Nonivamide (Synonyms: Nonanoic Acid Vanillylamide, NSC 172795, Pelargonic Acid Vanillylamide, Pseudocapsaicin, N-Vanillylnonanamide, N-Vanillylpelargonamide)

Nonivamide is a agonist, which exhibits 4d-EC50 value of 5.1 mg/L in static toxicity tests.

Nonivamide, a synthetic derivate of natural capsaicin, has an effective antifouling activity. Capsaicin exhibits 4d-EC50 values of 5.5±0.5 mg/L, 23±2 mg/L, 6.9±0.2 mg/L, and 15.6±0.4 mg/L in static toxicity tests conducted using Pseudomonas putida, Lake Erie bacteria, Vibrio natriegens, and Vibrio parahaemolyticus, respectively. A significant growth inhibitory effect (p<0.01) is observed in the group treated with 1 mg/L of Nonivamide for 4 d, and the EC50 value (4 d-EC50) is 5.1 mg/L[1]. Nonivamide treatment causes calcium release from the ER and altered the transcription of growth arrest- and DNA damage-inducible transcript 3 (GADD153), GADD45α, GRP78/BiP, ATF3, CCND1, and CCNG2) in a manner comparable with prototypical ER stress-inducing agents. ER calcium flux is evaluated by pretreating cells with 2.5 μM thapsigargin for 5 min followed by addition of 2.5 μM Nonivamide. Treatment of TRPV1-overexpressing cells with 2.5 μM Nonivamide produces marked increases in cytosolic calcium due to release of calcium from ER stores. Treatment of TRPV1-overexpressing cells with 1 μM Nonivamide causes an approximate 50% loss in cell viability after a 24-h period. BEAS-2B cells treated with 100 and 200 μM Nonivamide also exhibits a shift in the relative amount of EIF2α-P and an increase in the expression of GADD153 mRNA and protein[2]. Treatment with Nonivamide reduces lipid accumulation to a similar extent as CAP; the effects are not different from the effects after CAP treatment at any of the tested concentrations. Compared to untreated control cells, treatment with Nonivamide decreases lipid accumulation by 5.34±1.03% (P<0.05) at 0.01 µM up to 10.4±2.47% (P<0.001) at 1 µM[3].

References:
[1]. Zhou J, et al. Toxic effects of environment-friendly antifoulant Nonivamide on Phaeodactylum tricornutum. Environ Toxicol Chem. 2013 Apr;32(4):802-9.
[2]. Thomas KC, et al. Transient receptor potential vanilloid 1 agonists cause endoplasmic reticulum stress and cell death in human lung cells. J Pharmacol Exp Ther. 2007 Jun;321(3):830-8.
[3]. Rohm B, et al. Nonivamide enhances miRNA let-7d expression and decreases adipogenesis PPARγ expression in 3T3-L1 cells. J Cell Biochem. 2015 Jun;116(6):1153-63.