Evernic Acid

Evernic Acid is an orally active thioredoxin reductase 1 (TrxR1) inhibitor and antiproliferative agent. Evernic Acid inhibits the proliferation and migration of human breast cancer cells. Evernic Acid blocks the NF-κB pathway by inhibiting p65 nuclear translocation and IκBα phosphorylation, thereby suppressing downstream inflammatory mediators. Evernic Acid acts as an antioxidant, anti-inflammatory agent and neuroprotective agent, protects neurons from cell death, mitochondrial dysfunction and oxidative stress damage, reduces astrocyte activation, and ameliorates dopaminergic neuron loss and neuroinflammation. Evernic Acid inhibits enoyl reductases FabI and FabZ of Plasmodium falciparum. Evernic Acid downregulates the expression of lasB and rhlA genes in Pseudomonas aeruginosa, inhibits quorum sensing and biofilm formation, and exerts antibacterial activity against Gram-positive bacteria, Gram-negative bacteria and fungi. Evernic Acid is applicable to research related to breast cancer, Parkinson's disease, bacterial infections and fungal infections^[1][2][3]. In Vitro: Evernic acid (10-150 μg/mL; 24-52 h) exerts dose-dependent antiproliferative effects on human breast cancer MCF-7 and MDA-MB-453 cell lines, with an IC₅₀ of 33.79 μg/mL at 52 h for MCF-7 cells and 121.40 μg/mL at 48 h for MDA-MB-453 cells^[1].
Evernic acid (33.79-121.40 μg/mL; 48-52 h) upregulates TrxR1 gene expression in human breast cancer MCF-7 cells and downregulates TrxR1 gene expression in MDA-MB-453 cells when treated at respective IC₅₀ concentrations for 52 h (MCF-7) and 48 h (MDA-MB-453)^[1].
Evernic acid (33.79-121.40 μg/mL; 12-24 h) inhibits migration of human breast cancer MCF-7 and MDA-MB-453 cell lines when treated at respective IC₅₀ concentrations, with significant inhibition observed at 24 h for MCF-7 cells and at 12 and 24 h for MDA-MB-453 cells^[1].
Evernic acid (33.79-121.40 μg/mL; 48-52 h) suppresses intracellular TrxR1 enzyme activity by 25% in human breast cancer MCF-7 cells and 30% in MDA-MB-453 cells when treated at respective IC₅₀ concentrations for 52 h (MCF-7) and 48 h (MDA-MB-453)^[1].
Evernic acid (1-100 μM; 6 h pre-incubation followed by 24 h co-treatment with MPP⁺) suppresses MPP⁺-induced apoptotic morphological changes in primary rat cortical neurons, and 100 μM evernic acid normalizes MPP⁺-altered Bcl-2/Bax protein expression balance^[2].
Evernic acid (100 μM; 6 h pre-incubation followed by 6 h co-treatment with MPP⁺) protects primary rat cortical neurons from MPP⁺-induced mitochondrial membrane potential loss^[2].
Evernic acid (0.1-100 μM; 6 h pre-incubation prior to MPP⁺ co-treatment) dose-dependently suppresses MPP⁺-induced ROS generation in primary rat cortical neurons^[2].
Evernic acid (100 μM; 6 h pre-incubation followed by 1 h or 24 h co-treatment with MPP⁺) inhibits the NF-κB signaling pathway in primary rat astrocytes exposed to MPP⁺, by blocking p65 nuclear translocation, reducing IκBα phosphorylation, and lowering COX-2 expression^[2].
Evernic acid (100 μM; 6 h pre-incubation prior to MPP⁺ co-treatment) suppresses MPP⁺-induced increases in pro-inflammatory cytokine (IL-1β, IL-6, TNF-α) and chemokine (CCL2) mRNA expression in primary rat astrocytes^[2].
Evernic acid (as the primary component of fraction VI) inhibits the growth of Staphylococcus aureus ATCC 29213 (MIC 0.98 μg/mL), Pseudomonas aeruginosa ATCC 27853 (MIC 31.25 μg/mL), Escherichia coli ATCC 25922 (MIC 125 μg/mL), and Candida albicans ATCC 90028 (MIC 62.5 μg/mL) in vitro^[3].
Evernic acid inhibits the expression of quorum-sensing-dependent virulence genes lasB and rhlA in Pseudomonas aeruginosa in vitro^[3]. In Vivo: Evernic acid (5-80 mg/kg; p.o.; daily; 10 days) significantly accelerates motor function recovery, attenuates dopaminergic neuronal loss, and suppresses astroglial activation in MPTP-induced Parkinson’s disease model mice^[2].