Aculeacin A
Aculeacin A is a β-1,3-glucan synthase inhibitor. Aculeacin A is an antifungal antibiotic. Aculeacin A inhibits cell wall glucan synthesis in growing yeast cells, induces cell lysis, osmotic fragility, cell aggregation and abnormal cell morphology, without affecting the synthesis of proteins, nucleic acids or mannan. Aculeacin A acts only on growing yeast cells and has a narrow antifungal spectrum, mainly targeting Candida and Torulopsis species. Aculeacin A shows reduced activity in human serum and exhibits a paradoxical dose-response pattern. Aculeacin A has an inoculum effect against some Candida albicans strains, and its activity is pH-stable. Aculeacin A can be used in studies of fungal infections, such as those caused by Candida, Torulopsis and other species.
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- CAS. Nr.: 58814-86-1
- Formel: C50H81N7O16
- Molecular Weight:1036.22
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
Beschreibung
IC50 & Target
[4]|
Lipopeptide |
In Vitro
Aculeacin A (0.05-0.5 μg/mL; up to 20 hours) completely inhibits the growth of Saccharomyces cerevisiae Hansen 0209 strain at a concentration of 0.5 μg/mL, and partially inhibits its growth at 0.2 μg/mL, when incubated in glucose-peptone medium for up to 20 hours[2].
Aculeacin A (0.5-50 μg/mL; up to 4 h) exhibits fungicidal activity against actively growing cells of Saccharomyces cerevisiae Hansen 0209 strain, and reduces cell viability within 2 h of incubation, but has no effect on the viability of non-growing resting cells even at the highest concentration of 50 μg/mL[2].
Aculeacin A (5 μg/mL; 1 hour) causes cell lysis at the budding tips of Saccharomyces cerevisiae Hansen 0209 strain within 1 hour of incubation in glucose-peptone medium[2].
Aculeacin A (5 μg/mL; 10 minutes pre-incubation, followed by incubation for up to 90 minutes) inhibits the incorporation of [U-14C]glucose into acid-insoluble fractions of Saccharomyces cerevisiae Hansen 0209 cells, but exerts no effect on the incorporation of [1-14C]leucine or [2-14C]uridine after up to 90 minutes of incubation with the radioactive precursors[2].
Aculeacin A (5 μg/mL; 10 minutes pre-incubation followed by 30 minutes treatment) selectively inhibits the incorporation of [U-14C] glucose into the glucan component of the cell wall of Saccharomyces cerevisiae Hansen 0209 strain, reducing the incorporation level to 45.7% of that in the control group, while exerting minimal effects on mannan synthesis[2].
Aculeacin A (10-100 μg/mL) weakly induces protoplast lysis of Saccharomyces cerevisiae Hansen 0209 only at the relatively high concentration of 100 μg/mL, while no effect is observed at 10 μg/mL[2].
Aculeacin A (5 μg/mL; 1 hour) induces membrane invagination and the formation of membranous spherical bodies in the gap between the cell wall and cytoplasm in intact Saccharomyces cerevisiae Hansen 0209 strain cells after 1 hour of incubation[2].
The inhibitory activity of Aculeacin A against 6 strains of Candida albicans is almost unaffected by variations in medium pH within the range of 3.0 to 8.0[3].
Aculeacin A (0.02-20 μg/mL; 6 hours) exhibits fungicidal activity against actively growing Candida albicans, Candida tropicalis, and Torulopsis glabrata, with its lethal activity peaking at concentrations ranging from 0.08 to 0.31 μg/mL, while higher concentrations reduce its fungicidal effect[3].
Aculeacin A (0.02-20 μg/mL; up to 6 hours) exerts paradoxical fungicidal and growth-inhibitory effects on exponentially growing Candida albicans MTU 12077 cells, with activity peaking at 0.08~1.25 μg/mL and decreasing at higher concentrations[4].
Studies show that Aculeacin A (0.31 μg/mL; 0-6 hours) exerts no effect on non-proliferating Candida albicans cells, but significantly reduces the viability of proliferating cells at the same concentration[4].
Aculeacin A (0.08-1.25 μg/mL; 30 minutes) induces visible aggregates in exponentially growing susceptible yeast cells, including Candida albicans, but does not induce aggregation in non-susceptible yeast strains[4].
Aculeacin A (0.08-20 μg/mL; 6 hours) induces concentration-dependent morphological changes in exponentially growing Candida albicans MTU 12077 cells. It causes cell lysis at concentrations ranging from 0.08 to 0.31 μg/mL, and induces abnormally large cell morphology at a concentration of 20 μg/mL[4].
Aculeacin A (0.31-20 μg/mL; 3 hours) induces osmotically sensitive cells in Candida albicans MTU 12077, with lower concentrations resulting in greater sensitivity, while osmotic stabilization inhibits the drug-induced cell aggregation[4].
Aculeacin A (0.01-100 μg/mL; 20 minutes pre-incubation) preferentially inhibits the synthesis of alkali-insoluble glucan in osmotically stabilized exponential-phase Candida albicans MTU 12077 cells (with an inhibition rate of approximately 80% at 0.31 μg/mL), and exhibits an anomalous dose-response: the inhibitory effect reaches a peak at 0.31 μg/mL, while the inhibition weakens at higher concentrations[4].
Aculeacin A (0.31-20 μg/mL; 3 hours) induces alkali-insoluble glucan-deficient Candida albicans MTU 12077 cells, with their glucan content reduced to ~20-23% of that in the control group, while other cellular components are minimally affected[4].
Aculeacin A (0.08-80 μg/mL; 60 minutes) inhibits β-(1,3)-glucan synthase activity in cell-free extracts of Candida albicans MTU 12077 and Saccharomyces cerevisiae MTU 09018 (with maximum inhibition rates of up to 64% at 8 μg/mL and up to 75% at 0.8 μg/mL), and the inhibitory effect weakens at higher concentrations[4].
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 Hansen 0209 cells
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Concentration:0.05 μg/mL, 0.2 μg/mL, 0.5 μg/mL
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Incubation Time:up to 20 hours
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Result:Completely inhibited growth over the 20-hour incubation period at 0.5 μg/mL.
Partially reduced growth compared to untreated controls at 0.2 μg/mL.
Showed minimal growth inhibition relative to higher concentrations at 0.05 μg/mL.
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Cell Line:Saccharomyces cerevisiae strain Hansen 0209 cells
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Concentration:tested concentrations (growth-permissive medium); 5 μg/mL, 50 μg/mL (non-growth buffer)
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Incubation Time:up to 4 hours (growth-permissive medium); up to 4 hours (non-growth buffer)
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Result:Exerted a fungicidal effect at all tested concentrations in growth-permissive glucose-peptone medium, with a distinct decrease in viable cells occurring within the first 2 hours, followed by a gradual reduction in the rate of cell death.
Caused no decrease in viable cells at 5 μg/mL or 50 μg/mL over 4 hours in non-growth 0.1 M phosphate buffer.
Chemical Information
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CAS. Nr. 58814-86-1
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Molecular Weight 1036.22
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Formel C50H81N7O16
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SMILES
CCCCCCCCCCCCCCCC(NC1C(NC(C(O)C)C(N2C(CC(O)C2)C(NC(C(O)C(O)C3=CC=C(O)C=C3)C(NC(C(O)C)C(N4C(C(O)C(C)C4)C(NC(O)C(O)C1)=O)=O)=O)=O)=O)=O)=O
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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Research Protocol for Drug Screening technologies
Drug screening technologies are experimental and computational strategies used to identify small molecules or chemical probes that modulate a defined molecular target, signaling pathway, cellular phenotype, disease model, or patient-derived response profile. High-throughput screening tests many compounds in miniaturized assay formats, while quantitative high-throughput screening tests compounds across concentration ranges so that potency and efficacy can be inferred from concentration-response behavior rather than from a single-point signal. The core biological function of a drug-screening strategy is to connect compound exposure with measurable pathway activity, target modulation, cell-state change, viability, cytotoxicity, morphology, or disease-relevant phenotype. Assay performance must be evaluated before screening because hit identification depends on the separation between positive and negative controls, control variability, plate effects, outliers, and the statistical framework
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Suspension Spheroid Formation (Low-Adhesion/Forced Aggregation)
Suspension spheroid formation by low-adhesion or forced aggregation is a scaffold-free 3D culture method in which cells are prevented from attaching to plastic and are guided to interact with each other, forming compact multicellular aggregates through cell-cell adhesion, gravity-driven settling, microwell confinement, or centrifugation-assisted aggregation. The method detects the capacity of a cell population to self-assemble into spheroids, and the main readouts are spheroid formation efficiency, morphology, compactness, projected area or diameter, circularity, viability, proliferation, and experimental responses such as drug sensitivity. Classic implementations include hanging drops, agarose or hydrogel microwells, ultra-low-attachment round-bottom wells, and centrifugation-assisted aggregation in non-adherent wells. Low-adhesion culture shifts the system away from cell-substrate adhesion and toward cell-cell adhesion, while round-bottom or microwell geometry concentrates cells into
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Protein Extraction
Protein extraction uses physical, chemical or biological methods, such as ultrasonic disruption, salting out, cell lysis, electrophoresis, etc., to destroy the cell membrane structure and to separate the proteins from different components according to their characteristics.
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Hanging Drop Spheroid Culture
Hanging drop spheroid culture is a scaffold-free 3D culture method in which a small droplet of cell suspension is inverted so that suspended cells sediment by gravity toward the lowest point of the drop, aggregate, and form a multicellular spheroid with direct cell-cell contact. Spheroids generated by this method are used to study 3D cell cohesion, cell-ECM interactions, drug response, co-culture organization, and tumor-like microenvironmental behavior. The primary readouts are spheroid formation efficiency, spheroid size, circularity or compactness, viability, and treatment response; these can be measured by bright-field microscopy, fluorescence viability staining, ATP-, fluorescence-, or colorimetric-based assays, and image-based diameter or volume calculations.
Reinheit & Dokumentation
Verweise
[1]. Zhang F, et al. Biochemical and genetic characterization of fungal proline hydroxylase in echinocandin biosynthesis. Applied microbiology and biotechnology. 2018 Sep;102(18):7877-7890. [Content Brief]
[2]. Mizoguchi J, et al. On the mode of action of a new antifungal antibiotic, aculeacin A: inhibition of cell wall synthesis in Saccharomyces cerevisiae. The Journal of antibiotics. 1977 Apr;30(4):308-13. [Content Brief]
[3]. Iwata K et al. In vitro studies of aculeacin A, a new antifungal antibiotic. J Antibiot (Tokyo). 1982 Feb;35(2):203-9. [Content Brief]
[4]. Yamaguchi H et al. Studies on the mechanism of antifungal action of aculeacin A. J Antibiot (Tokyo). 1982 Feb;35(2):210-9. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)