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.).
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- 純度 : 95.00%
- CAS 番号: 100513-53-9
- 分子式: C58H107NO23
- 分子量:1186.46
-
保管条件:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
MedChemExpress(MCE)の使用を引用している文献 Blasticidin A
MoreAntibiotic アイソフォーム固有の製品をすべて表示
More
生物活性
製品説明
体外実験
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.
-
Cell Line:Saccharomyces cerevisiae strain W303
-
Concentration:1 μM
-
Incubation Time:30 min
-
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.
化学情報
-
CAS 番号 100513-53-9
-
性状 Solid
-
分子量 1186.46
-
分子式 C58H107NO23
-
Color White to off-white
-
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
-
別名
(+)-Blasticidin A
-
輸送条件
Room temperature in continental US; may vary elsewhere.
-
保管条件
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Publications (1)
-
Journal Impact Factor
-
Most Recent
-
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
プロトコル
-
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.
純度とドキュメンテーション
-
データシート (269 KB)
-
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)
-
取扱説明書 (2659 KB)
参考文献
[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
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)