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| Other Sizes |
| Targets |
Oxamic acid targets lactate dehydrogenase (LDH), an enzyme that catalyzes the interconversion of pyruvate and lactate with concomitant interconversion of NADH and NAD+. LDH is a key enzyme in anaerobic glycolysis and is often upregulated in cancer cells (the Warburg effect). Oxamic acid inhibits LDH, particularly LDHA, which is expressed in tumor cells. The compound binds to the substrate-binding site of LDH, competing with pyruvate. Inhibition of LDH leads to reduced lactate production, altered cellular metabolism, and may induce apoptosis in cancer cells.
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| ln Vitro |
Oxamic acid suppresses the proliferation, migration and invasion of both A2780 and SKOV3 cells[1]. Oxamic acid (10 μM; 24-72 h) inhibits cell proliferation in a dose- and time-dependent manner in both NPC cancer cells[2] . Oxamic acid (0-100 mM; 24 h) induces cell cycle arrest in the G2/M phase in CNE-1 and CNE-2 cells[2]. (0-100 mM; 48 h) induces apoptosis via caspase-3 activation and the mitochondrial pathway in NPC cells[2]. Oxamic acid (0-100 mM; 24 h) increases ROS levels in NPC cells[2].
In vitro, oxamic acid inhibits lactate dehydrogenase (LDH) activity in enzyme assays and in intact Ehrlich ascites tumor cells. It has been shown to inhibit human lactate dehydrogenase A (LDHA) with an IC50 of approximately 7 mM (range varies depending on assay conditions). In cell culture, oxamic acid (10-50 mM) reduces lactate production, decreases intracellular ATP levels, and induces cell death in various cancer cell lines (e.g., HeLa, MCF-7, A549). It is widely used as a tool compound for studying glycolysis and the Warburg effect in cancer research. |
| ln Vivo |
Oxamic acid (intraperitoneal injection; 750 mg/kg; once daily; 3 w) treatment improves the efficacy of tumor inhibition in vivo when combined with irradiation treatment[2].
In vivo, oxamic acid has not been extensively studied because its relatively high IC50 (millimolar range) makes it a weak LDH inhibitor requiring large doses. Limited studies in tumor-bearing mice have shown that high-dose oxamic acid (500-1000 mg/kg, i.p.) can reduce tumor growth modestly, but such doses may cause systemic toxicity. It is not used clinically due to its low potency. Instead, more potent LDH inhibitors (e.g., FX-11, GNE-140) have been developed. Oxamic acid remains a research tool for in vitro studies of glycolysis and LDH inhibition. |
| Enzyme Assay |
Enzyme inhibition assay for LDH: Recombinant human LDHA (10-50 ng) is incubated with varying concentrations of oxamic acid (0.1-100 mM) in reaction buffer (100 mM Tris-HCl, 0.2 mM NADH, 1 mM pyruvate, pH 7.4). The reaction is initiated by addition of pyruvate, and NADH oxidation is monitored by measuring absorbance decrease at 340 nm over 1-5 minutes at 25-37degC using a UV-Vis spectrophotometer. The rate of NADH consumption (deltaA340/min) is calculated. IC50 values are determined by fitting a sigmoidal dose-response curve. For oxamic acid, the IC50 against LDHA is approximately 5-10 mM (depending on pyruvate concentration). Ki is approximately 1-2 mM (competitive inhibition).
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| Cell Assay |
Cell Proliferation Assay[2]
Cell Types: CNE-1 and CNE-2 Tested Concentrations: 10 μM Incubation Duration: 24-72 hours Experimental Results: Showed IC50s of 74.6, 32.4 and 17.8 mM and 62.3, 44.5, 31.6 mM at 24, 48 and 72 h in the CNE-1 and CNE-2 cancer cells, respectively. Apoptosis Analysis[2] Cell Types: CNE-1 and CNE-2 Tested Concentrations: 0, 20, 50 and 100 mM Incubation Duration: 48 hours Experimental Results: Showed the increasement of early and late apoptotic cells in a dose-dependent manner. Increased the expression of pro-apoptotic Bax and cleaved-caspase-3, while reduced the anti-apoptotic signals of Bcl-2 and pro-caspase-3. Cell Cycle Analysis[2] Cell Types: CNE-1 and CNE-2 Tested Concentrations: 0, 20, 50 and 100 mM Incubation Duration: 24 hours Experimental Results: Showed a dose-dependent increase in the numbers of CNE-1 and CNE-2 cells in the G2/M phase. Cell-based assay for LDH inhibition and lactate production: Cancer cells (e.g., HeLa, MCF-7, A549) are seeded in 96-well plates (5,000-10,000 cells/well) and allowed to attach overnight. Cells are then treated with varying concentrations of oxamic acid (1-100 mM) in fresh medium for 24-48 hours. After treatment, the culture supernatant is collected, and lactate concentration is measured using a colorimetric lactate assay kit. Intracellular ATP levels are measured using a luciferase-based ATP assay kit. Cell viability is assessed by MTT or CCK-8 assay. EC50 values for lactate reduction and cytotoxicity are calculated. For oxamic acid, significant LDH inhibition requires millimolar concentrations (10-50 mM). |
| Animal Protocol |
Animal/Disease Models: Female Balb/c nude mice injected with CNE-1 cells[2]
Doses: 750 mg/kg Route of Administration: Intraperitoneal injection; 750 mg/kg; once daily; 3 weeks Experimental Results: Inhibited the tumor growth when compared to either oxamate alone or irradiation alone. In vivo efficacy protocol for LDH inhibitor: female athymic nude mice (6-8 weeks old) are implanted subcutaneously with cancer cells (e.g., 5×10⁶ HeLa or A549 cells in Matrigel). When tumors reach approximately 100-150 mm3, mice are randomized into groups (n=6-8). Oxamic acid is administered intraperitoneally (500-1000 mg/kg daily) or by oral gavage (1000-2000 mg/kg daily) in saline (pH adjusted to 7.4) for 14-21 days. Control groups receive vehicle. Tumor volume is measured every 2-3 days with calipers. Body weight is monitored for signs of toxicity. At study termination, tumors are excised and analyzed for LDH activity, lactate concentration, ATP levels, and markers of apoptosis (cleaved caspase-3). Due to low potency, high doses are required, often causing toxicity and limiting efficacy. |
| ADME/Pharmacokinetics |
Pharmacokinetic data for oxamic acid are limited. As a small polar molecule, it is likely to have high water solubility and low plasma protein binding. Oral absorption is expected to be moderate due to its polar nature. Following intravenous administration, the half-life is likely short (minutes to hours) due to rapid renal excretion. The high doses required for LDH inhibition (gram amounts in humans) preclude clinical use. For laboratory use, powder stored at 2-8degC in a dry, dark place. In solution, store at -20degC or -80degC for up to 6 months.
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| Toxicity/Toxicokinetics |
Oxamic acid is of low acute toxicity. The LD50 in rats has been reported to be approximately 5-10 g/kg orally. However, the compound is irritating to skin, eyes, and the respiratory tract. GHS classification: H315 (Causes skin irritation), H319 (Causes serious eye irritation), H335 (May cause respiratory irritation). Precautionary measures: wear protective gloves, eye protection, and face protection; wash hands thoroughly after handling; avoid breathing dust/fume/gas/mist/vapors/spray; use only outdoors or in a well-ventilated area. Oxamic acid is not classified as a carcinogen or reproductive toxin.
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| References |
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| Additional Infomation |
Oxamic Acid is a dicarboxylic acid monoamide formed by the condensation of a carboxyl group of oxalic acid with an amino group. It is a metabolite of *E. coli* and the conjugate acid of oxalamide. Oxaamide is a metabolite found or produced in *E. coli* (K12 strain, MG1655 strain). Oxaamide has also been reported in bees and beans, with relevant data available. It is an amino-substituted glyoxylic acid derivative. See also: Oxaamide (insect repellent) (note moved to).
Oxamic acid is a simple organic acid that is the monoamide of oxalic acid. It is an ozone oxidation product and is used in the synthesis of hydroxybenzimidazoles as potential antitumor agents targeting human lactate dehydrogenase A (LDHA). It is also a metabolite in the biodegradation of nitrogen-containing compounds. Oxamic acid is suitable for lactate dehydrogenase (LDH)-related research, particularly studies on glycolysis, cancer metabolism, and the Warburg effect. No clinical trials or regulatory approvals as an anti-cancer drug exist. |
| Molecular Formula |
C2H3NO3
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|---|---|
| Molecular Weight |
89.05
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| Exact Mass |
89.011
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| CAS # |
471-47-6
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| Related CAS # |
Oxamic acid sodium; 565-73-1; Oxamic acid; 471-47-6
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| PubChem CID |
974
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| Appearance |
White to off-white solid powder
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| Density |
1.563g/cm3
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| Boiling Point |
306.3ºC at 760mmHg
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| Melting Point |
207-210 °C (dec.)(lit.)
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| Vapour Pressure |
0.000177mmHg at 25°C
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| Source |
Originated from microorganisms
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| LogP |
0
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
1
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| Heavy Atom Count |
6
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| Complexity |
86.8
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| Defined Atom Stereocenter Count |
0
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| SMILES |
C(=O)(C(=O)O)N
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| InChi Key |
SOWBFZRMHSNYGE-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C2H3NO3/c3-1(4)2(5)6/h(H2,3,4)(H,5,6)
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| Chemical Name |
oxamic acid
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| Synonyms |
Oxamidic acid
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
H2O : ~125 mg/mL (~1403.71 mM; with ultrasonication)
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 11.2296 mL | 56.1482 mL | 112.2965 mL | |
| 5 mM | 2.2459 mL | 11.2296 mL | 22.4593 mL | |
| 10 mM | 1.1230 mL | 5.6148 mL | 11.2296 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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