10574-01-3

Basic information

• Product Name: (Z)-N-isopropyl-9-octadecenamide
• Synonyms: (Z)-N-isopropyl-9-octadecenamide;9-Octadecenamide, N-(1-methylethyl)-, (9Z)-;(Z)-N-(1-Methylethyl)-9-octadecenamide;N-Isopropyloleic amide;Einecs 234-161-5;Oleic acid, isopropylamide
• CAS NO: 10574-01-3
• Molecular Formula: C₂₁H₄₁NO
• Molecular Weight: 323.55634
• EINECS: 234-161-5
• Mol File: 10574-01-3.mol
• Article Data: 4

Chemical Properties

• Boiling Point: 461.6 °C at 760 mmHg
• Flash Point: 288 °C
• Appearance: /
• Density: 0.862 g/cm³
• Vapor Pressure: 1.06E-08mmHg at 25°C
• Refractive Index: 1.461
• CAS DataBase Reference: (Z)-N-isopropyl-9-octadecenamide(CAS DataBase Reference)
• NIST Chemistry Reference: (Z)-N-isopropyl-9-octadecenamide(10574-01-3)
• EPA Substance Registry System: (Z)-N-isopropyl-9-octadecenamide(10574-01-3)

Safety Data

• Hazardous Substances Data: 10574-01-3(Hazardous Substances Data)

Usage

General Description

"(Z)-N-isopropyl-9-octadecenamide" is a chemical compound with the molecular formula C22H43NO. It is also known as oleamide, and it is a member of the fatty acid primary amides. (Z)-N-isopropyl-9-octadecenamide is a white crystalline solid that is insoluble in water but soluble in organic solvents. It is commonly used as a slip agent, lubricant, and anti-foaming agent in the production of plastic and rubber materials. It also has potential applications as a surfactant, corrosion inhibitor, and anti-static agent. Additionally, (Z)-N-isopropyl-9-octadecenamide has been studied for its potential role in the regulation of sleep and as a neurotransmitter in the central nervous system.

InChI:InChI=1/C21H41NO/c1-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-21(23)22-20(2)3/h11-12,20H,4-10,13-19H2,1-3H3,(H,22,23)/b12-11-

Upstream product

• 112-80-1 cis-Octadecenoic acid 
• 75-31-0 isopropylamine 
• 112-77-6 (Z)-9-octadecenoyl chloride 

Relevant articles and documents

N-morpholino- and N-diethyl-analogues of palmitoylethanolamide increase the sensitivity of transfected human vanilloid receptors to activation by anandamide without affecting fatty acid amidohydrolase activity

The abilities of 19 analogues of palmitoylethanolamide and two analogues of oleoylethanolamide to affect the Ca2+ influx into human embryonic kidney cells expressing the human vanilloid receptor (hVR1-HEK293 cells) in response to anandamide (AEA) have been investigated using a FLIPR assay and a bovine serum albumin-containing assay medium. Only palmitoylethanolamide produced any effect in the absence of AEA. The ability of palmitoylethanolamide to potentiate the response to AEA was retained when the N-CH2CH2OH group was replaced by N-CH2CH2Cl,whereas replacement with N-alkyl substituents [from -H up to -(CH2)12CH3] resulted either in a reduction or in a complete loss of this activity. The tertiary amide N-(CH2CH3)2 (19) and N-morpholino (20) analogues of palmitoylethanolamide potentiated the response to 1 μM AEA to a greater degree than the parent compound, whereas the N-(CH3)2 analogue was inactive. 19 and 20 produced leftward shifts in the dose-response curve for AEA activation of Ca2+ influx into hVR1-HEK293 cells. EC50 values for AEA to produce Ca2+ influx into hVR1-HEK293 cells were 1.1, 1.1, 0.54 and 0.36 μM in the presence of 0, 1, 3 and 10 μM 19, respectively. The corresponding values for 20 were 1.5, 1.3, 0.77 and 0.17 μM, respectively. The compounds did not affect the dose-response curves to capsaicin. The ability of oleoylethanolamide to potentiate AEA is retained by the N-CH2CH3 and N-CH(CH3)2 analogues (22 and 23, respectively). 22 and 23 produced a small (～25%) inhibition of the binding of [3H]-CP55,940 and [3H]-WIN 55,212-2 to CB1 and CB2 receptors, respectively, expressed in CHO cells. The compounds inhibited the metabolism of 2 μM [3H]-AEA by rat brain fatty acid amidohydrolase with IC50 values of 5.6 and 11 μM, respectively. In contrast, 19 and 20 were without effect on either binding to CB receptors or fatty acid amidohydrolase activity. Minor reductions in the accumulation of 10 μM [3H]-AEA into C6 glioma cells were seen at 10 μM concentrations of 19 and 20. It is concluded that 19 and 20 selectively enhance AEA effects upon VR1 receptors without potentially confounding effects upon CB receptors or fatty acid amidohydrolase activity.

USE OF ENDOCANNABINOID-LIKE COMPOUNDS FOR TREATING CNS DEGENERATIVE DISORDERS

no abstract published