| Size | Price | Stock | Qty |
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| 50mg |
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| 100mg |
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| Other Sizes |
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
This study investigated the metabolism of 20 mg/kg of 14C-labeled fusaric acid in male and pregnant rats. Thirty minutes after administration, most of the radioactive material was present in the kidneys, liver, and plasma of male rats, subsequently decreasing rapidly. Within 24 hours of administration, the majority (92.9%) of the dose was found in the urine, and within 48 hours, 93.1% of the dose was found in the urine. Within 1 hour of administration, a significant amount of radioactive material was found in the bile. Autoradiography in pregnant rats showed that the radioactive material readily translocates to the fetus. No radioactive material was detected in the fetus within 24 hours. Metabolism/Metabolites Zinc, cobalt, and molybdenum enhance the biosynthesis of fusaric acid by Fusarium oxysporum. Nicotinic acid has a mild stimulating effect, while tryptophan, cysteine, and the combination of indoleacetic acid and serine significantly stimulate synthesis. Indoleacetic acid alone inhibits the production of fusarium acid by Fusarium oxysporum, but indoleacetic acid combined with serine has a stimulatory effect. The combination of indoleacetic acid, serine, and tryptophan inhibits biosynthesis. Homoserine exhibits stimulatory activity independent of other tested compounds, as it is unaffected by them. The biosynthetic pathway of fusarium acid was investigated using 1-(13)C-labeled and 2-(13)C-labeled aspartic acid. Carbons 2, 3, 4, and 7 are derived from acetic acid via aspartic acid or related C4 dicarboxylic acids, while carbons 5, 6, 8, 9, 10, and 11 are more directly derived from acetic acid. Aspartic acid is apparently metabolized to fusarium acid via oxaloacetate, while L-aspartic acid acts as a nitrogen donor in aminotransferase reactions, transferring to a pool primarily derived from endogenous oxaloacetate. In rats, the major metabolite of 5-(n-butyl)pyridinecarboxamide is fusaric acid, a dopamine β-hydroxylase inhibitor. Therefore, administration of this drug reduces the concentration of endogenous L-norepinephrine in the brain, heart, and spleen. |
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| Toxicity/Toxicokinetics |
Toxicity Summary
Fusarium oxytocin affects neurotransmitter levels by partially inhibiting tyrosine hydroxylase and dopamine β-hydroxylase. Studies have shown that this leads to elevated levels of serotonin, 5-hydroxyindoleacetic acid, tyrosine, and dopamine in the brain, and decreased levels of norepinephrine. These changes in neurotransmitter levels may lead to symptoms such as hypotension, behavioral and motor function alterations, neurological disorders, and developmental problems. (A3020, A3021, A3022, A3023) Interactions When male mice were intraperitoneally injected with nitrofurantoin (100 mg/kg) 6 hours after alcohol withdrawal, the concentrations of norepinephrine, dopamine, and serotonin in the brain were 112.8, 186.4, and 652.8 ng/g, respectively, 4 hours later. Nitrofurantoin administration reduced norepinephrine levels in the brain and was associated with exacerbation of alcohol withdrawal syndrome. |
| Additional Infomation |
Fusarium acid belongs to the pyridine class of compounds and is an aromatic carboxylic acid. It has been reported to be found in Fusarium fujikuroi, Fusarium verticillioides, and Fusarium solani, with available data. Fusarium acid is a mycotoxin found in various Fusarium species, such as Fusarium moniliforme. It has been proposed for various therapeutic uses, but primarily used as a research tool. Fusarium acid is moderately toxic and is found in contaminated corn and grains, including barley, wheat, millet, and sorghum. (L1963, A3020) It is a pyridinecarboxylic acid derivative isolated from various Fusarium species. It has been proposed for various therapeutic uses, but primarily used as a research tool. Its mechanism of action is not fully understood. It may inhibit dopamine β-hydroxylase, the enzyme that converts dopamine to norepinephrine. It may also have other effects, including inhibiting cell proliferation and DNA synthesis.
Mechanism of Action Fusarium oxysine inhibits rapid eye movement (REM) sleep in cats, but has no significant effect on slow-wave sleep. REM sleep usually recovers after the drug-induced REM sleep inhibition period, suggesting that although fusarium oxysine inhibits the peripheral manifestations of REM sleep, the biological requirements for REM sleep remain unchanged. Fusarium oxysine inhibits the uptake of norepinephrine and dopamine in the hypothalamus and striatum synapses of rats. Fusarium oxysine stimulates basal spillover of norepinephrine and dopamine in brainstem and striatum sections. Data show that the dopamine β-hydroxylase inhibitor fusarium oxysine also has significant effects on the central nervous system by interfering with other synaptic functions. Fusarium oxytocin (100 mg/kg, intraperitoneal injection) increased the levels of tryptophan, serotonin, and 5-hydroxyindoleacetic acid in the rat brain, as well as the level of free tryptophan in the blood, indicating that in addition to affecting the central nervous system, fusarium oxytocin can also exert peripheral effects on serotonin metabolism by inhibiting the binding of tryptophan to serum albumin. Fusarium oxytocin (75 mg/kg, intraperitoneal injection) is a dopamine β-hydroxylase inhibitor that can effectively alleviate Parkinson's disease-related tremor, rigidity, and speech difficulties, and can increase serotonin levels in the rat brain and decrease norepinephrine levels in the brain. Nitrofurantoin (FA) increases monosynaptic reflex activity in cats in a dose-dependent manner. FA does not raise blood pressure, but inhibits dopamine synthesis of norepinephrine. Therapeutic Uses Dopamine derivatives; enzyme inhibitors; nucleic acid synthesis inhibitors Experimental Application: Administration of fluoxacin (100 mg/kg, intraperitoneal injection) 1.5 hours before water immersion stress almost completely prevented the formation of gastric ulcers in rats. Fluoxacin may prevent gastric ulcers by reducing the release of norepinephrine in the central nervous system. |
| Molecular Formula |
C10H13NO2
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| Molecular Weight |
179.22
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| Exact Mass |
179.095
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| CAS # |
536-69-6
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| PubChem CID |
3442
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| Appearance |
White to off-white solid powder
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| Density |
1.113g/cm3
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| Boiling Point |
329.2ºC at 760mmHg
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| Melting Point |
96-100 °C
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| Flash Point |
152.9ºC
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| LogP |
2.122
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
4
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| Heavy Atom Count |
13
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| Complexity |
170
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
DGMPVYSXXIOGJY-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C10H13NO2/c1-2-3-4-8-5-6-9(10(12)13)11-7-8/h5-7H,2-4H2,1H3,(H,12,13)
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| Chemical Name |
5-butylpyridine-2-carboxylic 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) |
DMSO: 62.5 mg/mL (348.73 mM)
H2O: 50 mg/mL (278.99 mM) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (11.61 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.08 mg/mL (11.61 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.08 mg/mL (11.61 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 5.5797 mL | 27.8987 mL | 55.7973 mL | |
| 5 mM | 1.1159 mL | 5.5797 mL | 11.1595 mL | |
| 10 mM | 0.5580 mL | 2.7899 mL | 5.5797 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.