60563-13-5

Usage

Uses

Used in Pharmaceutical Industry:
Ethyl homovanillate is used as an inhibitor for monoamine oxidase A (MAOA) due to its strong inhibitory effects on the enzyme. This application is particularly relevant in the treatment of various psychiatric and neurological disorders, as MAOA inhibition can help regulate the levels of monoamines in the brain, which are essential for mood regulation and cognitive function.
Used in Nutraceutical Industry:
In the nutraceutical industry, ethyl homovanillate can be used as a dietary supplement or additive to promote overall brain health and cognitive function. Its MAOA inhibitory properties can contribute to the enhancement of mood and the prevention of age-related cognitive decline.
Used in Cosmetic Industry:
Ethyl homovanillate can also be utilized in the cosmetic industry for its potential anti-aging and skin health benefits. ETHYL HOMOVANILLATE's ability to inhibit MAOA may help promote skin cell regeneration and improve overall skin health, making it a valuable ingredient in anti-aging and skincare products.
Used in Research and Development:
Due to its strong inhibitory effects on MAOA, ethyl homovanillate can be used in research and development for the creation of new drugs and therapies targeting psychiatric and neurological disorders. Its unique chemical properties make it a valuable tool for understanding the role of monoamines in these conditions and for developing novel treatment strategies.

InChI:InChI=1/C11H14O4/c1-3-15-11(13)7-8-4-5-9(12)10(6-8)14-2/h4-6,12H,3,7H2,1-2H3

Upstream product

• 64-17-5 ethanol 
• 306-08-1 Homovanillic acid 
• 90-05-1 2-methoxy-phenol 
• 55-10-7 4-hydroxy-3-methoxy-mandelic acid 
• 498-00-0 4-hydroxymethyl-2-methoxyphenol 
• 50-81-7 ascorbic acid 

Downstream Products

• 107512-56-1 2-(4-Hydroxy-3-methoxy-phenyl)-N-((E)-octadec-9-enyl)-acetamide 
• 154051-81-7 ethyl 3-methoxy-4-trimethylacetoxyphenylacetate 
• 925439-19-6 [3-methoxy-4-(2-pyrrolidin-1-yl-ethoxy)-phenyl]-acetic acid ethyl ester 
• 960041-24-1 [3-methoxy-4-(2-methoxyethoxy)phenyl]acetic acid ethyl ester 
• 765302-46-3 ethyl (3-methoxy-4-{[(trifluoromethyl)sulfonyl]oxy}phenyl)acetate 
• 148452-82-8 3-Methoxy-4-(tetradecyloxy)benzeneacetic acid ethyl ester 
• 111627-50-0 4-(3-chloropropoxy)-3-methoxybenzeneacetic acid ethyl ester 
• 1207544-60-2 C₁₈H₁₆ClNO₄ 
• 1037077-53-4 2-(4-hydroxy-3-methoxyphenyl)ethyl acetate 
• 1092166-83-0 [3-methoxy-4-(2-methoxy-ethoxymethoxy)-phenyl]-ethyl acetate 
• 1258845-38-3 (3-bromo-4-hydroxy-5-methoxyphenyl)acetic acid ethyl ester 
• 1258845-44-1 (3-methoxy-4-methoxymethoxyphenyl)acetic acid ethyl ester 
• 934231-71-7 ethyl [3-methoxy-4-(piperidin-4-yloxy)phenyl]acetate hydrochloride 
• 180304-16-9 ethyl 4-(2-azidoethoxy)-3-methoxyphenylacetate 

Relevant academic research and scientific papers

METHOD FOR PRODUCING ESTERS OF HOMOVANILLIC ACID

The present invention primarily relates to a method for producing a compound of formula (I) and/or a physiologically acceptable salt thereof from vanillylmandelic acid and/or a physiologically acceptable salt thereof. The present invention further relates to the simultaneous use of one or more iodide salt(s) or hydrate(s) thereof, one or more reducing agent(s), one or more inorganic and/or organic acid(s) other than phosphonic acid, and methanol and/or a physiologically acceptable salt thereof or an alcohol of formula (II) as defined herein and/or a physiologically acceptable salt thereof for converting vanillylmandelic acid and/or a physiologically acceptable salt thereof into a compound of formula (I) and/or a physiologically acceptable salt thereof or into a compound of formula (III) as defined herein and/or a physiologically acceptable salt thereof.

Phenylacetic acid ester compound and use thereof

The invention relates to a phenylacetate compound as shown in a general formula (I) and a pharmaceutical composition containing the phenylacetate compound, as well as application in anesthesia and sedation.

Biological evaluation of natural and synthesized homovanillic acid esters as inhibitors of intestinal fatty acid uptake in differentiated Caco-2 cells

With raising prevalence of obesity, the regulation of human body fat is increasingly relevant. The modulation of fatty acid uptake by enterocytes represents a promising target for body weight maintenance. Recent results demonstrated that the trigeminal active compounds capsaicin, nonivamide, and trans-pellitorine dose-dependently reduce fatty acid uptake in differentiated Caco-2 cells as a model for the intestinal barrier. However, non-pungent alternatives have not been investigated and structural determinants for the modulation of intestinal fatty acid uptake have not been identified so far. Thus, based on the previous results, we synthesized 23 homovanillic acid esters in addition to the naturally occurring capsiate and screened them for their potential to reduce intestinal fatty acid uptake using the fluorescent fatty acid analog Bodipy-C12 in differentiated Caco-2 cells as an enterocyte model. Whereas pre-incubation with 100 μM capsiate did not change fatty acid uptake by Caco-2 enterocytes, a maximum inhibition of ?47% was reached using 100 μM 1-methylpentyl-2-(4-hydroxy-3-methoxy-phenyl)acetate. Structural analysis of the 24 structural analogues tested in the present study revealed that a branched fatty acid side chain, independent of the chain length, is one of the most important structural motifs associated with inhibition of fatty acid uptake in Caco-2 enterocytes. The results of the present study may serve as an important basis for designing potent dietary inhibitors of fatty acid uptake.

HOMOVANILLIC ESTER, MORE PARTICULARLY FOR ACHIEVING AN IMPRESSION OF HEAT AND/OR SPICINESS

Compounds of formula (I) and novel uses of compounds of formula (I), such as for flavour compositions. New preparations and new methods using compounds of formula (I).

The SAR analysis of TRPV1 agonists with the α-methylated B-region

A series of TRPV1 agonists with amide, reverse amide, and thiourea groups in the B-region and their corresponding α-methylated analogues were investigated. Whereas the α-methylation of the amide B-region enhanced the binding affinities and potencies as agonists, that of the reverse amide and thiourea led to a reduction in receptor affinity. The analysis indicated that proper hydrogen bonding as well as steric effects in the B-region are critical for receptor binding.

Receptor activity and conformational analysis of 5′-halogenated resiniferatoxin analogs as TRPV1 ligands

A series of 5′-halogenated resiniferatoxin analogs have been investigated in order to examine the effect of halogenation in the A-region on their binding and the functional pattern of agonism/antagonism for rat TRPV1 heterologously expressed in Chinese hamster ovary cells. Halogenation at the 5-position in the A-region of RTX and of 4-amino RTX shifted the agonism of parent compounds toward antagonism. The extent of antagonism was greater as the size of the halogen increased (I > Br > Cl > F) while the binding affinities were similar, as previously observed for our potent agonists. In this series, 5-bromo-4-amino RTX (39) showed very potent antagonism with K i (ant) = 2.81 nM, which was thus 4.5-fold more potent than 5′-iodo RTX, previously reported as a potent TRPV1 antagonist. Molecular modeling analyses with selected agonists and the corresponding halogenated antagonists revealed a striking conformational difference. The 3-methoxy of the A-region in the agonists remained free to interact with the receptor whereas in the case of the antagonists, the compounds assumed a bent conformation, permitting the 3-methoxy to instead form an internal hydrogen bond with the C4-hydroxyl of the diterpene.

Halogenation of 4-hydroxy/amino-3-methoxyphenyl acetamide TRPV1 agonists showed enhanced antagonism to capsaicin

As an extension of our analysis of the effect of halogenation on thiourea TRPV1 agonists, we have now modified selected 4-hydroxy(or 4-amino)-3- methoxyphenyl acetamide TRPV1 agonists by 5- or 6-halogenation on the aromatic A-region and evaluated them for potency for TRPV1 binding and regulation and for their pattern of agonism/antagonism (efficacy). Halogenation shifted the functional activity at TRPV1 toward antagonism with a greater extent of antagonism as the size of the halogen increased (I > Br > Cl), as previously observed for the thiourea series. The extent of antagonism was greater for halogenation at the 5-position than at the 6-position, in contrast to SAR for the thiourea series. In this series, compounds 55 and 75 showed the most potent antagonism, with Ki (ant) = 2.77 and 2.19 nM, respectively, on rTRPV1 expressed in Chinese hamster ovary cells. The compounds were thus ca. 40-60-fold more potent than 6′-iodononivamide.