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Non-competitive MAGL inhibitor. Exhibits selectivity for MAGL over FAAH, diacylglycerol lipase and COX2. Blocks 2-AG hydrolysis in rat brain slices. Enhances stress-induced analgesia in rats.
|Storage||Store at +4°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 295.38. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||3.39 mL||16.93 mL||33.85 mL|
|5 mM||0.68 mL||3.39 mL||6.77 mL|
|10 mM||0.34 mL||1.69 mL||3.39 mL|
|50 mM||0.07 mL||0.34 mL||0.68 mL|
References are publications that support the biological activity of the product.
Hohmann et al (2005) An endocannabinoid mechanism for stress-induced analgesia. Nature. 435 1108 PMID: 15973410
Makara et al (2005) Selective inhibition of 2-AG hydrolysis enhances endocannabinoid signaling in hippocampus. Nat.Neurosci. 8 1139 PMID: 16116451
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Keywords: URB 602, URB 602 supplier, URB602, non-competitive, MAGL, inhibitors, inhibits, monoacylglycerol, lipases, 6020, Tocris Bioscience
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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The key feature of drug addiction is the inability to stop using a drug despite clear evidence of harm. This poster describes the brain circuits associated with addiction, and provides an overview of the main classes of addictive drugs and the neurotransmitter systems that they target.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.