Fusaric acid

Fusaric acid is an orally active multi-pathway inhibitor with the activity of inducing oxidative stress and apoptosis. Fusaric acid can chelate divalent metal cations, damage mitochondrial membrane structure, and activate apoptosis-related proteases such as Caspase-3/7, -8, and -9. Fusaric acid also regulates Bax/Bcl-2 protein, inhibits fibrosis-related signaling pathways such as NF-κB, TGF-β1/SMADs, and PI3K/AKT/mTOR, and reduces collagen deposition. Fusaric acid is also a dopamine β-hydroxylase inhibitor, which reduces endogenous levels of norepinephrine and epinephrine in the brain, heart, spleen, and adrenal glands. Fusaric acid can play a role in myocardial fibrosis and improve cardiac hypertrophy in heart disease, and can also be used in the study of esophageal cancer and liver cancer[1][2][3][4].

Product Specifications

CAS Number

[536-69-6]

UNSPSC

12352005

Hazard Statement

H302

Target

Adrenergic Receptor; Akt; Apoptosis; Dopamine β-hydroxylase; mTOR; NF-κB; PI3K; TGF-beta/Smad

Type

Natural Products

Related Pathways

Apoptosis; GPCR/G Protein; Metabolic Enzyme/Protease; Neuronal Signaling; NF-κB; PI3K/Akt/mTOR; Stem Cell/Wnt; TGF-beta/Smad

Applications

Metabolism-sugar/lipid metabolism

Field of Research

Cancer; Endocrinology; Cardiovascular Disease

Assay Protocol

https://www.medchemexpress.com/fusaric-acid.html

Concentration

10mM

Purity

99.94

Solubility

DMSO : 62.5 mg/mL (ultrasonic; warming; heat to 60°C) |H2O : 50 mg/mL (ultrasonic)

Smiles

O=C(C1=NC=C(CCCC)C=C1)O

Molecular Formula

C10H13NO2

Molecular Weight

179.22

Precautions

H302

References & Citations

[1]Devnarain N, et al. Fusaric acid induces oxidative stress and apoptosis in human cancerous oesophageal SNO cells. Toxicon. 2017 Feb;126:4-11.|[2]Jiao J, et al. Hydrogen peroxide production and mitochondrial dysfunction contribute to the fusaric acid-induced programmed cell death in tobacco cells. J Plant Physiol. 2014 Aug 15;171 (13) :1197-203.|[3]Li X, et al. Fusaric acid (FA) protects heart failure induced by isoproterenol (ISP) in mice through fibrosis prevention via TGF-β1/SMADs and PI3K/AKT signaling pathways. Biomed Pharmacother. 2017 Sep;93:130-145.|[4]Nagatsu T, et al. Inhibition of dopamine beta-hydroxylase by fusaric acid (5-butylpicolinic acid) in vitro and in vivo. Biochem Pharmacol. 1970 Jan;19 (1) :35-44.