OCTANOIC ACID
Relevant Data
Food Additives Approved by WHO:
Flavouring Substances Approved by European Union:
General Information
| Mainterm | OCTANOIC ACID |
| Doc Type | ASP |
| CAS Reg.No.(or other ID) | 124-07-2 |
| Regnum |
178.1010 173.370 173.315 173.340 172.210 172.860 184.1025 |
From www.fda.gov
Computed Descriptors
Download SDF| 2D Structure | |
| CID | 379 |
| IUPAC Name | octanoic acid |
| InChI | InChI=1S/C8H16O2/c1-2-3-4-5-6-7-8(9)10/h2-7H2,1H3,(H,9,10) |
| InChI Key | WWZKQHOCKIZLMA-UHFFFAOYSA-N |
| Canonical SMILES | CCCCCCCC(=O)O |
| Molecular Formula | C8H16O2 |
| Wikipedia | caprylic acid |
From Pubchem
Computed Properties
| Property Name | Property Value |
|---|---|
| Molecular Weight | 144.214 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 2 |
| Rotatable Bond Count | 6 |
| Complexity | 89.3 |
| CACTVS Substructure Key Fingerprint | A A A D c e B w M A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A G g A A C A A A C A C A g A A C C A A A A g A I A A C Q C A A A A A A A A A A A A A E A A A A A A B I A A A A A Q A A E A A A A A A G I y K C A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A = = |
| Topological Polar Surface Area | 37.3 |
| Monoisotopic Mass | 144.115 |
| Exact Mass | 144.115 |
| Compound Is Canonicalized | True |
| Formal Charge | 0 |
| Heavy Atom Count | 10 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Isotope Atom Count | 0 |
| Covalently-Bonded Unit Count | 1 |
From Pubchem
Food Additives Biosynthesis/Degradation
ADMET Predicted Profile --- Classification
| Model | Result | Probability |
|---|---|---|
| Absorption | ||
| Blood-Brain Barrier | BBB+ | 0.9488 |
| Human Intestinal Absorption | HIA+ | 0.9888 |
| Caco-2 Permeability | Caco2+ | 0.8326 |
| P-glycoprotein Substrate | Non-substrate | 0.6321 |
| P-glycoprotein Inhibitor | Non-inhibitor | 0.9598 |
| Non-inhibitor | 0.9277 | |
| Renal Organic Cation Transporter | Non-inhibitor | 0.9266 |
| Distribution | ||
| Subcellular localization | Mitochondria | 0.5152 |
| Metabolism | ||
| CYP450 2C9 Substrate | Non-substrate | 0.7886 |
| CYP450 2D6 Substrate | Non-substrate | 0.8956 |
| CYP450 3A4 Substrate | Non-substrate | 0.6982 |
| CYP450 1A2 Inhibitor | Inhibitor | 0.8326 |
| CYP450 2C9 Inhibitor | Non-inhibitor | 0.8808 |
| CYP450 2D6 Inhibitor | Non-inhibitor | 0.9554 |
| CYP450 2C19 Inhibitor | Non-inhibitor | 0.9578 |
| CYP450 3A4 Inhibitor | Non-inhibitor | 0.9484 |
| CYP Inhibitory Promiscuity | Low CYP Inhibitory Promiscuity | 0.9647 |
| Excretion | ||
| Toxicity | ||
| Human Ether-a-go-go-Related Gene Inhibition | Weak inhibitor | 0.9322 |
| Non-inhibitor | 0.8868 | |
| AMES Toxicity | Non AMES toxic | 0.9865 |
| Carcinogens | Non-carcinogens | 0.6452 |
| Fish Toxicity | High FHMT | 0.9144 |
| Tetrahymena Pyriformis Toxicity | High TPT | 0.9990 |
| Honey Bee Toxicity | High HBT | 0.6691 |
| Biodegradation | Ready biodegradable | 0.8795 |
| Acute Oral Toxicity | IV | 0.6378 |
| Carcinogenicity (Three-class) | Non-required | 0.7057 |
From admetSAR
ADMET Predicted Profile --- Regression
| Model | Value | Unit |
|---|---|---|
| Absorption | ||
| Aqueous solubility | -3.5022 | LogS |
| Caco-2 Permeability | 1.3950 | LogPapp, cm/s |
| Distribution | ||
| Metabolism | ||
| Excretion | ||
| Toxicity | ||
| Rat Acute Toxicity | 1.3275 | LD50, mol/kg |
| Fish Toxicity | 1.8920 | pLC50, mg/L |
| Tetrahymena Pyriformis Toxicity | 0.3852 | pIGC50, ug/L |
From admetSAR
Toxicity Profile
| Route of Exposure | Ingestion |
|---|---|
| Mechanism of Toxicity | It has been demonstrated that octanoic (OA) and decanoic (DA) acids compromise the glycolytic pathway and citric acid cycle functioning, increase oxygen consumption in the liver and inhibit some activities of the respiratory chain complexes and creatine kinase in rat brain . These fatty acids were also shown to induce oxidative stress in the brain . Experiments suggest that OA and DA impair brain mitochondrial energy homeostasis that could underlie at least in part the neuropathology of MCADD. |
| Metabolism | The enzyme MCAD (medium-chain acyl-CoA dehydrogenase) is responsible for the dehydrogenation step of fatty acids with chain lengths between 6 and 12 carbons as they undergo beta-oxidation in the mitochondria. Fatty acid beta-oxidation provides energy after the body has used up its stores of glucose and glycogen. This typically occurs during periods of extended fasting or illness when caloric intake is reduced, and energy needs are increased. Beta-oxidation of long chain fatty acids produces two carbon units, acetyl-CoA and the reducing equivalents NADH and FADH2. NADH and FADH2 enter the electron transport chain and are used to make ATP. Acetyl-CoA enters the Krebs Cycle and is also used to make ATP via the electron transport chain and substrate level phosphorylation. When the supply of acetyl-CoA (coming from the beta-oxidation of fatty acids) exceeds the capacity of the Krebs Cycle to metabolize acetyl-CoA, the excess acetyl-CoA molecules are converted to ketone bodies (acetoacetate and beta-hydroxybutyrate) by HMG-CoA synthase in the liver. Ketone bodies can also be used for energy especially by the brain and heart; in fact they become the main sources of energy for those two organs after day three of starvation. (Wikipedia) |
| Toxicity Values | Oral rat LD<sub>50</sub>: 10080 mg/kg. Intravenous mouse LD<sub>50</sub>: 600 mg/kg. Skin rabbit LD<sub>50</sub>: over 5000 mg/kg. |
| Lethal Dose | |
| Carcinogenicity (IARC Classification) | No indication of carcinogenicity to humans (not listed by IARC). |
| Minimum Risk Level | |
| Health Effects | Octanoic (OA) and decanoic (DA) acids are the predominant metabolites accumulating in medium-chain acyl-CoA dehydrogenase (MCAD; E.C. 1.3.99.3) deficiency (MCADD), the most common inherited defect of fatty acid oxidation. Glycine and l-carnitine bind to these fatty acids giving rise to derivatives that also accumulate in this disorder. The clinical presentation typically occurs in early childhood but can occasionally be delayed until adulthood. The major features of the disease include hypoglycemia, vomiting, lethargy and encephalopathy after fasting, infection or other metabolic stressors. (A15457) |
| Treatment | Management of acute MCADD includes rapid correction of hypoglycemia, rehydration and treatment of the underlying infection or other stress factor. Current long-term therapy includes avoidance of fasting and a high carbohydrate low-fat diet, but it does not fully prevent the crises and the neurological alterations. |
| Reference |
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From T3DB
Taxonomic Classification
| Kingdom | Organic compounds |
|---|---|
| Superclass | Lipids and lipid-like molecules |
| Class | Fatty Acyls |
| Subclass | Fatty acids and conjugates |
| Intermediate Tree Nodes | Not available |
| Direct Parent | Medium-chain fatty acids |
| Alternative Parents | |
| Molecular Framework | Aliphatic acyclic compounds |
| Substituents | Medium-chain fatty acid - Straight chain fatty acid - Monocarboxylic acid or derivatives - Carboxylic acid - Carboxylic acid derivative - Organic oxygen compound - Organic oxide - Hydrocarbon derivative - Organooxygen compound - Carbonyl group - Aliphatic acyclic compound |
| Description | This compound belongs to the class of organic compounds known as medium-chain fatty acids. These are fatty acids with an aliphatic tail that contains between 4 and 12 carbon atoms. |
From ClassyFire
Targets
- General Function:
- 3-oxoacyl-[acyl-carrier-protein] synthase activity
- Specific Function:
- Catalyzes the condensation reaction of fatty acid synthesis by the addition to an acyl acceptor of two carbons from malonyl-ACP. Specific for elongation from C-10 to unsaturated C-16 and C-18 fatty acids.
- Gene Name:
- fabB
- Uniprot ID:
- P0A953
- Molecular Weight:
- 42612.995 Da
- General Function:
- Phospholipase activity
- Specific Function:
- Hydrolyzes only long chain acyl thioesters (C12-C18). Specificity similar to chymotrypsin.
- Gene Name:
- tesA
- Uniprot ID:
- P0ADA1
- Molecular Weight:
- 23621.955 Da
- General Function:
- Zinc ion binding
- Specific Function:
- Ligand-activated transcription factor. Key regulator of lipid metabolism. Activated by the endogenous ligand 1-palmitoyl-2-oleoyl-sn-glycerol-3-phosphocholine (16:0/18:1-GPC). Activated by oleylethanolamide, a naturally occurring lipid that regulates satiety. Receptor for peroxisome proliferators such as hypolipidemic drugs and fatty acids. Regulates the peroxisomal beta-oxidation pathway of fatty acids. Functions as transcription activator for the ACOX1 and P450 genes. Transactivation activity requires heterodimerization with RXRA and is antagonized by NR2C2. May be required for the propagation of clock information to metabolic pathways regulated by PER2.
- Gene Name:
- PPARA
- Uniprot ID:
- Q07869
- Molecular Weight:
- 52224.595 Da
From T3DB