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Merck

A6855

Arachidonoyl-AMC

fatty acid amide hydrolase substrate, 99% (HPLC), solid

Synonym(s):

AAMCA

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About This Item

Empirical Formula (Hill Notation):
C30H39NO3
Molecular Weight:
461.64
UNSPSC Code:
12352204
PubChem Substance ID:
24891145
NACRES:
NA.32
MDL number:
MFCD08062144

Product Name

Arachidonoyl-AMC, fatty acid amide hydrolase substrate

SMILES string

CCCCC\C=C/C\C=C/C\C=C/C\C=C/CCCC(=O)Nc1ccc2C(C)=CC(=O)Oc2c1

InChI key

IQPBUDMTXHWSHB-ZKWNWVNESA-N

InChI

1S/C30H39NO3/c1-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-20-29(32)31-26-21-22-27-25(2)23-30(33)34-28(27)24-26/h7-8,10-11,13-14,16-17,21-24H,3-6,9,12,15,18-20H2,1-2H3,(H,31,32)/b8-7-,11-10-,14-13-,17-16-

assay

99% (HPLC)

form

solid

storage condition

under inert gas

solubility

DMSO: soluble

storage temp.

−20°C

Quality Level

100

Application

Fluorogenic substrate used in a selective and sensitive assay of fatty acid amide hydrolase (FAAH).

Storage Class

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Certificates of Analysis (COA)

Lot/Batch Number
MKCZ5455
MKCZ5721
MKCV0794
MKCS7574
MKCM6219

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Simona Di Martino et al.
Journal of medicinal chemistry, 63(7), 3634-3664 (2020-03-17)
Sphingolipids (SphLs) are a diverse class of molecules that are regulated by a complex network of enzymatic pathways. A disturbance in these pathways leads to lipid accumulation and initiation of several SphL-related disorders. Acid ceramidase is one of the key
Enrico Dainese et al.
Scientific reports, 10(1), 2292-2292 (2020-02-12)
Fatty acid amide hydrolase (FAAH) is a membrane-bound homodimeric enzyme that in vivo controls content and biological activity of N-arachidonoylethanolamine (AEA) and other relevant bioactive lipids termed endocannabinoids. Parallel orientation of FAAH monomers likely allows both subunits to simultaneously recruit
Xinwen Zhang et al.
Neuropharmacology, 128, 269-281 (2017-10-25)
Monoacylglycerol lipase (MGL) hydrolyzes 2-arachidonoylglycerol to arachidonic acid and glycerol. Inhibition of MGL may attenuate neuroinflammation by enhancing endocannabinoid signaling and decreasing prostaglandin (PG) production. Almost half of HIV infected individuals are afflicted with HIV-associated neurocognitive disorder (HAND), a neuroinflammatory

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