Am630

Manufactured by Merck Group

Sourced in United States

The AM630 is a laboratory instrument designed for conducting cellular and molecular biology experiments. It is capable of performing various analytical tasks, including cell counting, viability assessment, and fluorescence-based assays. The AM630 utilizes advanced optical and detection technologies to provide accurate and reproducible results. For detailed specifications and intended use, please consult the product literature or contact our sales team.

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Lab products found in correlation

Am251, by Merck Group (6 mentions) Am1241, by Merck Group (2 mentions) Gw842166x, by Cayman Chemical (2 mentions) 6 ohda, by Merck Group (2 mentions) Gw842166x, by Merck Group (2 mentions) Am630, by Cayman Chemical (2 mentions) Jwh015, by Merck Group (2 mentions) Rimonabant, by Merck Group (2 mentions) Carrageenan, by Merck Group (2 mentions) Calcein am, by Thermo Fisher Scientific (1 mentions) Rpmi 1640, by Merck Group (1 mentions) Streptomycin, by Thermo Fisher Scientific (1 mentions) Polycarbonate filter, by Neuro Probe (1 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (1 mentions) 4 6 diamidino 2 phenylindole (dapi), by Thermo Fisher Scientific (1 mentions) Laemmli buffer, by Merck Group (1 mentions) Rhodamine labeled phalloidin, by Thermo Fisher Scientific (1 mentions) Sphingosine 1 phosphate (s1p), by Merck Group (1 mentions) Ml 193, by Bio-Techne (1 mentions) O 1602, by Cayman Chemical (1 mentions)

22 protocols using am630

Cannabinoid Receptor Modulation in Neuropathic Pain

Cited 2 times

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TMX (Sigma T5648) was dissolved into corn oil and was injected intraperitoneally (i.p.) once every other day, a total of five times, 2 mg/day (10 mg total dose) (Feil et al., 2009 (link); Anastassiadis et al., 2010 (link)). Subsequent verification and CCI modeling were performed 14 days after the final injection.
AM1241 (Sigma A6478) is a CB2 agonist, and AM630 (Sigma SML0327) is a highly specific CB2 antagonist. The drug was dissolved in dimethyl sulfoxide (DMSO), Tween 80, and normal saline (the ratio is 1:2:7). To determine the relationship between neuropathic pain and CB2, 36 WT mice were randomly divided into WT CCI + vehicle (DMSO:Tween 80:normal saline = 1:2:7), WT CCI + 0.1, 1, 3 mg/kg AM1241 (Sigma A6478; Wu et al., 2021 (link); Lozano-Ondoua et al., 2010 (link); Ma et al., 2021 (link)) groups, and WT CCI + 1, 3 mg/kg AM630 (Sigma SML0327; Malan et al., 2001 (link); Buffon et al., 2020 (link); Sultana et al., 2021 (link)) groups (n = 6 at each group). Fifteen CB1cKO mice were randomly divided into CB1cKO CCI + vehicle and CB1cKO CCI + 3, 5 mg/kg AM630 (n = 5 at each group). AM1241/AM630 or its vehicle (0.1 ml) was injected i.p. daily from 12th to 17th day after CCI surgery.

Liu Y., Jia M., Wu C., Zhang H., Chen C., Ge W., Wan K., Lan Y., Liu S., Li Y., Fang M., He J., Pan H.L., Si J.Q, & Li M. (2022). Transcriptomic Profiling in Mice With CB1 receptor Deletion in Primary Sensory Neurons Suggests New Analgesic Targets for Neuropathic Pain. Frontiers in Pharmacology, 12, 781237.

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Investigating GPR55 Signaling in Immune Cells

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Monoclonal IgE (clone SPE7), RPMI 1640, 2-mercaptoethanol (2-ME), Laemmli buffer, L-α-lysophosphatidylinositol (LPI), and sphingosine-1-phosphate (S1P) were purchased from Sigma-Aldrich (St. Louis, MO, USA). HEPES, non-essential amino acids (NEAA), penicillin, streptomycin, and fetal bovine serum (FBS) were obtained from Gibco-BRL-Life Technologies (Gaithersburg, MD, USA). Interleukin (IL)-3 was purchased from PeproTech (Rocky Hill, NJ, USA). The GPR55 synthetic agonist, O-1602, was purchased from Cayman Chemical (Ann Arbor, MI, USA), while the GPR55 antagonist, ML-193, was purchased from TOCRIS (Bristol, UK). The CB2 antagonist, AM630, was from Sigma-Aldrich (St. Louis, MO, USA). Anti-p-cofilin (pSer 3) antibodies were obtained from Cell Signaling Technology (Danvers, MA, USA). Anti-p-LIMK (pThr 508/505) and anti-β-actin (C-terminal) antibodies were purchased from Santa Cruz Biotechnology (Dallas, TX, USA). The secondary antibodies, HRP-coupled anti-mouse and anti-rabbit, were obtained from Jackson ImmunoResearch (West Grove, PA, USA). Rhodamine-labeled phalloidin and calcein-AM were obtained from Life Technologies (Carlsbad, CA, USA). DAPI was purchased from Invitrogen (Carlsbad, CA, USA). The polycarbonate filters were from Neuro Probe, and bovine skin gelatin from Sigma-Aldrich (St. Louis, MO, USA)

Martínez-Aguilar L.M., Ibarra-Sánchez A., Guerrero-Morán D.J., Macías-Silva M., Muñoz-Bello J.O., Padilla A., Lizano M, & González-Espinosa C. (2023). Lysophosphatidylinositol Promotes Chemotaxis and Cytokine Synthesis in Mast Cells with Differential Participation of GPR55 and CB2 Receptors. International Journal of Molecular Sciences, 24(7), 6316.

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Propofol Preconditioning Attenuates Myocardial I/R Injury

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Young rat myocardial I/R injury models were used. Before ischemia, the rats were preconditioned with or without propofol. We further tested the role of receptor signaling in propofol conditioning by intravenous injection of selective CB1R antagonists AM251 (Sigma, 1 mg/kg) or selective CB2R antagonists AM630 (Sigma, 1 mg/kg) 1.5 hours prior to ischemia irrespective of propofol conditioning or not. The dosage and timing of AM251 or AM630 were taken from the study by Hajrasouliha et al. [17 (link)]. The two drugs were used separately in our study which comprised seven groups with six rats for each group. 24 hours after reperfusion, infarct area was evaluated using Evans blue plus TTC staining. Serum cTnI levels were measured 2 hours after ischemia. Oxidative-redox state indicators including serum MDA, MPO, and SOD were also measured at 24 hours of reperfusion.

Sun H.J., Lu Y., Wang H.W., Zhang H., Wang S.R., Xu W.Y., Fu H.L., Yao X.Y., Yang F, & Yuan H.B. (2017). Activation of Endocannabinoid Receptor 2 as a Mechanism of Propofol Pretreatment-Induced Cardioprotection against Ischemia-Reperfusion Injury in Rats. Oxidative Medicine and Cellular Longevity, 2017, 2186383.

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Macrophage Differentiation Modulation

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The RAW264.7 mouse macrophage cells (ATCC, Manassas, VA, USA) were culture in DMEM (Gibco BRL, MD, USA), which contained heat-inactivated FBS of 10%, 100 U/mL penicillin, 100 U/mL streptomycin and 2 mM l-glutamine under 37 °C in a 5% CO₂ incubator.
We treated RAW264.7 cells by RANKL of 100 ng/mL without or with 2 μM AM1241 or 200 nM AM630 for 5 days. RANKL, AM1241, and AM630 (Sigma-Aldrich, St. Louis, USA).

Li W, & Sun Y. (2020). Nrf2 is required for suppressing osteoclast RANKL-induced differentiation in RAW 264.7 cells via inactivating cannabinoid receptor type 2 with AM630. Regenerative Therapy, 14, 191-195.

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6-OHDA-Induced Neurodegeneration Model

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The 6-OHDA was purchased from Sigma-Aldrich (St. Louis, MO, USA). D-amphetamine was provided by the NIDA Drug Supply Program. GW842166X and AM630 were purchased from Cayman Chemical Company (Ann Arbor, MI, USA). GW842166X and AM630 were first dissolved in DMSO (Sigma-Aldrich) and then mixed with TWEEN-80 (Sigma-Aldrich). Then, sterile saline was added to the mix solution to create a final working solution with 2.5% DMSO + 2.5% TWEEN-80 + 95% saline. Picrotoxin and all other common chemicals were obtained from Sigma-Aldrich. 6-Cyano-7-nitroquinoxaline-2,3-dione disodium salt (CNQX) and D-(-)-2-Amino-5-phosphonopentanoic acid (D-AP5) were obtained from Tocris Bioscience (Ellisville, MO, USA).

Yu H., Liu X., Chen B., Vickstrom C.R., Friedman V., Kelly T.J., Bai X., Zhao L., Hillard C.J, & Liu Q.S. (2021). The Neuroprotective Effects of the CB2 Agonist GW842166x in the 6-OHDA Mouse Model of Parkinson’s Disease. Cells, 10(12), 3548.

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Cardiac Effects of CB1/CB2 Receptor Antagonists

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The cannabinoid receptor-1 (CB1) antagonist, AM251 (Sigma Chemicals), was administered either acutely (3 mg/kg, iv) in the experiments involving ventricular pressure-volume studies and measurement of changes in ESPVR or chronically (3 mg/kg/day, SC × 2 days) in the hemorrhage studies. The CB-2 receptor antagonist AM630 (Sigma) was administered acutely (3 mg/kg iv) in ventricular pressure-volume experiments. Gadolinium chloride (12 mg/kg iv daily × 2 days, Sigma) was used to deplete monocytes and macrophages from cardiac tissue.

Gaskari S.A., Liu H., D’Mello C., Kunos G, & Lee S.S. (2015). Blunted cardiac response to hemorrhage in cirrhotic rats is mediated by local macrophage-released endocannabinoids. Journal of hepatology, 62(6), 1272-1277.

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Cannabinoid Receptor Modulation in Pain

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The following drugs were used in this study: N-(Piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-car boxamide (AM251), a CB₁ cannabinoid receptor inverse agonist; 6-Iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl](4-methoxyphenyl)methanone (AM630), a CB₂ cannabinoid receptor inverse agonist; (5Z,8Z,11Z,14Z)-5,8,11,14-eicosatetraenyl-methylester phosphonofluoridic acid (MAFP), an irreversible nonselective FAAH inhibitor; 4-[Bis(1,3-benzodioxol-5-yl)hydroxymethyl]-1-piperidinecarboxylic acid 4-nitrophenyl ester (JZL184), a potent and selective monoacylglycerol lipase inhibitor; (5Z,8Z,11Z,14Z)N(4Hydroxy2methylphenyl)5,8,11,14eicosatetraenamide (VDM11), a selective inhibitor of AEA cellular reuptake. All drugs were purchased from Tocris Bioscience (Ellisville, MO, USA). AM251, AM630 and JZL184 were dissolved in a physiological saline and dimethyl sulphoxide (20%, Sigma-Aldrich, St. Louis, MO, USA) vehicle. MAFP was dissolved in a physiological saline and ethanol (20%, Merck, New Jersey, NJ, USA) vehicle, and VDM11 was dissolved in a Tocrisolve (Tocris, Ellisville, MO, USA) vehicle. All drugs were administered in volumes of 1 mL/kg subcutaneous (s.c.), 10 μL intrathecal (i.t.) and 5 μL intracerebroventricular (i.c.v.). Each one of the substances, vehicles or diluents was tested alone and did not alter the nociceptive threshold.

Galdino G., Romero T., da Silva J.F., Aguiar D., de Paula A.M., Cruz J., Parrella C., Piscitelli F., Duarte I., Di Marzo V, & Perez A. (2014). Acute Resistance Exercise Induces Antinociception by Activation of the Endocannabinoid System in Rats. Anesthesia and analgesia, 119(3), 702-715.

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Intrathecal CB2R Agonist and Antagonist Study

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The CB2R agonist JWH015 (2 µg; sigma, USA) and antagonist AM630 (1 µg; sigma, USA) were dissolved in 5 µL of 20% dimethyl sulfoxide (DMSO) (in normal saline). On day 14 after sarcoma cells implantation, mice in the tumor+JWH015 group received a single intrathecal injection of 2 µg of JWH015. Mice in the tumor+AM630+JWH015 group received a single intrathecal injection of 1 µg of AM630 30 min before the injection of JWH015. Mice in the tumor+vehicle group received the same volume of 20% DMSO under identical conditions as the control. Doses of these compounds were based on our previous study.18 (link)

Wang C., Xu K., Wang Y., Mao Y., Huang Y., Liang Y., Liu Y., Hao J., Gu X., Ma Z, & Sun Y. (2020). Spinal cannabinoid receptor 2 activation reduces hypersensitivity associated with bone cancer pain and improves the integrity of the blood–spinal cord barrier. Regional Anesthesia and Pain Medicine, 45(10), 783-791.

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CBD Effects on NHEK Cells

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NHEKs were isolated from human foreskin tissues according to the method described previously and were cultured in Keratinocyte Growth Medium 2 (KGM2) (PromoCell, #C-20011, Heidelberg, Germany) under standard conditions.22 (link) Cells were seeded into 6-well culture plates at a cell density of 1×10⁵ cells per well. CBD solution (Sorrento Therapeutics, CA, USA) were dissolved in KGM2. CB2 receptor antagonist AM630 (Sigma, #SML0327, MO, USA) and TRPV1 antagonist Capsazepine (Sigma, #C191, MO, USA) were dissolved in dimethyl sulfoxide (DMSO). For the CEV group and (CEV+CBD) group, cells were treated with either the vehicle or CBD for 18 h, and then stimulated with CEVs. For the (CEV+AM630/Capsazepine) group, cells were treated with AM630 or Capsazepine for 20 h, and then stimulated with CEVs. For the (CEV+CBD+AM630/Capsazepine) group, cells were sequentially treated with AM630 or Capsazepine for 2 h, CBD for 18 h, and CEVs for 12 h.

Jiang Z., Jin S., Fan X., Cao K., Liu Y., Wang X., Ma Y, & Xiang L. (2022). Cannabidiol Inhibits Inflammation Induced by Cutibacterium acnes-Derived Extracellular Vesicles via Activation of CB2 Receptor in Keratinocytes. Journal of Inflammation Research, 15, 4573-4583.

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Curcumin Modulates Cardiac Biomarkers

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Curcumin, AM630, STZ, and ISO were procured from Sigma-Aldrich, Saint Louis, MO, USA. Curcumin was dispersed in 0.5% w/v carboxymethyl cellulose prior to administration. The kits for the determination of creatine kinase-MB (CK-MB) isoenzyme, lactate dehydrogenase (LDH), serum transaminase, total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) were procured from ERBA Diagnostics, Germany. The mice ELISA kit for tumor necrosis factor (TNF-α), interleukin-6 (IL-6) and IL-1β was purchased from eBioscience, San Diego, CA, USA. Other reagents of analytical grade were procured from local suppliers.

Pawar H.D., Mahajan U.B., Nakhate K.T., Agrawal Y.O., Patil C.R., Meeran M.F., Sharma C., Ojha S, & Goyal S.N. (2022). Curcumin Protects Diabetic Mice against Isoproterenol-Induced Myocardial Infarction by Modulating CB2 Cannabinoid Receptors. Life, 12(5), 624.

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