5-Butylpyridin-3-carbonsaeure

Warning

H302 (98.6%): Harmful if swallowed [Warning Acute toxicity, oral]

P264, P270, P301+P317, P330, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 69 reports by companies from 2 notifications to the ECHA C&L Inventory.；Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

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 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)

DOPAMINE BETA-HYDROXYLASE INHIBITOR & HYPOTENSIVE ACTIVITY...

IN THE MOUSE & RAT, A MAX DAILY DOSE OF 125 MG/KG ORALLY CAUSED NO DEFECTS BUT DELAY IN OSSIFICATION & GROWTH OF THE MOUSE FETUSES WAS FOUND. AT THE SAME DOSE, NO EFFECTS WERE FOUND IN THE RABBIT. /FUSARIC ACID-CA/

FUSARIC ACID (10 MG/KG, IV) CAUSED A RAPID & DOSE-RELATED HYPOTENSION, TACHYCARDIA, TACHYPNEA, INCREASE IN BLOOD FLOW IN THE UPPER MESENTERIC ARTERY, & DECREASE IN BLOOD FLOW IN THE FEMORAL ARTERY IN DOGS. FUSARIC ACID (0.3-3 MG) HAD A DOSE-DEPENDENT NEGATIVE INOTROPIC & NODAL RHYTHM DECREASING ACTIVITY IN NODAL & PAPILLARY MUSCLE PREPARATIONS.

THE EFFECTS OF FUSARIC ACID (FA), A DOPAMINE-BETA-HYDROXYLASE INHIBITOR, WERE DETERMINED ON AGGRESSION, MOTOR ACTIVITY, & BRAIN MONAMINES AT DOSES OF 3.2-60 MG/KG FOLLOWING ADMIN OF DIETARY SUPPLEMENTS OF L-TYROSINE OR BALANCED PROTEIN TO MALE ALBINO MICE. COMPARED TO SALINE-INJECTED CONTROL ANIMALS, BOTH AGGRESSION & MOTOR ACTIVITY WERE REDUCED BY THE HIGHEST DOSES OF FUSARIC ACID. TREATMENT WITH FA AT DOSES OF 30 TO 60 MG/KG DECREASED BRAIN NOREPINEPHRINE, DOPAMINE, & BRAIN TYROSINE IN ANIMALS FED THE TYROSINE SUPPLEMENT. IN CONTRAST, FA INCREASED 5-HYDROXYTRYPTAMINE & CAUSED MARKED INCREASES IN 5-HYDROXYINDOLEACETIC ACID AT THE HIGHEST DOSES.

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.

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.

Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.

Any drugs that are used for their effects on dopamine receptors, on the life cycle of dopamine, or on the survival of dopaminergic neurons.

Compounds that inhibit cell production of DNA or RNA.

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.

MEDICATION

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 can be found in contaminated corn and cereal grains including barley, wheat, millets and sorghum. (L1963, A3020)

HARDEGGER, NIKLES, HELV CHIM ACTA 39, 505 (1956)...

LARGE QUANTITIES OF FUSARIC ACID WERE PRODUCED BY FUSARIUM SPECIES GROWN ON A MODIFIED RICHARDS MEDIUM CONTAINING 2 MOLAR, BUT NOT 0.05 MOLAR GLUCOSE.

ANTIBIOTIC (WILTING AGENT) FIRST ISOLATED FROM THE FUNGUS FUSARIUM HETEROSPORIUM, NEES: YABUTA ET AL, J AGR CHEM SOC JAPAN 10, 1059 (1934). ISOLATION FROM OTHER FUSARIUM SPECIES & FROM GIBBERELLA FUJIKUROI & SYNTHESIS: PLATTNER ET AL, HELV CHIM ACTA 37, 1379 (1954).

2-Pyridinecarboxylic acid, 5-butyl-: INACTIVE

ADDITION OF EXCESSIVE AMOUNTS OF ZINC (30 MG/L) TO THE MEDIUM OF VIRULENT STRAIN OF FUSARIUM OXYSPORUM VASINFECTUM DECREASED THE CONTENT OF FUSARIC ACID BY 40% IN COMPARISON TO THAT IN THE SAME STRAIN GROWN ON MEDIUM WITH A NORMAL AMOUNT OF ZINC (0.2 MG/L). EXCESSIVE ZINC APPARENTLY ALTERS THE METABOLIC PATHWAY ASSOCIATED WITH FUSARIC ACID FORMATION & LEADS TO ACTIVATION OF THE DEHYDROGENASE SYSTEM. THE MAIN EFFECT OF EXCESSIVE ZINC APPEARS NOT TO BE LOSS OF VIABILITY BY PATHOGENIC FORMS, BUT LOSS OF VIRULENCE.