Vaccine Lab / Alfa Chemistry
Sodium Octanoate

Our customer services representatives are available 24 hours a day, from Monday to Sunday.

CONTACT US

Sodium Octanoate

Catalog Number ACM1984061-2
CAS 1984-06-1
Structure
Synonyms Octanoic acid-2,4,6,8-13C4 sodium salt
IUPAC Name sodium;octanoate
Molecular Weight 166.19
Molecular Formula C8H15NaO2
Canonical SMILES CCCCCCCC(=O)[O-].[Na+]
InChI InChI=1S/C8H16O2.Na/c1-2-3-4-5-6-7-8(9)10;/h2-7H2,1H3,(H,9,10);/q;+1/p-1
InChI Key BYKRNSHANADUFY-UHFFFAOYSA-M
Melting Point 245 °C (dec.)
Purity ≥99%
Solubility Soluble in water
Appearance Powder
Complexity 94.1
Covalently-Bonded Unit Count 2
Defined Atom Stereocenter Count 0
EC Number 217-850-5
Exact Mass 166.09697400
Heavy Atom Count 11
Hydrogen Bond Acceptor Count 2
Hydrogen Bond Donor Count 0
Isomeric SMILES CCCCCCCC(=O)[O-].[Na+]
Monoisotopic Mass 166.09697400
pH 8.0-10.5 (100g/L in H₂O, 20°C)
Physical State Solid
Rotatable Bond Count 6
Storage Conditions Room temperature
Topological Polar Surface Area 40.1 Ų
Knowledge & Learning Case Study Q&A

The Protective Role of Sodium Octanoate in Traumatic Cardiac Arrest

Sodium octanoate alleviates cardiac and cerebral injury after traumatic cardiac arrest in a porcine model Lin Y, et al. The American Journal of Emergency Medicine, 2024, 78, 48-56.

The study indicates that early administration of sodium octanoate can significantly alleviate cardiac and cerebral injuries following traumatic cardiac arrest (TCA) by inhibiting apoptosis and ferroptosis. These findings suggest that sodium octanoate could offer a novel therapeutic approach for improving outcomes in TCA patients by protecting against post-resuscitation damage.
Methods: The study utilized 22 male domestic pigs, divided into three groups: Sham (n = 7), TCA (n = 7), and sodium octanoate (SO) (n = 8). TCA was induced by hemorrhage via the right femoral artery. The Sham group underwent endotracheal intubation and catheterization without blood loss or resuscitation. Five minutes post-resuscitation, the SO group received a continuous infusion of sodium octanoate, while the TCA group received saline. Biomarkers for cardiac and cerebral injury were monitored at baseline and various time points, and samples of heart and brain tissues were analyzed for apoptosis, iron deposition, oxidative stress, and ferroptosis-related protein expression (ACSL4 and GPX4).
Results: Sodium octanoate infusion significantly improved mean arterial pressure, cardiac output, and ejection fraction post-TCA. The SO group exhibited lower levels of serum biomarkers indicative of cardiac and cerebral injury compared to the TCA group. Furthermore, sodium octanoate reduced apoptosis rates in cardiomyocytes and cerebral cortex cells and decreased iron deposition and oxidative stress. It also downregulated ferroptosis by modulating ACSL4 and GPX4 protein levels.

Our products and services are for research use only and cannot be used for any clinical purposes.

Online Inquiry
Verification code