Fusaric acid   中文名称: 萎蔫酸

Absorption, Distribution and Excretion
THE METABOLISM OF (14)C-LABELED FUSARIC ACID WAS STUDIED IN MALE & PREGNANT RATS AFTER ORAL ADMIN OF 20 MG/KG. THE MAJOR PART OF RADIOACTIVITY RETAINED IN THE BODY OF MALE RATS WAS IN THE KIDNEY, LIVER, & PLASMA 30 MIN AFTER ADMIN, & DECLINED RAPIDLY THEREAFTER. MOST (92.9%) OF THE DOSE APPEARED IN URINE BY 24 HR AFTER ADMIN & 93.1% BY 48 HR. A CONSIDERABLE AMOUNT OF RADIOACTIVITY APPEARED IN BILE WITHIN 1 HR AFTER ADMIN. AN EASY TRANSFER OF RADIOACTIVITY INTO THE FETUS WAS SHOWN BY RADIOAUTOGRAPHY OF PREGNANT RATS. THE ACTIVITY WAS NOT DETECTED IN THE FETUS IN 24 HR.

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Metabolism / Metabolites
ZINC, COBALT, & MOLYBDENUM ENHANCE THE BIOSYNTHESIS OF FUSARIC ACID BY FUSARIUM OXYSPORUM. NICOTINIC ACID WAS SLIGHTLY STIMULATORY, & TRYPTOPHAN, CYSTEINE, & THE COMBINATION OF INDOLEACETATE & SERINE MARKEDLY STIMULATED THE SYNTHESIS.
INDOLEACETIC ACID ALONE INHIBITED FUSARIC ACID FORMATION BY FUSARIUM OXYSPORUM, BUT INDOLEACETATE WITH SERINE HAD A STIMULATORY EFFECT. THE COMBINATION OF INDOLEACETATE & SERINE WITH TRYPTOPHAN INHIBITED THE BIOSYNTHESIS. HOMOSERINE SHOWED STIMULATORY ACTIVITY INDEPENDENT OF THE OTHER COMPOUNDS TESTED SINCE IT WAS NOT AFFECTED BY THEIR PRESENCE.
THE BIOSYNTHETIC PATHWAY FOR FUSARIC ACID WAS INVESTIGATED USING 1-(13)C-LABELED & 2-(13)C-LABELED ASPARTATE. CARBON ATOMS 2, 3, 4, & 7 WERE DERIVED FROM ACETATE VIA ASPARTATE OR A RELATED C4 DICARBOXYLIC ACID, WHEREAS CARBONS 5, 6, 8, 9, 10, & 11 WERE DERIVED MORE DIRECTLY FROM ACETATE. ASPARTIC ACID APPARENTLY IS METABOLIZED TO FUSARIC ACID VIA OXALOACETATE, & L-ASPARTATE SERVES AS A DONOR OF NITROGEN, IN AN AMINOTRANSFERASE REACTION, TO A SEPARATE OXALACETATE POOL OF PRIMARILY ENDOGENOUS ORIGIN.
IN RATS, THE MAJOR METABOLITE OF 5-(N-BUTYL)PICOLINAMIDE IS FUSARIC ACID, WHICH IS A DOPAMINE-BETA-HYDROXYLASE INHIBITOR. HENCE, ADMIN OF THE DRUG LOWERS THE CONCN OF ENDOGENOUS L-NORADRENALINE IN THE BRAIN, HEART, & SPLEEN.

Toxicity Summary
Fusaric acid affects neurotransmitter levels by acting as a partial inhibitor on tyrosine-hydroxylase and an inhibitor on dopamine-beta-hydroxylase. This has been shown to cause elevated serotonin, 5-hydroxyindoleacetic acid, tyrosine, and dopamine levels in the brain, as well as decreased norepinephrine levels. These changes in neurotransmitter levels may be responsible for effects such as hypotension, altered behavior and locomotive activity, neurological disorders, and developmental problems. (A3020, A3021, A3022, A3023)

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Interactions
WHEN FUSARIC ACID (100 MG/KG, IP) WAS ADMIN TO MALE MICE 6 HR AFTER ALCOHOL WITHDRAWAL, BRAIN NORADRENALINE, DOPAMINE, & SEROTONIN CONCN WERE 112.8, 186.4, & 652.8 NG/G 4 HR LATER. FUSARIC ACID ADMIN DECREASED BRAIN NORADRENALINE LEVEL ACCOMPANIED BY AN ENHANCED ALCOHOL WITHDRAWAL SYNDROME.

Fusaric acid is a member of pyridines and an aromatic carboxylic acid.
Fusaric acid has been reported in Fusarium fujikuroi, Fusarium verticillioides, and Fusarium solani with data available.
Fusaric acid is a mycotoxin found in various Fusarium species such as Fusarium moniliforme. It has been proposed for a various therapeutic applications but is primarily used as a research tool. Fusaric acid is moderately toxic and can be found in contaminated corn and cereal grains including barley, wheat, millets and sorghum. (L1963, A3020)
A picolinic acid derivative isolated from various Fusarium species. It has been proposed for a variety of therapeutic applications but is primarily used as a research tool. Its mechanisms of action are poorly understood. It probably inhibits DOPAMINE BETA-HYDROXYLASE, the enzyme that converts dopamine to norepinephrine. It may also have other actions, including the inhibition of cell proliferation and DNA synthesis.

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Mechanism of Action
FUSARIC ACID SUPPRESSED RAPID EYE MOVEMENT (REM) SLEEP IN CATS BUT HAD NO SIGNIFICANT EFFECT ON SLOW WAVE SLEEP. REM SLEEP USUALLY REBOUNDED AFTER A PERIOD OF DRUG-INDUCED SUPPRESSION, INDICATING THAT, ALTHOUGH FUSARIC ACID SUPPRESSED THE PERIPHERAL MANIFESTATIONS OF REM, THE BIOLOGICAL NEED FOR REM WAS NOT ALTERED.
FUSARIC ACID INHIBITED NORADRENALINE & DOPAMINE UPTAKE IN SYNAPTOSOMES FROM RAT HYPOTHALAMUS & CORPUS STRIATUM. THE BASAL OVERFLOW OF NORADRENALINE & DOPAMINE FROM BRAIN STEM & CORPUS STRIATUM SLICES WAS STIMULATED BY FUSARIC ACID. THE DATA SHOW THAT FUSARIC ACID, A DOPAMINE-BETA-HYDROXYLASE INHIBITOR, ALSO EXERTS MARKED EFFECTS IN THE CNS BY INTERFERING WITH OTHER SYNAPTOSOMAL FUNCTIONS.
FUSARIC ACID (100 MG/KG, IP) INCREASED THE LEVELS OF TRYPTOPHAN, SEROTONIN, & 5-HYDROXYINDOLEACETIC ACID IN RAT BRAIN & THE LEVEL OF FREE TRYPTOPHAN IN THE BLOOD INDICATING THAT IN ADDITION TO ITS CNS EFFECT, FUSARIC ACID EXERTS A PERIPHERAL ACTION ON SEROTONIN METABOLISM BY INHIBITING TRYPTOPHAN BINDING TO SERUM ALBUMIN.
FUSARIC ACID (75 MG/KG, IP), AN INHIBITOR OF DOPAMINE BETA-HYDROXYLASE, EFFECTIVE IN THE RELIEF OF TREMORS, RIGIDITY, & SPEECH DIFFICULTIES ASSOCIATED WITH PARKINSONS DISEASE, INCREASED THE BRAIN SEROTONIN LEVELS & DECREASED THE BRAIN NORADRENALINE LEVELS OF RATS.
FUSARIC ACID (FA) INCREASED MONOSYNAPTIC REFLEX NEURAL ACTIVITY IN A DOSE-DEPENDENT MANNER IN CATS. FA DID NOT INCREASE THE BLOOD PRESSURE BUT INHIBITED THE SYNTHESIS OF NOREPINEPHRINE FROM DOPAMINE.

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Therapeutic Uses
Dopamine Agents; Enzyme Inhibitors; Nucleic Acid Synthesis Inhibitors
EXPTL USE: FUSARIC ACID (100 MG/KG, IP) GIVEN 1.5 HR PRIOR TO WATER-IMMERSION STRESS ALMOST COMPLETELY PREVENTED GASTRIC ULCER FORMATION IN RATS. FUSARIC ACID PROBABLY PREVENTS GASTRIC ULCERATION BY DECREASING NORADRENALINE RELEASE IN THE CNS.

C10H13NO2

179.22

179.095

536-69-6

3442

White to off-white solid powder

1.113g/cm3

329.2ºC at 760mmHg

96-100 °C

152.9ºC

2.122

50.19

1

3

4

13

170

0

DGMPVYSXXIOGJY-UHFFFAOYSA-N

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)

5-butylpyridine-2-carboxylic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: 62.5 mg/mL (348.73 mM)
H2O: 50 mg/mL (278.99 mM)

配方 1 中的溶解度: ≥ 2.08 mg/mL (11.61 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 20.8 mg/mL澄清DMSO储备液加入400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.08 mg/mL (11.61 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.08 mg/mL (11.61 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。