Pathways

Butoconazole is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Butoconazole passes through the liver and is then excreted from the body mainly through the kidney.

Butoconazole is an imidazole antifungal used to treat vulvovaginal candidiasis. The exact mechanism of the antifungal action of butoconazole is unknown, however, it is presumed to function as other imidazole derivatives via inhibition of steroid synthesis. Imidazoles generally inhibit the conversion of lanosterol to ergosterol via the inhibition of the enzyme cytochrome P450 14α-demethylase. Butoconazole inhibits lanosterol 14-alpha demethylase in the endoplasmic reticulum of fungal cells. Lanosterol 14-alpha demethylase is the enzyme that catalyzes the synthesis of 4,4'-dimethyl cholesta-8,14,24-triene-3-beta-ol from lanosterol. With this enzyme inhibited ergosterol synthesis cannot occur which causes a significant low concentration of ergosterol in the fungal cell. Ergosterol is essential in maintaining membrane integrity in fungi. Without ergosterol, the fungus cell cannot synthesize membranes thereby increasing fluidity and preventing growth of new cells. This leads to cell lysis which causes it to collapse and die.

Metabolites of Butobarbital are predicted with biotransformer.

Butobarbital, also known as butethal or butobarbitone, functions as both a sedative and a hypnotic drug, primarily intended for treating insomnia. Belonging to the barbiturate group of medicines, it is presumed to act on GABA receptors in the brain, leading to the release of the neurotransmitter GABA. This chemical release inhibits specific brain areas, inducing a state of sleepiness. By binding to a specific site linked to a Cl- ionopore at the GABAA receptor, butobarbital prolongs the opening duration of the Cl- ionopore. This extension results in the prolonged post-synaptic inhibitory influence of GABA in the thalamus. This overall effect is coupled with significant reductions in GABA-sensitive neuronal calcium conductance (gCa). Barbiturate action ultimately results in the acute enhancement of inhibitory GABAergic tone. Additionally, barbiturates act by directly inhibiting excitatory AMPA-type glutamate receptors, leading to a marked suppression of glutamatergic neurotransmission. Butobarbital is swiftly absorbed after oral administration. Symptoms of overdose encompass severe confusion, diminished or absent reflexes, pronounced drowsiness, fever, persistent irritability, decreased body temperature, impaired judgment, slow or labored breathing, slow heartbeat, slurred speech, unsteady gait, sleep disturbances, abnormal eye movements, and severe weakness.

Butenafine is a topical antifungal used to treat tinea versicolor, tinea pedis, tinea cruris, and tinea corporis due to the fungi E. floccosum, T. mentagrophytes, T. rubrum, and T. tonsurans.The exact mechanism of action has not been established, but it is suggested that butenafine's antifungal activity is exerted through the alteration of cellular membranes, which results in increased membrane permeability, and growth inhibition. Butenafine is mainly active against dermatophytes and has superior fungicidal activity against this group of fungi when compared to that of terbinafine, naftifine, tolnaftate, clotrimazole, and bifonazole. It is also active against candida albicans, and it is more active than terbinafine. Butenafine works by inhibiting squalene monooxygenase which is an essential enzyme of Ergosterol biosynthesis. Butenafine is transported into the fungal cell vis diffusion. Squalene monooxygenase catalyzes the synthesis of (S)-2,3-epoxysqualene from squalene. Since it is inhibited, it cannot continue on to synthesize lanosterol which is essential in the synthesis of ergosterol. Without ergosterol in the cell membrane, the cell membrane sees increased permeability which allows intracellular components to leak out of the cell. Ergosterol is also essential in cell membrane integrity so without that, eventually the cell collapses and dies.. The fungal cell also cannot synthesize new cell membranes for new fungus cells if there is no ergosterol. The inhibition of squalene monooxygenase also causes a buildup of squalene which is toxic to the fungal cell.

Butanoate or butyrate is the traditional name for the conjugate base of butanoic acid (also known as butyric acid). Butanoate metabolism includes L-glutamate degradation into the signal molecule GABA followed by subsequent reactions to make further products. Glutamate decarboxylase is an enzyme in the cytosol that catalyzes the conversion of L-glutamate into 4-aminobutanoate (GABA). It requires pyridoxal 5'-phosphate as a cofactor. This is followed by GABA permease, belonging to the APC Family of transport proteins, transporting GABA from the cytosol into the mitochondria matrix. Next, gamma-aminobutyrate transaminase degrades gamma-amino butyric acid (GABA) into succinate semialdehyde and uses either pyruvate or glyoxylate as an amino-group acceptor. The pyruvate-dependent activity is reversible while the glyoxylate-dependent activity is irreversible. Afterwards, succinate-semialdehyde dehydrogenase oxidizes succinate semialdehyde into succinate. A predicted succinate semialdehyde transporter in the mitochondria inner membrane is theorized to export succinate semialdehyde from the mitochondrial matrix into the cytosol. There, glyoxylate/succinic semialdehyde reductase catalyzes the reversible conversion of succinate semialdehyde into 4-hydroxybutanoate. Butanoate metabolism in Arabidopsis thaliana also includes reactions involving acetyl-CoA and acetoacetyl-CoA. 3-hydroxybutyryl-CoA dehydrogenase is a predicted enzyme (coloured orange in the image) in the cytosol that is theorized to catalyze the reversible conversion of 3-hydroxybutanoyl-CoA into acetoacetyl-CoA. Acetyl-CoA acetyltransferase then catalyzes the reversible conversion of acetoacetyl-CoA into acetyl-CoA. Then, hydroxymethylglutaryl-CoA synthase condenses acetyl-CoA with acetoacetyl-CoA to form 3-hydroxy-3-methylglutaryl-CoA. This is followed by a predicted 3-hydroxy-3-methylglutaryl-CoA transporter localized to the mitochondria inner membrane that is theorized to import 3-hydroxy-3-methylglutaryl-CoA into the mitochondrial matrix from the cytosol. Once there, hydroxymethylglutaryl-CoA lyase catalyzes the synthesis of acetoacetate and acetyl-CoA from 3-hydroxy-3-methylglutaryl-CoA.