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Table 1 Characteristics of selected cannabinoid receptor ligands

From: Cannabinoid-based drugs targeting CB1 and TRPV1, the sympathetic nervous system, and arthritis

Ligand Target receptors Ki at CB1 in nM Ki at CB2 in nM Emax/IC50 at TRPV1 (nM) Route of degradation
Anandamide CB1, CB2, GPR55, TRPV1, TRPA1, TRPM8 (antagonist) 239.2 ± 61.77 [158] 439.5 ± 95.89 [158] 458 (Emax) [159] FAAH, FAAH-2, NAAA, COX-2, LOX [160]
2-AG CB1, CB2, TRPV1, GABAA 3423.6 ± 3288.24 [158] 1193.8 ± 327.71 [158] 750 ± 40 (IC50) [161] MAGL, COX-2, LOX, ABHD6/12 [160,162]
Delta9-THC CB1, CB2, GPR18 25.1 ± 5.54 [158] 35.2 ± 5.86 [158] NA CYP2C [163]
Rimonabant CB1, MOR 1.98 ± 0.36 [164] NA NA CYP3A [165]
  1. Anandamide, 2-arachidonylglycerol (2-AG) and tetrahydrocannabinol (THC) are CB1/CB2 agonists, rimonabant is a CB1/MOR antagonist/inverse agonist. Anandamide and THC are partial CB1/CB2 agonists, 2-AG is a full agonist at both receptors. The main degrading enzyme for each compound is highlighted in bold. ABHD, α/β-hydrolase domain; CB 1 /CB 2 , cannabinoid receptor I/II; COX-2, cyclooxygenase-2; CYP, cytochrome P450; Delta9 THC, delta9 tetrahydrocannabinol; Emax, maximal functional response; FAAH, fatty acid amide hydrolase; IC50, half maximal inhibitory concentration; Ki, dissociation constant; LOX, lipoxygenase; MAGL, monoacylglycerol lipase; MOR, μ opoid receptor; NA, not applicable; NAAA, N-acylethanolamine-hydrolyzing acid amidase; TRPA1, transient receptor potential ankyrin I; TRPM8, transient receptor potential melastatin 8; TRPV1, transient receptor potential vanilloid I