JWH-210 is an analgesic chemical from the naphthoylindole family, which acts as a potent cannabinoid agonist at both the CB1 and CB2 receptors. JWH-210 is one of the most potent 4-substituted naphthoyl derivatives in the naphthoylindole series, having a higher binding affinity. The physiological and toxicological properties of this compound have not been evaluated in humans.

AM-679 is a drug that acts as a moderately potent agonist for the cannabinoid receptors. AM-679 is a 5-lipoxygenase-activating protein inhibitor. AM-679, found in Italy for the first time, but also identified during a seizure made by Hungarian authorities, almost concurrent with the Italian seizure.

JWH-250 or (1-pentyl-3-(2-methoxyphenylacetyl)indole) is an analgesic chemical from the phenylacetylindole family that acts as a cannabinoid agonist at both the CB1 and CB2 receptors, with a Ki of 11 nM at CB1 and 33 nM at CB2. JWH-250 does not have any therapeutic application, however it is found in many herbal products that are smoked for their psychoactive effects. JWH-250 is a controlled substance by FDA.

LY-320135 is a substituted benzofuran which is structurally distinct from the aminoalkylindole and pyrazole type cannabinoid antagonists, AM630 and SR141716A, respectively. LY-320135 is a potent and selective canniboid CB1 receptor antagonist/inverse agonist. LY-320135 is selective (~70 fold) over canniboid CB2 receptors. LY-320135 is widely used in research, particularly for elucidating the mechanisms by which many CB1 antagonists act as inverse agonists at higher doses. LY-320135 shows weak binding to both 5-HT2 (Ki = 6.4 uM) and muscarinic receptors (Ki = 2.1 uM).

(S)-AM-1241 is enantiomer of the CB2 modulator, that has most penetrated the literature, has proven an important research tool for investigating CB2-mediated antinociception. (R, S)-AM1241 produces antinociception following local and systemic administration in naive rats. Behavioral, neurochemical, and electrophysiological studies suggest that (R, S)-AM1241 suppresses persistent pain through a CB2-specific mechanism. In cAMP inhibition assays, (R, S)-AM1241 was found to be an agonist at human CB(2), but an inverse agonist in rat and mouse CB(2) receptors. (R)-AM1241 bound with more than 40-fold higher affinity than (S)-AM1241, to all three CB(2) receptors and displayed a functional profile similar to that of the racemate. In contrast, S-AM1241 was an agonist at all three CB(2) receptors. In pain models, S-AM1241 was more efficacious than either R-AM1241 or the racemate. In preclinical studies (R, S)-AM1241, (R)-AM1241, and (S)-AM1241 produced antinociception to thermal, but not mechanical, stimulation of the hind paw in naive rats. Antinociception produced by (R, S)-AM1241 and (S)-AM1241 exhibited an inverted U-shaped dose-response curve. (R)-AM1241 produced greater antinociception than either (S)-AM1241 or (R, S)-AM1241. (R, S)-AM1241, (R)-AM1241, and (S)-AM1241 each produced CB2-mediated antinociception that was blocked by SR144528 but not by rimonabant. Local and systemic naloxone blocked morphine-induced antinociception but did not block antinociceptive effects of (R, S)-AM1241, (R)-AM1241, or (S)-AM1241. The physiological and toxicological properties of (S)-AM-1241 have not been evaluated in humans.

WIN 55212-2 is the synthetic cannabimimetic compound. It is a potent aminoalkylindole cannabinoid receptor agonist. WIN 55,212-2 increases expression of anti-oxidant Cu/Zn SOD and is able to prevent inflammation induced by Aβ1-42 in cultured astrocytes. It exerts neuroprotective and anti-inflammatory actions against Aβ damage through both CB₁ and CB₂ receptors. WIN 55212-2 attenuates hyperalgesia and allodynia in a rat model of neuropathic pain. In the clinical trial, it was revealed that WIN 55212-2, applied topically, decreases the intraocular pressure of human glaucoma resistant to conventional therapies within the first 30 min.

AM-251 is a 123I radioisotope and potent CB1 receptor antagonist derivative of the CB1 cannabinoid receptor inverse agonist SR141716A, presenting a radioprobe for in vivo binding studies at the CB1 receptor with a higher affinity (Ki = 7.49 nM) for CB1 than the parent compound (Ki = 11.5 nM). AM-251 has been employed in competitive binding studies to identify CB1 affinity of different cannabimimetic agonists in vivo. AM-251 is also a potent activator of the GPR55 receptor. Daily injection of AM-251 in obese Zucker rats produced a marked and sustained decrease in daily food intake and body weight and a considerable increase in energy expenditure in comparison with untreated obese Zucker rats. AM-251 administration to obese rats significantly reduced plasma levels of glucose, leptin, AST, ALT, Gamma GT, total bilirubin and LDL cholesterol whereas HDL cholesterol plasma levels increased. AM-251 represents a promising therapeutic strategy for the treatment of obesity and metabolic syndrome.

(R)-AM-1241 is enantiomer of the CB2 modulator, that has most penetrated the literature, has proven an important research tool for investigating CB2-mediated antinociception. (R, S)-AM1241 produces antinociception following local and systemic administration in naive rats. Behavioral, neurochemical, and electrophysiological studies suggest that (R, S)-AM1241 suppresses persistent pain through a CB2-specific mechanism. In cAMP inhibition assays, (R, S)-AM1241 was found to be an agonist at human CB(2), but an inverse agonist in rat and mouse CB(2) receptors. (R)-AM1241 bound with more than 40-fold higher affinity than (S)-AM1241, to all three CB(2) receptors and displayed a functional profile similar to that of the racemate. In contrast, S-AM1241 was an agonist at all three CB(2) receptors. In pain models, S-AM1241 was more efficacious than either R-AM1241 or the racemate. In preclinical studies (R, S)-AM1241, (R)-AM1241, and (S)-AM1241 produced antinociception to thermal, but not mechanical, stimulation of the hind paw in naive rats. Antinociception produced by (R, S)-AM1241 and (S)-AM1241 exhibited an inverted U-shaped dose-response curve. (R)-AM1241 produced greater antinociception than either (S)-AM1241 or (R, S)-AM1241. (R, S)-AM1241, (R)-AM1241, and (S)-AM1241 each produced CB2-mediated antinociception that was blocked by SR144528 but not by rimonabant. Local and systemic naloxone blocked morphine-induced antinociception but did not block antinociceptive effects of (R, S)-AM1241, (R)-AM1241, or (S)-AM1241. The physiological and toxicological properties of (R)-AM-1241 have not been evaluated in humans.

HU-210 is a synthetic cannabinoid. HU-210 is a highly potent cannabinoid receptor agonist. Also, it displays agonist activity at GPR55. HU-210 administration in adult rats results in a dose-dependent inhibition of plasma growth hormone, follicle stimulating hormone, and luteinizing hormone; modifications of plasma adrenocorticotropic hormone (ACTH) and corticosterone levels reveal a dose-dependent action on the pituitary-adrenal axis after acute exposure. HU-210 block beta-amyloid peptide-induced activation of cultured microglial cells, as judged by mitochondrial activity, cell morphology, and tumor necrosis factor-alpha release; these effects are independent of the antioxidant action of cannabinoid compounds and are also exerted by a CB2-selective agonist. HU-210 induced a spatial deficit in the water maze in learning a reference memory task in numerous parameters together with alterations in hippocampal firing patterns of single principal neurons.