OXALIC ACID
General Information
| Mainterm | OXALIC ACID |
| CAS Reg.No.(or other ID) | 144-62-7 |
| Regnum |
177.1010 177.2410 |
From www.fda.gov
Computed Descriptors
Download SDF| 2D Structure | |
| CID | 971 |
| IUPAC Name | oxalic acid |
| InChI | InChI=1S/C2H2O4/c3-1(4)2(5)6/h(H,3,4)(H,5,6) |
| InChI Key | MUBZPKHOEPUJKR-UHFFFAOYSA-N |
| Canonical SMILES | C(=O)(C(=O)O)O |
| Molecular Formula | C2H2O4 |
| Wikipedia | oxalic acid |
From Pubchem
Computed Properties
| Property Name | Property Value |
|---|---|
| Molecular Weight | 90.034 |
| Hydrogen Bond Donor Count | 2 |
| Hydrogen Bond Acceptor Count | 4 |
| Rotatable Bond Count | 1 |
| Complexity | 71.5 |
| CACTVS Substructure Key Fingerprint | A A A D c Q B A O 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 C g A A C A A A A A A A g A A A C A A A A g A I A A C Q C A I A A A A A A A A A A A B A A A A B A A A A A A A A A A A A A A A B 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 = = |
| Topological Polar Surface Area | 74.6 |
| Monoisotopic Mass | 89.995 |
| Exact Mass | 89.995 |
| XLogP3 | None |
| XLogP3-AA | -0.3 |
| Compound Is Canonicalized | True |
| Formal Charge | 0 |
| Heavy Atom Count | 6 |
| 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+ | 0.8251 |
| Human Intestinal Absorption | HIA+ | 0.5405 |
| Caco-2 Permeability | Caco2- | 0.8810 |
| P-glycoprotein Substrate | Non-substrate | 0.7820 |
| P-glycoprotein Inhibitor | Non-inhibitor | 0.9872 |
| Non-inhibitor | 0.9886 | |
| Renal Organic Cation Transporter | Non-inhibitor | 0.9680 |
| Distribution | ||
| Subcellular localization | Mitochondria | 0.7734 |
| Metabolism | ||
| CYP450 2C9 Substrate | Non-substrate | 0.8612 |
| CYP450 2D6 Substrate | Non-substrate | 0.9274 |
| CYP450 3A4 Substrate | Non-substrate | 0.8021 |
| CYP450 1A2 Inhibitor | Non-inhibitor | 0.9621 |
| CYP450 2C9 Inhibitor | Non-inhibitor | 0.9267 |
| CYP450 2D6 Inhibitor | Non-inhibitor | 0.9593 |
| CYP450 2C19 Inhibitor | Non-inhibitor | 0.9828 |
| CYP450 3A4 Inhibitor | Non-inhibitor | 0.9751 |
| CYP Inhibitory Promiscuity | Low CYP Inhibitory Promiscuity | 0.9962 |
| Excretion | ||
| Toxicity | ||
| Human Ether-a-go-go-Related Gene Inhibition | Weak inhibitor | 0.9936 |
| Non-inhibitor | 0.9809 | |
| AMES Toxicity | Non AMES toxic | 0.9132 |
| Carcinogens | Non-carcinogens | 0.6444 |
| Fish Toxicity | High FHMT | 0.7964 |
| Tetrahymena Pyriformis Toxicity | Low TPT | 0.9558 |
| Honey Bee Toxicity | High HBT | 0.6171 |
| Biodegradation | Ready biodegradable | 0.8559 |
| Acute Oral Toxicity | IV | 0.6275 |
| Carcinogenicity (Three-class) | Non-required | 0.7539 |
From admetSAR
ADMET Predicted Profile --- Regression
| Model | Value | Unit |
|---|---|---|
| Absorption | ||
| Aqueous solubility | 0.4427 | LogS |
| Caco-2 Permeability | -0.2542 | LogPapp, cm/s |
| Distribution | ||
| Metabolism | ||
| Excretion | ||
| Toxicity | ||
| Rat Acute Toxicity | 1.1107 | LD50, mol/kg |
| Fish Toxicity | 1.8609 | pLC50, mg/L |
| Tetrahymena Pyriformis Toxicity | -1.2055 | pIGC50, ug/L |
From admetSAR
Toxicity Profile
| Route of Exposure | |
|---|---|
| Mechanism of Toxicity | The affinity of divalent metal ions is sometimes reflected in their tendency to form insoluble precipitates. Thus in the body, oxalic acid also combines with metals ions such as Ca2+, Fe2+, and Mg2+ to deposit crystals of the corresponding oxalates, which irritate the gut and kidneys. (2) Therefore the toxicity of oxalic acid is due to kidney failure caused by precipitation of solid calcium oxalate, the main component of kidney stones. Oxalic acid can also cause joint pain due to the formation of similar precipitates in the joints. Ingestion of ethylene glycol results in oxalic acid as a metabolite that can also cause acute kidney failure. |
| Metabolism | Oxalic acid is not metabolized but excreted in the urine. |
| Toxicity Values | |
| Lethal Dose | Oral LDLo (lowest published lethal dose) of 600 mg/kg. It has been reported that the lethal oral dose is 15 to 30 grams. |
| Carcinogenicity (IARC Classification) | No indication of carcinogenicity (not listed by IARC). |
| Minimum Risk Level | |
| Health Effects | Because it binds vital nutrients such as calcium, long-term consumption of foods high in oxalic acid can be problematic. Healthy individuals can safely consume such foods in moderation, but those with kidney disorders, gout, rheumatoid arthritis, or certain forms of chronic vulvar pain (vulvodynia) are typically advised to avoid foods high in oxalic acid or oxalates. The calcium oxalate precipitate (better known as kidney stones) obstruct the kidney tubules. Conversely, calcium supplements taken along with foods high in oxalic acid can cause calcium oxalate to precipitate out in the gut and drastically reduce the levels of oxalate absorbed by the body (by 97% in some cases.) Chronically high levels of oxalic acid are associated with at least 2 inborn errors of metabolism including: Type I primary hyperoxaluria and Primary hyperoxaluria. Oxalate stones in primary hyperoxaluria tend to be severe, resulting in relatively early kidney damage (before age 20), which impairs the excretion of oxalate leading to a further acceleration in accumulation of oxalate in the body. After the development of renal failure patients may develop oxalate deposits in the bones, joints and bone marrow. Severe cases may develop haematological problems such as anaemia and thrombocytopaenia. The deposition of oxalate in the body is sometimes called "oxalosis" to be distinguished from "oxaluria" which refers to oxalate in the urine. |
| Treatment | Acute Exposure: If oxalic acid is swallowed, immediately give the person water or milk, unless instructed otherwise by a health care provider. DO NOT give water or milk if the person is having symptoms (such as vomiting, convulsions, or a decreased level of alertness) that make it hard to swallow. If acute exposure occurs to the eyes, irrigate opened eyes for several minutes under running water. Chronic exposure: in some patients with primary hyperoxaluria type 1, pyridoxine treatment (vitamin B6) may decrease oxalate excretion and prevent kidney stone formation. |
| Reference |
|
From T3DB
Taxonomic Classification
| Kingdom | Organic compounds |
|---|---|
| Superclass | Organic acids and derivatives |
| Class | Carboxylic acids and derivatives |
| Subclass | Dicarboxylic acids and derivatives |
| Intermediate Tree Nodes | Not available |
| Direct Parent | Dicarboxylic acids and derivatives |
| Alternative Parents | |
| Molecular Framework | Aliphatic acyclic compounds |
| Substituents | Dicarboxylic acid or derivatives - Carboxylic acid - 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 dicarboxylic acids and derivatives. These are organic compounds containing exactly two carboxylic acid groups. |
From ClassyFire
Targets
- General Function:
- Sh3/sh2 adaptor activity
- Specific Function:
- Non-receptor protein tyrosine kinase which is activated following engagement of many different classes of cellular receptors including immune response receptors, integrins and other adhesion receptors, receptor protein tyrosine kinases, G protein-coupled receptors as well as cytokine receptors. Participates in signaling pathways that control a diverse spectrum of biological activities including gene transcription, immune response, cell adhesion, cell cycle progression, apoptosis, migration, and transformation. Due to functional redundancy between members of the SRC kinase family, identification of the specific role of each SRC kinase is very difficult. SRC appears to be one of the primary kinases activated following engagement of receptors and plays a role in the activation of other protein tyrosine kinase (PTK) families. Receptor clustering or dimerization leads to recruitment of SRC to the receptor complexes where it phosphorylates the tyrosine residues within the receptor cytoplasmic domains. Plays an important role in the regulation of cytoskeletal organization through phosphorylation of specific substrates such as AFAP1. Phosphorylation of AFAP1 allows the SRC SH2 domain to bind AFAP1 and to localize to actin filaments. Cytoskeletal reorganization is also controlled through the phosphorylation of cortactin (CTTN). When cells adhere via focal adhesions to the extracellular matrix, signals are transmitted by integrins into the cell resulting in tyrosine phosphorylation of a number of focal adhesion proteins, including PTK2/FAK1 and paxillin (PXN). In addition to phosphorylating focal adhesion proteins, SRC is also active at the sites of cell-cell contact adherens junctions and phosphorylates substrates such as beta-catenin (CTNNB1), delta-catenin (CTNND1), and plakoglobin (JUP). Another type of cell-cell junction, the gap junction, is also a target for SRC, which phosphorylates connexin-43 (GJA1). SRC is implicated in regulation of pre-mRNA-processing and phosphorylates RNA-binding proteins such as KHDRBS1. Also plays a role in PDGF-mediated tyrosine phosphorylation of both STAT1 and STAT3, leading to increased DNA binding activity of these transcription factors. Involved in the RAS pathway through phosphorylation of RASA1 and RASGRF1. Plays a role in EGF-mediated calcium-activated chloride channel activation. Required for epidermal growth factor receptor (EGFR) internalization through phosphorylation of clathrin heavy chain (CLTC and CLTCL1) at 'Tyr-1477'. Involved in beta-arrestin (ARRB1 and ARRB2) desensitization through phosphorylation and activation of ADRBK1, leading to beta-arrestin phosphorylation and internalization. Has a critical role in the stimulation of the CDK20/MAPK3 mitogen-activated protein kinase cascade by epidermal growth factor. Might be involved not only in mediating the transduction of mitogenic signals at the level of the plasma membrane but also in controlling progression through the cell cycle via interaction with regulatory proteins in the nucleus. Plays an important role in osteoclastic bone resorption in conjunction with PTK2B/PYK2. Both the formation of a SRC-PTK2B/PYK2 complex and SRC kinase activity are necessary for this function. Recruited to activated integrins by PTK2B/PYK2, thereby phosphorylating CBL, which in turn induces the activation and recruitment of phosphatidylinositol 3-kinase to the cell membrane in a signaling pathway that is critical for osteoclast function. Promotes energy production in osteoclasts by activating mitochondrial cytochrome C oxidase. Phosphorylates DDR2 on tyrosine residues, thereby promoting its subsequent autophosphorylation. Phosphorylates RUNX3 and COX2 on tyrosine residues, TNK2 on 'Tyr-284' and CBL on 'Tyr-731'. Enhances DDX58/RIG-I-elicited antiviral signaling. Phosphorylates PDPK1 at 'Tyr-9', 'Tyr-373' and 'Tyr-376'. Phosphorylates BCAR1 at 'Tyr-128'. Phosphorylates CBLC at multiple tyrosine residues, phosphorylation at 'Tyr-341' activates CBLC E3 activity. Required for podosome formation (By similarity).
- Gene Name:
- SRC
- Uniprot ID:
- P12931
- Molecular Weight:
- 59834.295 Da
References
- Berman HM, Westbrook J, Feng Z, Gilliland G, Bhat TN, Weissig H, Shindyalov IN, Bourne PE: The Protein Data Bank. Nucleic Acids Res. 2000 Jan 1;28(1):235-42. [10592235 ]
- General Function:
- Thrombospondin receptor activity
- Specific Function:
- Thrombin, which cleaves bonds after Arg and Lys, converts fibrinogen to fibrin and activates factors V, VII, VIII, XIII, and, in complex with thrombomodulin, protein C. Functions in blood homeostasis, inflammation and wound healing.
- Gene Name:
- F2
- Uniprot ID:
- P00734
- Molecular Weight:
- 70036.295 Da
References
- Sekiya K, Okuda H: Inhibitory action of soluble elastin on thromboxane B2 formation in blood platelets. Biochim Biophys Acta. 1984 Mar 1;797(3):348-53. [6320905 ]
- General Function:
- Ubiquinone binding
- Specific Function:
- Membrane-anchoring subunit of succinate dehydrogenase (SDH) that is involved in complex II of the mitochondrial electron transport chain and is responsible for transferring electrons from succinate to ubiquinone (coenzyme Q).
- Gene Name:
- SDHD
- Uniprot ID:
- O14521
- Molecular Weight:
- 17042.82 Da
References
- Wozniak AJ, Glisson BS, Hande KR, Ross WE: Inhibition of etoposide-induced DNA damage and cytotoxicity in L1210 cells by dehydrogenase inhibitors and other agents. Cancer Res. 1984 Feb;44(2):626-32. [6318974 ]
- General Function:
- Succinate dehydrogenase activity
- Specific Function:
- Flavoprotein (FP) subunit of succinate dehydrogenase (SDH) that is involved in complex II of the mitochondrial electron transport chain and is responsible for transferring electrons from succinate to ubiquinone (coenzyme Q). Can act as a tumor suppressor.
- Gene Name:
- SDHA
- Uniprot ID:
- P31040
- Molecular Weight:
- 72690.975 Da
References
- Wozniak AJ, Glisson BS, Hande KR, Ross WE: Inhibition of etoposide-induced DNA damage and cytotoxicity in L1210 cells by dehydrogenase inhibitors and other agents. Cancer Res. 1984 Feb;44(2):626-32. [6318974 ]
- General Function:
- Ubiquinone binding
- Specific Function:
- Iron-sulfur protein (IP) subunit of succinate dehydrogenase (SDH) that is involved in complex II of the mitochondrial electron transport chain and is responsible for transferring electrons from succinate to ubiquinone (coenzyme Q).
- Gene Name:
- SDHB
- Uniprot ID:
- P21912
- Molecular Weight:
- 31629.365 Da
References
- Wozniak AJ, Glisson BS, Hande KR, Ross WE: Inhibition of etoposide-induced DNA damage and cytotoxicity in L1210 cells by dehydrogenase inhibitors and other agents. Cancer Res. 1984 Feb;44(2):626-32. [6318974 ]
- General Function:
- Succinate dehydrogenase activity
- Specific Function:
- Membrane-anchoring subunit of succinate dehydrogenase (SDH) that is involved in complex II of the mitochondrial electron transport chain and is responsible for transferring electrons from succinate to ubiquinone (coenzyme Q).
- Gene Name:
- SDHC
- Uniprot ID:
- Q99643
- Molecular Weight:
- 18610.03 Da
References
- Wozniak AJ, Glisson BS, Hande KR, Ross WE: Inhibition of etoposide-induced DNA damage and cytotoxicity in L1210 cells by dehydrogenase inhibitors and other agents. Cancer Res. 1984 Feb;44(2):626-32. [6318974 ]
From T3DB