HuagongsheHuagongshe Chemistry Print Report · For research reference only
HCID 5460307Generated: October 23, 2026
Fumarate
FUMARATE · Fumarate(2-) · Fumarate dianion · (E)-2-Butenedioate · Fumaric acid dianion · Fumaric acid, ion(2-) · (E)-3-Carboxyacrylate · (E)-2-Butenedioic acidanion
https://huagongshe.com/en/chemical/5460307
Identifiers & Physical Properties
| CAS No. | 142-42-7 |
|---|
| Molecular formula | C4H2O4-2 |
|---|
| Average molar mass | 114.06 g/mol |
|---|
| Monoisotopic mass | 113.9964057 g/mol |
|---|
| SMILES | O=C([O-])/C=C/C(=O)[O-] |
|---|
| InChIKey | VZCYOOQTPOCHFL-OWOJBTEDSA-L |
|---|
| PubChem CID | 5460307 |
|---|
| ChEBI | CHEBI:29806 |
|---|
| DTXSID | DTXSID9037660 |
|---|
Chemical & Physical Properties
| XLogP | 1 |
|---|
| Topological polar surface area | 80.3 |
|---|
| Hydrogen bond donors | 0 |
|---|
| Hydrogen bond acceptors | 4 |
|---|
| Rotatable bonds | 0 |
|---|
| Heavy atoms | 8 |
|---|
| Formal charge | -2 |
|---|
| Complexity | 108 |
|---|
| Collision Cross Section | 116.9 Ų [M-H]- [CCS Type: DTMethod: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)] |
|---|
Safety & Regulations
| Treatment | Acute exposure: EYES: irrigate opened eyes for several minutes under running water. INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice. SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention.
Chronic Exposure: There is no treatment for fumarase deficiencies. Only palliative care is possible. For cancers caused by intracellular fumarate excess, there are a wide variety of cancer treatments including drugs and surgery. |
|---|
| Health effects | Acute exposure to fumaric acid can cause skin redness (skin contact), cough or sore throat (inhalation), abdominal cramps, nausea and diarrhea (ingestion). Chronically high levels of fumaric acid are associated with at least 3 inborn errors of metabolism including: 2-Ketoglutarate dehydrogenase complex deficiency, Fumarase deficiency and Pyruvate carboxylase deficiency. Fumarase deficiency causes encephalopathy, severe mental retardation, unusual facial features, brain malformation, and epileptic seizures. High intracellular fumaric acid levels are associated with the development of renal cancer, leiomyomata, renal cysts, and tumors. |
|---|
| Exposure routes | Endogenous, ingestion, contact (skin and eyes) |
|---|
| Toxicity summary | Acute Toxicity: Fumarate is also an endogenous electrophile and reacts spontaneously with cysteine residues in proteins by a Michael addition reaction to form S-(2-succinyl) cysteine, a process termed succination. Lachrymators such as fumarate are thought to act by attacking sulfhydryl functional groups in enzymes. One of the most probable protein targets is the TRPA1 ion channel that is expressed in sensory nerves (trigeminal nerve) of the eyes, nose, mouth and lungs.
Chronic Toxicity: Fumarate is increasingly being identified as an oncometabolite. Fumarase or fumarate hydratase (FH) is a tumor suppressor, whose mutation is associated with the development of leiomyomata, renal cysts, and tumors. Loss of FH enzymatic activity results in accumulation of intracellular fumarate which has been proposed to act as a competitive inhibitor of 2-oxoglutarate-dependent oxygenases including the hypoxia-inducible factor (HIF) hydroxylases, thus activating oncogenic HIF pathways. Mitochondrial dysfunction is also associated with FH deficiency. Fumarate hydratase-deficient cells and tumors have been shown to accumulate fumarate to very high levels with multiple consequences including the activation of oncogenic pathways (A15199). Fumarate (and succinate) inhibit the activity or function of other members of the 2-oxoglutarate-dependent oxygenase superfamily, including histone demethylase enzymes (HDMs) and the TET family of 5-methlycytosine (5mC) hydroxylases which are critical in epigenetic regulation of gene expression.. Fumarate accumulation may also affect cytosolic pathways by inhibiting the reactions involved in the biosynthesis of arginine and purine. More recently it has been found that fumarate promotes p65 phosphorylation and p65 accumulation at the HIF-1α promoter through non-canonical signaling via the upstream Tank Binding Kinase 1 (TBK1). Fumarate is also an endogenous electrophile and reacts spontaneously with cysteine residues in proteins by a Michael addition reaction to form S-(2-succinyl) cysteine, a process termed succination. Accumulation of cellular fumarate has been shown to correlate directly with an increase in succinated proteins. Targets for succination include the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase, adiponectin, cytoskeletal proteins, and endoplasmic reticulum chaperone proteins. Furthermore, evidence suggests that succination of these proteins in cells may impair their functions. |
|---|
| Signs and Symptoms | Acute exposure to fumaric acid can cause eye and skin irritation, cough or sore throat (inhalation), abdominal cramps, nausea and diarrhea (ingestion). |
|---|
| Carcinogen Classification | Not listed by IARC. Has been implicated in oncogenesis (A15088, A15092). |
|---|
