128502-58-9

Upstream product

• 593-71-5 Chloroiodomethane 
• 1462-75-5 3-phenylpropylmagnesium bromide 
• 61440-32-2 8-phenyloctyl chloride 
• 10472-97-6 8-phenyloctan-1-ol 

Downstream Products

• 1026866-56-7 6-Methyl-3-(8-phenyl-octyloxy)-pyridine-2-carbaldehyde 
• 159977-14-7 ethyl 2-(4-nitrophenyl)-10-phenyldecanoate 
• 1415221-93-0 8--phenyloctyl--N--Boc--(2S)--2--amino--3--(1--(8--phenyloctyl)--1H--indol--3-yl)propanoate 

Relevant academic research and scientific papers

One-pot, one- and multi-carbon homologation of alkyl halides; reaction of Grignard reagents with chloroiodomethane

Reaction of a Grignard reagent (RMgX) with chloroiodomethane affords the corresponding iodide (RI) and, depending on R, solvent and temperature, iodides which are one-carbon and multicarbon homologs of RX. Allyl iodide but not allyl bromide can be monohomologated by the combined action of chloroiodomethane and isopropyl Grignard.

Non-proteinogenic amino acids in the pThr-2 position of a pentamer peptide that confer high binding affinity for the polo box domain (PBD) of polo-like kinase 1 (Plk1)

We report herein that incorporating long-chain alkylphenyl-containing non-proteinogenic amino acids in place of His at the pT-2 position of the parent polo-like kinase 1 (Plk1) polo box domain (PBD)-binding pentapeptide, PLHSpT (1a) increases affinity. Fo

Sulfonyl fluoride inhibitors of fatty acid amide hydrolase

Sulfonyl fluorides are known to inhibit esterases. Early work from our laboratory has identified hexadecyl sulfonylfluoride (AM374) as a potent in vitro and in vivo inhibitor of fatty acid amide hydrolase (FAAH). We now report on later generation sulfonyl

MONOACYLGLYCEROL LIPASE INHIBITORS FOR MODULATION OF CANNABINOID ACTIVITY

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

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.

1,3-benzenedimethanamines useful as central nervous system active agents

Pharmaceutical compounds of the formula: STR1 R1 to R8 are each hydrogen or C1-4 alkyl, m, n and p are each 0, 1, or 2, q is 0, 1, 2 or 3, X and Z are each C1-4 alkyl, C1-4 alkoxy, hydroxy, nitro, cyano, halo, trihalomethyl, carboxy, C1-4 alkoxy-carbonyl or phenyl, and in addition z, together with the phenyl ring to which it is attached, can be: STR2 Y is --O--, --S-- or --CH2 --, V is --(CH2)r -- or --(CH2)r S-- where r is 1 to 15, and W is hydrogen or optionally substituted phenyl; and salts thereof.