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ethyl 7-(phenoxy)heptanoate is a chemical with a specific purpose. Lookchem provides you with multiple data and supplier information of this chemical.

857787-75-8

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857787-75-8 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 857787-75-8 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 8,5,7,7,8 and 7 respectively; the second part has 2 digits, 7 and 5 respectively.
Calculate Digit Verification of CAS Registry Number 857787-75:
(8*8)+(7*5)+(6*7)+(5*7)+(4*8)+(3*7)+(2*7)+(1*5)=248
248 % 10 = 8
So 857787-75-8 is a valid CAS Registry Number.

857787-75-8Relevant academic research and scientific papers

Regioselective Alkoxycarbonylation of Allyl Phenyl Ethers Catalyzed by Pd/dppb under Syngas Conditions

Amézquita-Valencia, Manuel,Alper, Howard

, p. 3860 - 3867 (2016/05/24)

A simple and regioselective synthesis of phenoxy esters and phenylthio esters is reported. The products are obtained by selective alkoxycarbonylation catalyzed by Pd2(dba)3, 1,4-bis(diphenylphisphino)butane (dppb), and syngas (CO/H2) in chloroform/alcohol. This methodology affords bifunctional products in good yield with excellent n-selectivity and without the need to use additives.

DUAL MODULATION OF ENDOCANNABINOID TRANSPORT AND FATTY-ACID AMIDE HYDROLASE FOR TREATMENT OF EXCITOTOXICITY

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, (2010/09/18)

The endocannabinoid transporter and FAAH are sites of modulation that allow pharmacological enhancement of protective endocannabinergic signals. Selective inhibitors of the transporter and inhibitors of FAAH caused additive augmentation of endogenous signaling events mediated by the cannabinoid CB1 receptor.Disruption of such signals has been shown to prevent neuronal maintenance processes and increase vulnerability to brain damage. Here, blocking endocannabinoid inactivation enhanced cannabinergic activity and ameliorated cellular disturbances associated with excitotoxicity. Modulating the endocannabinoid system in this way also prevented excitotoxic behavioral abnormalities including memory impairment. Collectively, these results indicate that increasing endocannabinoid responses by inhibiting the endocannabinoid transported and/or the inhibiting FAAH leads to molecular, cellular, and functional protection against excitotoxic insults like stroke and traumatic brain injury.

MONOACYLGLYCEROL LIPASE INHIBITORS FOR MODULATION OF CANNABINOID ACTIVITY

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Page/Page column 114, (2009/05/28)

Disclosed are compounds and compositions that inhibit the action of monoacylglycerol lipase (MGL) and fatty acid amide hydrolase (FAAH), methods of inhibiting MGL and FAAH, methods of modulating cannabinoid receptors, and methods of treating various disorders related to the modulation of cannabinoid receptors.

FATTY ACID AMIDE HYDROLASE INHIBITORS

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Page/Page column 72-73, (2008/06/13)

Disclosed are compounds of formula R-X-Y that may be used to inhibit the action of fatty acid amide hydrolase (FAAH). Inhibition of fatty acid amide hydrolase (FAAH) will slow the normal degradation and inactivation of endogenous cannabinoid ligands by FAAH hydrolysis and allow higher levels of those endogenous cannabinergic ligands to remain present. These higher levels of endocannabinoid ligands provide increased stimulation of the cannabinoid CBl and CB2 receptors and produce physiological effects related to the activation of the cannabinoid receptors. They will also enhance the effects of other exogenous cannabinergic ligands and allow them to produce their effects at lower concentrations as compared to systems in which fatty acid amide hydrolase (FAAH) action is hot inhibited. Thus, a compound that inhibits the inactivation of endogenous cannabinoid ligands by fatty acid amide hydrolase (FAAH) may increase the levels of endocannabinoids and, thus, enhance the activation of cannabinoid receptors. Thus, the compound may not directly modulate the cannabinoid receptors but has the effect of indirectly stimulating the cannabinoid receptors by increasing the levels of endocannabinoid ligands. It may also enhance the effects and duration of action of other exogenous cannabinergic ligands that are administered in order to elicit a cannabinergic response.

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