Methyl syringate

Methyl syringate is a selective TRPA1 agonist. Methyl syringate regulates food intake and gastric emptying through a TRPA1-mediated pathway. Methyl syringate is an efficient phenolic mediator for bacterial and fungal laccases. Methyl syringate is a chemical marker of Asphodel monofloral honey. Methyl syringate contributes to the antibacterial activity of honey. Methyl syringate inhibits aflatoxin production. Methyl syringate can contribute to weight suppression. Methyl syringate can be studies for cancer prevention (e.g. lung cancer), suppression of hypoxia-induced inflammatory response and tumorigenesis^[1][2][3][4]. IC50 & Target:TRPA1^[3]. In Vitro:Methyl syringate (0.1-1 mM, pretreatment for 1 h then co-treatment under hypoxia for 24 h) effectively blocks hypoxia-induced COX-2 protein expression is a dose dependent manner and inhibits induction of COX-2 mRNA and promoter activity in A549 cells under hypoxic conditions^[4].
Methyl syringate (1 mM, 1 h) represses COX-2 and cell migration in HT-1080 cells^[4].
Methyl syringate (1-100 μM) inhibits catalytic activity of PTPN2 and PTPN6 with IC₅₀ values of 6.95 and 7.31 μM in E. coli cells overexpressing PTPN2 and PTPN6^[5].
Methyl syringate (10-20 μM, 6 h) stimulates the glucose uptake in differentiated 3T3-L1 adipocytes and C2C12 muscle cells^[5].
Methyl syringate (5-20 μM, 6 h) significantly increases AMPK phosphorylation in 3T3-L1 adipocytes at 10 or 20 μM dosage^[5].
Methyl syringate (1-20 μM, 6 d) does not affect adipocyte differentiation in differentiated 3T3-L1 preadipocytes, indicating it does not induce lipid accumulation^[5].
In Vivo:Methyl syringate (10 mg/kg, p.o., one single dose) significantly reduces the cumulative food intake 24 h after treatment in male ICR mice experienced fasting and allowed ad libitum access of food and water^[1].
Methyl syringate (0.1-10 mg/kg, p.o., one single dose) significantly decreases the food remaining in the stomach 28 h after treatment in male ICR mice ^[1].