Blasticidin A
Based on 1 publication(s) in Google Scholar
Blasticidin A ((+)-Blasticidin A) is a tetraamide acid derivative antibiotic produced by Streptomyces griseochromogenes, as well as a selective inhibitor of aflatoxin production. Blasticidin A exhibits antimicrobial activity against yeast. Blasticidin A can be used in research related to aflatoxin contamination (infection by Aspergillus sp.).
For research use only. We do not sell to patients.
- Purity : 95.00%
- CAS No.: 100513-53-9
- Formula: C58H107NO23
- Molecular Weight:1186.46
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Storage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
Publications Citing Use of MedChemExpress (MCE) Blasticidin A
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Biological Activity
Description
In Vitro
Blasticidin A (0.25-0.5 μM) dose-dependently inhibits aflatoxin production by Aspergillus parasiticus NRRL2999 in liquid culture, achieving near-complete inhibition at 0.5 μM without significantly reducing mycelial growth[1].
Blasticidin A (0.03-0.5 μg/mL) dose-dependently inhibits aflatoxin production by Aspergillus parasiticus NRRL2999 on agar plates, achieving complete inhibition at 0.5 μg/mL, while also dose-dependently reducing fungal hyphal extension and altering colony morphology at higher concentrations[1].
Blasticidin A (1 μM; 30 min) alters the proteome of Saccharomyces cerevisiae strain W303, reducing ribosomal protein abundance, increasing Gpd1p abundance, and promoting shifts to phosphorylated forms of key translational and chaperone proteins[2].
Blasticidin A (1 μM; 30 min) does not alter transcription of ribosomal protein genes ASC1 and RPP0 but increases transcription of GPD1 in Saccharomyces cerevisiae strain W303[2].
Blasticidin A (0.1-1 μM; 60 min) inhibits galactose-induced 6×His-LacZ protein synthesis in a dose-dependent manner in plasmid-transformed Saccharomyces cerevisiae strain W303[2].
Blasticidin A potently and selectively inhibits aflatoxin production in Aspergillus parasiticus NRRL2999, with an IC50 of 0.25 μM for aflatoxin production and an IC50 of 1.6 μM for fungal growth, giving a selectivity ratio of 6.4[2].
Blasticidin A (0.3 mM; 24-36 h) alters the proteome of Aspergillus flavus IMF47798, reducing abundances of aflatoxin biosynthetic enzymes after 36 h and reducing abundances of multiple metabolic and hypothetical proteins while increasing glutathione S-transferase abundances after both 24 h and 36 h[2].
Blasticidin A selectively inhibits aflatoxin production in Aspergillus flavus IMF47798, with an IC50 of 0.25 μM for aflatoxin production and an IC50 of 1.6 μM for fungal growth[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Saccharomyces cerevisiae strain W303
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Concentration:1 μM
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Incubation Time:30 min
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Result:Did not affect the mRNA levels of ribosomal protein genes ASC1 and RPP0.
Significantly increased the mRNA level of GPD1 relative to untreated control cells.
Chemical Information
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CAS No. 100513-53-9
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Appearance Solid
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Molecular Weight 1186.46
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Formula C58H107NO23
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Color White to off-white
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SMILES
OC(/C(C)=C/[C@@H](C)C[C@@H](C)C[C@@H](O)[C@H](O)[C@@H](C)[C@H](O)C[C@H](O)[C@H](C)[C@H](O)[C@@H](C)[C@H](O)C[C@H](O)C[C@H](O)C[C@H](O)C[C@H](O)[C@H](O)[C@@H](O)[C@H](O)[C@@H](O)C[C@H]1O[C@](O)([C@H]([C@H]([C@@H]1O)O)O)C[C@H](O)CCCCCCCCCC)=C2C(CN(C/2=O)C)=O
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Synonyms
(+)-Blasticidin A
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Publications (1)
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Journal Impact Factor
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Most Recent
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J Exp Clin Cancer Res
PHGDH activation fuels glioblastoma progression and radioresistance via serine synthesis pathway. [Abstract]2025 Mar 19;44(1):99. PMID: 40102981
Protocols
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
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Data Sheet (269 KB)
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SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 KB)
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Handling Instructions (2659 KB)
References
[1]. Sakuda S, et al. Blasticidin A as an inhibitor of aflatoxin production by Aspergillus parasiticus. J Antibiot (Tokyo). 2000;53(11):1265-1271. [Content Brief]
[2]. Yoshinari T, et al. Inhibitory activity of blasticidin A, a strong aflatoxin production inhibitor, on protein synthesis of yeast: selective inhibition of aflatoxin production by protein synthesis inhibitors. J Antibiot (Tokyo). 2010;63(6):309-314. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)