Azoxybacilin
* Please be kindly noted products are not for therapeutic use. We do not sell to patients.
| Category | Antibiotics |
| Catalog number | BBF-00247 |
| CAS | 157998-96-4 |
| Molecular Weight | 161.16 |
| Molecular Formula | C5H11N3O3 |
Online Inquiry
Description
Azoxybacilin is produced by the strain of Bacillus cereus NR2991. It can inhibit the sulfur fixation reaction in methionine biosynthesis and has strong anti-filamentous fungal activity: The IC80 of Aspergillus fumigata and Trichoderma was 0.71 ~ 1.3 μg/mL and 0.03 ~ 0.24 μg/mL, respectively. It had only moderate activity to yeast-based fungi, and the IC80 of Candida albicans was 4.2 ~ 5.8 μg/mL.
Specification
| Synonyms | (2s)-2-amino-4-[(z)-methyl-nno-azoxy]butanoic acid; Butanoic acid, 2-amino-4-[(1Z)-methyl-NNO-azoxy]-, (2S)- |
| IUPAC Name | [(3S)-3-amino-3-carboxypropyl]-methylimino-oxidoazanium |
| Canonical SMILES | CN=[N+](CCC(C(=O)O)N)[O-] |
| InChI | InChI=1S/C5H11N3O3/c1-7-8(11)3-2-4(6)5(9)10/h4H,2-3,6H2,1H3,(H,9,10)/t4-/m0/s1 |
| InChI Key | KFZWEFIJHQUPCM-BYPYZUCNSA-N |
Properties
| Appearance | Colorless Acicular Crystalline |
| Antibiotic Activity Spectrum | fungi |
| Melting Point | 203-205 °C |
| Solubility | Soluble in water, methanol, insoluble in acetone, n-hexane. |
Reference Reading
1. Antifungal azoxybacilin exhibits activity by inhibiting gene expression of sulfite reductase
Y Aoki, M Yamamoto, S M Hosseini-Mazinani, N Koshikawa, K Sugimoto, M Arisawa Antimicrob Agents Chemother. 1996 Jan;40(1):127-32. doi: 10.1128/AAC.40.1.127.
Azoxybacilin, produced by Bacillus cereus, has a broad spectrum of antifungal activity in methionine-free medium and has been suggested to inhibit sulfite fixation. We have further investigated the mode of action by which azoxybacilin kills fungi. The compound inhibited the incorporation of [35S] sulfate into acid-insoluble fractions of Saccharomyces cerevisiae under conditions in which virtually no inhibition was observed for DNA, RNA, or protein synthesis. It did not interfere with the activity of the enzymes for sulfate assimilation but clearly inhibited the induction of those enzymes when S. cerevisiae cells were transferred from rich medium to a synthetic methionine-free medium. Particularly strong inhibition was observed in the induction of sulfite reductase. Northern (RNA) analysis revealed that azoxybacilin decreased the level of mRNA of genes for sulfate assimilation, including MET10 for sulfite reductase and MET4, the transactivator of MET10 and other sulfate assimilation genes. When activities of azoxybacilin were compared for mRNA and enzyme syntheses from MET10, the concentration required for inhibition of transcription of the gene was about 10 times higher (50% inhibitory concentration = 30 micrograms/ml) than that required for inhibition of induction of enzyme synthesis (50% inhibitory concentration = 3 micrograms/ml). The data suggest that azoxybacilin acts on at least two steps in the expression of sulfite reductase; the transcriptional activation of MET4 and a posttranscriptional regulation in MET10 expression. We conclude that azoxybacilin exhibits antifungal activity by interfering with the regulation of expression of sulfite reductase activity.
2. Design of an antifungal methionine inhibitor not antagonized by methionine
Y Aoki, T Kamiyama, T Fujii, M Yamamoto, J Ohwada, M Arisawa Biol Pharm Bull. 1995 Sep;18(9):1267-71. doi: 10.1248/bpb.18.1267.
Only a few biosynthetic pathways in fungal cells have been used as antifungal targets. Therefore, the number of antifungals has been limited, and a cross-drug resistance among them has emerged in the therapy of mycoses. Under such circumstances, the identification of an antifungal with a new mode of action is highly desirable. By infecting mice with a mutant of C. albicans deficient in the sulfate assimilation pathway, we have discovered a new target for the discovery of antifungal agents. We have proven that azoxybacilin inhibits the sulfate assimilation pathway by showing its inhibitory activity for [35S]SO4 incorporation into proteins. We have also demonstrated that azoxybacilin was taken up into fungal cells via an active transport system specific for methionine. This sharing of the uptake system with methionine may explain the mechanism by which the antifungal activity of azoxybacilin is antagonized by methionine, and led us to design azoxybacilin derivatives that lack the structural feature of amino acids and, at the same time, have increased hydrophobicity to give higher non-specific permeability through the cell membrane. As a result, we have found that ester derivatives of azoxybacilin were not antagonized by methionine in their uptake, and that they showed antifungal activity independent of methionine. The benzyl ester of azoxybacilin was the same as azoxybacilin in its mode of action, but was not markedly antagonized by methionine at concentrations up to 1 mg/ml. These results suggest that azoxybacilin may not merely interfere with the sulfate assimilation pathway.
3. Ultradian metabolic oscillation of Saccharomyces cerevisiae during aerobic continuous culture: hydrogen sulphide, a population synchronizer, is produced by sulphite reductase
H Sohn, H Kuriyama Yeast. 2001 Jan 30;18(2):125-35. doi: 10.1002/1097-0061(20010130)18:23.0.CO;2-9.
We have reported that the consecutive cyclic production of H(2)S resulted in population synchrony of ultradian metabolic oscillation (Sohn et al., 2000). In order to understand the origin of H(2)S and its nature of periodic production, changes of sulphur compounds concentration and responsible enzymes were investigated. The concentrations of extracellular sulphate, intracellular glutathione and cysteine oscillated during metabolic oscillation but only the oscillation of sulphate concentration was out of phase with H(2)S production. The sulphate concentration in culture directly affected the amplitude and the period of metabolic oscillation: (a) the period of metabolic oscillation shortened from 50 min to 30 min when sulphate concentration in the medium was reduced from 46 mM to 2.5 mM; (b) the metabolic oscillation disappeared under sulphate-depletion conditions and arose again by the addition of sulphate. Pulse injection of sulphite (10 microM) perturbed metabolic oscillation with a burst production of H(2)S, while thiosulphate (up to 500 microM) was without apparent effect. Furthermore, addition of S-adenosyl methionine (100 microM) or azoxybacilin (3 mg/kg) decreased H(2)S production with perturbation of metabolic oscillation. The results presented here suggest that H(2)S, a population synchronizer, is produced by sulphite reductase in the sulphate assimilation pathway, and dynamic regulation of sulphate uptake plays an important role in ultradian metabolic oscillation.
Recommended Products
| BBF-03754 | CASTANOSPERMINE | Inquiry |
| BBF-03755 | Actinomycin D | Inquiry |
| BBF-02614 | Nystatin | Inquiry |
| BBF-01693 | Doxorubicin EP Impurity A (Daunorubicin) | Inquiry |
| BBF-01825 | Loganin | Inquiry |
| BBF-01826 | Deoxymannojirimycin | Inquiry |
Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
