Iodopravadoline (AM630) - CAS 164178-33-0
Catalog number: 164178-33-0
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
Cannabinoid Receptor
Iodopravadoline, also known as AM630, is an inverse agonist at the human cannabinoid CB1 receptor. Iodopravadoline has been found to attenuate the ability of a number of cannabinoids to inhibit electrically-evoked twitches of the mouse isolated vas deferens.
Solid powder
AM630; AM-630; AM 630; iodopravadoline.
Soluble in DMSO, not in water
Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).
Shelf Life:
2 years if stored properly
Canonical SMILES:
1.Endocannabinoid activation of CB
Sun L;Tai L;Qiu Q;Mitchell R;Fleetwood-Walker S;Joosten EA;Cheung CW Eur J Pain. 2017 May;21(5):804-814. doi: 10.1002/ejp.983. Epub 2017 Jan 20.
BACKGROUND: ;Spinal cord stimulation (SCS) has been shown to be effective in the management of certain neuropathic pain conditions, however, the underlying mechanisms are incompletely understood. In this study, we investigated repetitive SCS in a rodent neuropathic pain model, revealing long-lasting and incremental attenuation of hyperalgesia and a mechanism of action involving endocannabinoids.;METHOD: ;Animals were implanted with monopolar electrodes at the time of partial sciatic nerve injury. Dorsal columns at spinal segments T12/13 were stimulated 3 days later (early SCS), and again at day 7 (late SCS) using low-frequency parameters. Hypersensitivity to cutaneous mechanical stimuli was assessed using von Frey filaments. Pharmacological agents, selected to identify endocannabinoid and opioid involvement, were administered intraperitoneally, 10 min before SCS.;RESULTS: ;Early SCS caused partial reversal of mechanical hypersensitivity with corresponding changes in the biomarker of central sensitization, [phospho-Tyr;1472; ]-GluN2B. The partial reversal of hyperalgesia by early SCS was amplified by co-administration of LY 2183240, an inhibitor of endocannabinoid reuptake/breakdown.
2.Role of cannabinoidergic system on food intake in neonatal layer-type chicken.
Alizadeh A;Zendehdel M;Babapour V;Charkhkar S;Hassanpour S Vet Res Commun. 2015 Jun;39(2):151-7. doi: 10.1007/s11259-015-9636-3. Epub 2015 Apr 23.
Central regulatory mechanisms for neurotransmitters of food intake vary among animals. Endocannabinoids have crucial role on central food intake regulation in mammals but its role has not been studied in layer-type chicken. Thus, in this study 6 experiments designed to evaluate effects of intracerebroventricular (ICV) administration of 2-AG (2-Arachidonoylglycerol, selective CB1 receptors agonist), SR141716A (selective CB1 receptors antagonist), JWH015 (selective CB2 receptors agonist), AM630 (selective CB2 receptors antagonist) on feeding behavior in 3 h food deprived neonatal layer-type chickens. In experiment 1, birds ICV injected with control solution and 2-AG (0.25, 0.5 and 1 μg). In experiment 2: control solution, SR141716A (6.25, 12.5 and 25 μg) were ICV injected to birds. In experiment 3 animals received: control solution, SR141716A (6.25 μg), 2-AG (1 μg) and co-injection of SR141716A+2-AG. In experiment 4, chickens received control solution and JWH015 (6.25, 12.5 and 25 μg). In experiment 5, control solution and AM630 (1.25, 2.5 and 5 μg) were injected. In experiment 6, the birds received control solution, AM630 (1.25 μg), JWH015 (25 μg) and co-administration of AM630+JWH015.
3.Increase of mesenchymal stem cell migration by cannabidiol via activation of p42/44 MAPK.
Schmuhl E;Ramer R;Salamon A;Peters K;Hinz B Biochem Pharmacol. 2014 Feb 1;87(3):489-501. doi: 10.1016/j.bcp.2013.11.016. Epub 2013 Dec 1.
Migration and differentiation of mesenchymal stem cells (MSCs) are known to be involved in various regenerative processes such as bone healing. However, little is known about the pharmacotherapeutical options aiming at the mobilization and differentiation of MSCs. The present study therefore focussed on cannabinoids which have been demonstrated to exhibit tissue healing properties. Using Boyden chamber assays, the non-psychoactive phytocannabinoid cannabidiol (CBD) was found to increase the migration of adipose-derived MSCs in a time- and concentration-dependent manner. CBD-induced migration was inhibited by AM-630 (CB₂ receptor antagonist) and O-1602 (G protein-coupled receptor 55 [GRP55] agonist). Moreover, the promigratory effect of CBD was antagonized by inhibition of the p42/44 mitogen-activated protein kinase (MAPK) pathway which became activated upon CBD treatment. In line with this data, AM-630 and O-1602 attenuated CBD-induced p42/44 MAPK phosphorylation. A p42/44 MAPK-dependent promigratory effect was likewise demonstrated for the GPR55 antagonist O-1918 and the selective CB₂ receptor agonist JWH-133. Additional evidence for a functional effect of CBD on MSCs was provided by experiments demonstrating long-term stimulation with CBD to induce differentiation of MSCs into the osteoblastic lineage as evidenced by increased mineralization assessed by cresolphthalein complexone assay and enhanced activity of alkaline phosphatase.
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CAS 164178-33-0 Iodopravadoline (AM630)

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