (TGs, DRGs), n = 11 (BS, cSC), n = 8 (tSC, lSC) and n = 9 (cortex); For KML29: n = 8 (TGs, DRGs), n = 11 (BS, cSC), n = 8 (tSC, lSC) and n = 9 (cortex); For AKU-005: n = 4 (TGs, DRGs, BS, tSC, lSC), n = 5 (cSC, cortex).