Avenanthramide C is an orally active polyphenolic compound that penetrates the blood-brain barrier. Avenanthramide C is derived from oats. Avenanthramide C inhibits NF-κB nuclear translocation and inhibits the phosphorylation of PI3K, PLCγ1, Lyn, Syk, and Akt. Avenanthramide C inhibits the expression and activity of MMP-9 and inhibits MAPK phosphorylation. Avenanthramide C scavenges DPPH radicals, reduces intracellular ROS, and inhibits pro-inflammatory cytokine release and adhesion molecule expression. Avenanthramide C inhibits cell degranulation. Avenanthramide C attenuates active systemic anaphylaxis and inhibits passive cutaneous anaphylaxis. Avenanthramide C ameliorates PHZ-induced blood stasis. Avenanthramide C inhibits neuroinflammation, restores long-term potentiation, and improves recognition and spatial memory in Alzheimer's disease models. Avenanthramide C can be used for research on allergic inflammation, thrombosis, atherosclerosis, and Alzheimer's disease [1] [2] [3] [4] [5].
In Vivo, Avenanthramide C (0.1-10 mg/kg; p.o.; administered on days 9, 11, and 13) dose-dependently attenuates ovalbumin-induced active systemic anaphylaxis by suppressing the decrease in body temperature and reducing elevated serum histamine, IgE, and IL-4 levels[1]. Avenanthramide C (0.1-10 mg/kg; p.o.; single dose; 1 h before DNP-HSA challenge) dose-dependently inhibits IgE-mediated passive cutaneous anaphylaxis[1]. Avenanthramide C (6 mg/kg; p.o.; daily; 2 weeks) rescues impaired long-term potentiation in 5XFAD Alzheimer's disease model mice[5]. Avenanthramide C (6 mg/kg; p.o.; daily; 2 weeks) rescues impaired long-term potentiation in Tg2576 Alzheimer's disease model mice[5]. Avenanthramide C (6 mg/kg; p.o.; once daily; 2 weeks) inhibits neuroinflammation in the hippocampus of 5XFAD and Tg2576 Alzheimer's disease model mice[5].
In Vitro, Avenanthramide C (0.01-100 µM; 12 h) is not cytotoxic up to 100 µM in RBL-2H3 cells[1]. Avenanthramide C (1-100 nM; 1 h) concentration-dependently inhibits β-hexosaminidase release in DNP-HSA-stimulated RBL-2H3 cells[1]. Avenanthramide C (1-100 nM; 1 h) concentration-dependently inhibits histamine release in DNP-HSA-stimulated RBL-2H3 cells[1]. Avenanthramide C (1-100 nM) suppresses DNP-HSA-stimulated intracellular calcium elevation in a concentration-dependent manner in RBL-2H3 cells[1]. Avenanthramide C (1-100 nM; 1 h) inhibits DNP-HSA-stimulated phosphorylation of PI3K and PLCγ1 in RBL-2H3 cells[1]. Avenanthramide C (1-100 nM; 1 h) concentration-dependently inhibits the gene expression and release of IL-4, IL-6, and TNF-α in DNP-HSA-stimulated RBL-2H3 cells[1]. Avenanthramide C (1-100 nM; 1 h) inhibits the phosphorylation of Lyn, Syk, and Akt and suppresses IκBα degradation and NF-κB nuclear translocation in DNP-HSA-stimulated RBL-2H3 cells[1]. Avenanthramide C (0-100 μM; 24 h) dose-dependently suppresses the TNF-α-induced increase in MMP-9 mRNA levels in HASMC cells[3]. Avenanthramide C (100 μM) inhibits the MAPK signaling pathway by decreasing phosphorylation of ERK, JNK, and p38, and reduces IκB phosphorylation in TNF-α-stimulated HASMC cells[3]. Avenanthramide C (50 μM; 2 h) restores impaired LTP in ex vivo hippocampal slices from 5XFAD mice[5]. Avenanthramide C (50 μM; 2 h) restores impaired LTP in ex vivo hippocampal slices from Tg2576 mice[5]. Avenanthramide C (1.0625-100 μg mL-1; 30 min) acts as a potent free radical scavenger in the cell-free DPPH assay with an IC50 of 7.38 μg mL-1[2]. Avenanthramide C (6.25-100 μg mL-1; 24 h) is non-toxic to HUVECs at concentrations up to 25 μg mL-1 but exhibits cytotoxic effects at 50 and 100 μg mL-1[2]. Avenanthramide C (6.25-25 μg mL-1; 24 h) dose-dependently attenuates intracellular ROS accumulation induced by t-BOOH in HUVECs[2].
References:
[1]. Dhakal H, et al. Avenanthramide C from germinated oats exhibits anti-allergic inflammatory effects in mast cells. Scientific reports. 2019 May 03;9(1):6884.
[2]. Wang LW, et al. Avenanthramide C from underutilized oat glumes exhibits dual anti-oxidant and anti-thrombotic effects in oxidative damage and thrombosis models. Food & function. 2025 Jul 01;16(13):5380-5392.
[3]. Park J, et al. Avenanthramide C Suppresses Matrix Metalloproteinase-9 Expression and Migration Through the MAPK/NF- κB Signaling Pathway in TNF-α-Activated HASMC Cells. Frontiers in pharmacology. 2021;12:621854.
[4]. Matsukawa T, et al. Occurrence of avenanthramides and hydroxycinnamoyl-CoA:hydroxyanthranilate N-hydroxycinnamoyltransferase activity in oat seeds. Zeitschrift fur Naturforschung. C, Journal of biosciences. 2000;55(1-2):30-6.
[5]. Ramasamy VS, et al. Avenanthramide-C Restores Impaired Plasticity and Cognition in Alzheimer's Disease Model Mice. Molecular neurobiology. 2020 Jan;57(1):315-330.
In Vivo, Avenanthramide C (0.1-10 mg/kg; p.o.; administered on days 9, 11, and 13) dose-dependently attenuates ovalbumin-induced active systemic anaphylaxis by suppressing the decrease in body temperature and reducing elevated serum histamine, IgE, and IL-4 levels[1]. Avenanthramide C (0.1-10 mg/kg; p.o.; single dose; 1 h before DNP-HSA challenge) dose-dependently inhibits IgE-mediated passive cutaneous anaphylaxis[1]. Avenanthramide C (6 mg/kg; p.o.; daily; 2 weeks) rescues impaired long-term potentiation in 5XFAD Alzheimer's disease model mice[5]. Avenanthramide C (6 mg/kg; p.o.; daily; 2 weeks) rescues impaired long-term potentiation in Tg2576 Alzheimer's disease model mice[5]. Avenanthramide C (6 mg/kg; p.o.; once daily; 2 weeks) inhibits neuroinflammation in the hippocampus of 5XFAD and Tg2576 Alzheimer's disease model mice[5].
In Vitro, Avenanthramide C (0.01-100 µM; 12 h) is not cytotoxic up to 100 µM in RBL-2H3 cells[1]. Avenanthramide C (1-100 nM; 1 h) concentration-dependently inhibits β-hexosaminidase release in DNP-HSA-stimulated RBL-2H3 cells[1]. Avenanthramide C (1-100 nM; 1 h) concentration-dependently inhibits histamine release in DNP-HSA-stimulated RBL-2H3 cells[1]. Avenanthramide C (1-100 nM) suppresses DNP-HSA-stimulated intracellular calcium elevation in a concentration-dependent manner in RBL-2H3 cells[1]. Avenanthramide C (1-100 nM; 1 h) inhibits DNP-HSA-stimulated phosphorylation of PI3K and PLCγ1 in RBL-2H3 cells[1]. Avenanthramide C (1-100 nM; 1 h) concentration-dependently inhibits the gene expression and release of IL-4, IL-6, and TNF-α in DNP-HSA-stimulated RBL-2H3 cells[1]. Avenanthramide C (1-100 nM; 1 h) inhibits the phosphorylation of Lyn, Syk, and Akt and suppresses IκBα degradation and NF-κB nuclear translocation in DNP-HSA-stimulated RBL-2H3 cells[1]. Avenanthramide C (0-100 μM; 24 h) dose-dependently suppresses the TNF-α-induced increase in MMP-9 mRNA levels in HASMC cells[3]. Avenanthramide C (100 μM) inhibits the MAPK signaling pathway by decreasing phosphorylation of ERK, JNK, and p38, and reduces IκB phosphorylation in TNF-α-stimulated HASMC cells[3]. Avenanthramide C (50 μM; 2 h) restores impaired LTP in ex vivo hippocampal slices from 5XFAD mice[5]. Avenanthramide C (50 μM; 2 h) restores impaired LTP in ex vivo hippocampal slices from Tg2576 mice[5]. Avenanthramide C (1.0625-100 μg mL-1; 30 min) acts as a potent free radical scavenger in the cell-free DPPH assay with an IC50 of 7.38 μg mL-1[2]. Avenanthramide C (6.25-100 μg mL-1; 24 h) is non-toxic to HUVECs at concentrations up to 25 μg mL-1 but exhibits cytotoxic effects at 50 and 100 μg mL-1[2]. Avenanthramide C (6.25-25 μg mL-1; 24 h) dose-dependently attenuates intracellular ROS accumulation induced by t-BOOH in HUVECs[2].
References:
[1]. Dhakal H, et al. Avenanthramide C from germinated oats exhibits anti-allergic inflammatory effects in mast cells. Scientific reports. 2019 May 03;9(1):6884.
[2]. Wang LW, et al. Avenanthramide C from underutilized oat glumes exhibits dual anti-oxidant and anti-thrombotic effects in oxidative damage and thrombosis models. Food & function. 2025 Jul 01;16(13):5380-5392.
[3]. Park J, et al. Avenanthramide C Suppresses Matrix Metalloproteinase-9 Expression and Migration Through the MAPK/NF- κB Signaling Pathway in TNF-α-Activated HASMC Cells. Frontiers in pharmacology. 2021;12:621854.
[4]. Matsukawa T, et al. Occurrence of avenanthramides and hydroxycinnamoyl-CoA:hydroxyanthranilate N-hydroxycinnamoyltransferase activity in oat seeds. Zeitschrift fur Naturforschung. C, Journal of biosciences. 2000;55(1-2):30-6.
[5]. Ramasamy VS, et al. Avenanthramide-C Restores Impaired Plasticity and Cognition in Alzheimer's Disease Model Mice. Molecular neurobiology. 2020 Jan;57(1):315-330.