AM630
AM630 is a selective and competitive antagonist of cannabinoid receptors with Ki values of 5 μM and 31.2 nM for CB1 receptor and CB2 receptor, respectively [1].
In CB1-transfected CHO cells, AM630 significantly inhibited the production of cAMP stumilated by forskolin. In CB2-transfected cells, AM630 promoted forskolin to stimulate cyclic AMP production with EC50 value of 230.4 nM. AM630 also exerted to have inhibitory effect on the binding of GTPγS to membranes from CB2-transfected cells. Besides that, AM630 was found to activate the TRPA1 channels and subsequently desensitizing TRPA1 and TRPV1 channels in TG sensory neurons. Moreover, AM630 significantly weakened the thermal hyperalgesia induced by CAP (capsaicin) in WT mice [1, 2].
References:
1. Ross R A, Brockie H C, Stevenson L A, et al. Agonist-inverse agonist characterization at CB1 and CB2 cannabinoid receptors of L759633, L759656 and AM630. British journal of pharmacology, 1999, 126(3): 665-672.
2. Patil M, Patwardhan A, Salas M M, et al. Cannabinoid receptor antagonists AM251 and AM630 activate TRPA1 in sensory neurons. Neuropharmacology, 2011, 61(4): 778-788.
- 1. Bin Zhang, Feng Zheng, et al. "Activation of CB2 receptor inhibits pyroptosis and subsequently ameliorates cecal ligation and puncture-induced sepsis." Int Immunopharmacol. 2021 Oct;99:108038. PMID:34364304
- 2. Zou G, Zuo X, et al. "Cannabinoids Rescue Cocaine-Induced Seizures by Restoring Brain Glycine Receptor Dysfunction." Cell Rep. 2020;30(12):4209-4219.e7. PMID:32209479
- 3. Liu AP, Yuan QH, et al. "Cannabinoid receptor 2 activation alleviates septic lung injury by promoting autophagy via inhibition of inflammatory mediator release." Cell Signal. 2020;69:109556. PMID:32027949
| Physical Appearance | A solid |
| Storage | Store at -20°C |
| M.Wt | 504.36 |
| Cas No. | 164178-33-0 |
| Formula | C23H25IN2O3 |
| Synonyms | AM 630;AM-630 |
| Solubility | ≥25.2 mg/mL in DMSO; insoluble in H2O; ≥2.53 mg/mL in EtOH with gentle warming and ultrasonic |
| Chemical Name | [6-iodo-2-methyl-1-(2-morpholin-4-ylethyl)indol-3-yl]-(4-methoxyphenyl)methanone |
| SDF | Download SDF |
| Canonical SMILES | CC1=C(C2=C(N1CCN3CCOCC3)C=C(C=C2)I)C(=O)C4=CC=C(C=C4)OC |
| Shipping Condition | Small Molecules with Blue Ice, Modified Nucleotides with Dry Ice. |
| General tips | We do not recommend long-term storage for the solution, please use it up soon. |
| Cell experiment:[1] | |
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Cell lines |
Trigeminal ganglia (TG) sensory neurons |
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Reaction Conditions |
10 μM AM630 for 3 min incubation |
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Applications |
The application of cannabinoid receptor antagonist AM630 (10 μM) activated a robust Ca2+ accumulation in a subset (35 ~ 40%) of TG neurons. The AM630-evoked Ca2+ influxes into TG sensory neurons were concentration-dependent, with an EC50 value being 15.6 μM. |
| Animal experiment:[2] | |
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Animal models |
Swiss ICR mice |
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Dosage form |
1, 2 or 3 mg/kg Administered intraperitoneally twice a day for 7 days |
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Applications |
Chronic AM630 treatment alleviated anxiety-like behaviors in the light-dark box and elevated plus maze tests. Meanwhile, chronic AM630 treatment increased gene and reduced protein expression of CB2 receptors, GABAAα2 and GABAAγ2 in cortex and amygdala. |
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Note |
The technical data provided above is for reference only. |
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References: 1. Patil M, Patwardhan A, Salas MM, et al. Cannabinoid receptor antagonists AM251 and AM630 activate TRPA1 in sensory neurons. Neuropharmacology, 2011, 61(4): 778-788. 2. García-Gutiérrez MS, García-Bueno B, Zoppi S, et al. Chronic blockade of cannabinoid CB2 receptors induces anxiolytic-like actions associated with alterations in GABA(A) receptors. British Journal of Pharmacology, 2012, 165(4): 951-964. |
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