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Fig. 1 · Structure
Cat. No.
A10361
CAS No.
57-87-4
Formula
C28H44O
Mol. Weight
396.6

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Ergosterol

Cat. No. A10361 CAS 57-87-4
Ergosterol is a sterol and a biological precursor (a provitamin) to vitamin D2. Ergosterol is a component of fungal cell membranes, serving the same function that cholesterol serves in animal cells. Because ergosterol is present in fungal cell membranes yet absent in animal cell membranes, it is a useful target for antifungal drugs. .

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Biological Activity

Bioactivity / Mechanism

In MCF-7 and MDA-MB-231 cells, ergosterol reduced AKT phosphorylation and nuclear β-catenin signaling readouts. β-Catenin overexpression attenuated the localization response, supporting pathway involvement without establishing a direct molecular target. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Cellular Effect

Cell Line Activity Value Description Reference
A549 IC50 19.2 μM Antiproliferative activity against human A549 cells assessed as reduction in cell viability measured after 72 hrs by sulforhodamine B assay [PMID: 33691166]
BV-2 IC50 30.6 μM Antiinflammatory activity in mouse BV2 cells assessed as inhibition of LPS-induced iNOS-dependent nitrite production after 24 hrs by Griess method [PMID: 21028898]
COLO 205 IC50 4.9 μM Cytotoxicity against human COLO 205 cells assessed as reduction in cell viability measured after 24 hrs by MTT assay [PMID: 35293752]
COLO 320 IC50 6.5 μM Cytotoxicity against human COLO 320 cells assessed as reduction in cell viability measured after 24 hrs by MTT assay [PMID: 35293752]
HeLa IC50 0.91 μg/mL Inhibition of TNFalpha-induced NF-kappaB activity (unknown origin) expressed in HeLa cells cotreated with compound and 10 ng/ml TNF-alpha for 24 hr by reporter gene assay 10.1007/s00044-010-9409-z
L5178Y EC50 12.6 μM Cytotoxicity against mouse L5178Y cells by MTT assay [PMID: 27070198]
MRC5 IC50 0.5 μM Cytotoxicity against human MRC5 cells assessed as reduction in cell viability measured after 24 hrs by MTT assay [PMID: 35293752]
NCI-H157 IC50 23.3 μM Antiproliferative activity against human NCI-H157 cells assessed as reduction in cell viability measured after 72 hrs by sulforhodamine B assay [PMID: 33691166]

In Vitro Studies

Ergosterol reduced viability in two breast cancer cell lines and increased the G0/G1 cell-cycle fraction at 20 μM for 24 h. MCF-7 viability IC50 values were 6.70 ± 1.51 μM at 24 h and 9.52 ± 5.77 μM at 48 h; the MDA-MB-231 value was 15.55 ± 6.84 μM at 48 h (mean ± SD). These are assay-specific endpoints. [1]

Breast cancer cell viability and cell-cycle response

Cell-based study · Human MCF-7 and MDA-MB-231 breast cancer cells [1]

Ergosterol reduced the MTS viability signal with model- and time-dependent potency. At 20 μM for 24 h, both lines showed increased G0/G1 fractions relative to DMSO controls. The viability endpoint does not itself distinguish reduced proliferation from cell death.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
MCF-7 MTS viability after 24 hIC50 6.70 ± 1.51 μM[1]
MCF-7 MTS viability after 48 hIC50 9.52 ± 5.77 μM[1]
MDA-MB-231 MTS viability after 48 hIC50 15.55 ± 6.84 μM[1]
MDA-MB-231 viability at 20 μM, 24 hViability relative to vehicle 71.12 ± 4.18%[1]
Cell cycle at 20 μM, 24 hG0/G1 fraction Increased in both cell lines versus DMSO control[1]

Literature-Reported Treatment Conditions

Treatment concentration
2.5–40 μM for viability; 20 μM for cell cycle.
Exposure duration
24, 48 and 96 h for viability; 24 h for cell cycle. Quantitative IC50 values adopted only for the reported time points.
Method
Ergosterol treatment in cell culture; vehicle comparison.
Vehicle
0.1% DMSO (cell viability methods); DMSO control in Fig. 1b.
Reported limits
IC50 fitting procedure is not specified in the read methods. No normal breast-cell comparator was included in the selected experiment.
Methods and source locations

Compound reported in the paper: Ergosterol; Compound label in the paper: ER

Evidence applies to the reported ergosterol reagent in these cell models; supplier and lot equivalence to A10361 was not tested.

Results: Ergosterol inhibited the cell viability, cell cycle progression, and spheroid formation of breast cancer cells; Fig. 1a,b; Methods: Cell viability, Cell cycle analysis, Statistical analysis, Chemicals and reagents.

MCF-7 MTS viability after 24 h: MTS (CellTiter 96 AQueous One Solution); absorbance at 492 nm. Mean ± SD; three independent experiments as stated in statistical methods/caption. — Results first paragraph; Fig. 1a and caption; Cell viability; Statistical analysis

MCF-7 MTS viability after 48 h: Same viability experiment; reported mean ± SD, three independent experiments. — Results first paragraph; Fig. 1a and caption

MDA-MB-231 MTS viability after 48 h: Same viability experiment; reported mean ± SD, three independent experiments. — Results first paragraph; Fig. 1a and caption

MDA-MB-231 viability at 20 μM, 24 h: MTS viability; mean ± SD, three independent experiments. — Results first paragraph; Fig. 1a and caption

Cell cycle at 20 μM, 24 h: Propidium iodide flow cytometry; 10,000 events; Fig. 1b shows significant increases. No exact fraction estimated from the bars. — Fig. 1b and caption; Methods: Cell cycle analysis

Cellular AKT and β-catenin signaling response

Cell-based study · MCF-7 and MDA-MB-231 cells; vehicle controls and β-catenin overexpression/empty-vector comparisons [1]

Cellular assays associated ergosterol exposure with lower AKT phosphorylation and reduced nuclear β-catenin and reporter activity. β-Catenin overexpression attenuated the nuclear-localization response. These experiments support pathway involvement without proving direct target binding or β-catenin degradation.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
AKT Ser473 phosphorylationPhospho-AKT / total AKT Reduced from 6 to 24 h in both lines at 20 μM[1]
Nuclear β-catenin localization at 20 μM, 24 hNuclear colocalization Reduced in both cell lines relative to DMSO[1]
β-Catenin transcriptional reporter at 20 μM, 24 hRelative TOP/FOP luciferase activity 0.65 (MCF-7); 0.59 (MDA-MB-231); DMSO normalized to 1.00[1]
Nuclear β-catenin response under wild-type β-catenin overexpressionPerturbation control Ergosterol did not reduce the localization ratio in the overexpression condition as in the endogenous setting[1]

Literature-Reported Treatment Conditions

Treatment concentration
20 μM for adopted time-course, localization and reporter assays.
Exposure duration
AKT time course: 3, 6, 12 and 24 h; localization/reporter/overexpression comparisons: 24 h.
Method
Cellular exposure; serum-free treatment specified for immunofluorescence, transfection and Western blot methods.
Vehicle
DMSO control; 0.1% specified for immunofluorescence.
Co-treatment
β-Catenin expression construct versus empty vector is a mechanistic perturbation, not a drug combination.
Reported limits
Raw Western-blot SI PDF was acquired but not rendered/read. Direct ligand binding, isolated-enzyme potency and β-catenin degradation kinetics are not established by these selected assays.
Methods and source locations

Compound reported in the paper: Ergosterol; Compound label in the paper: ER

Evidence applies to the reported ergosterol reagent in these cell models; supplier and lot equivalence to A10361 was not tested.

Results: Ergosterol suppresses the nuclear translocation of β-catenin and its downstream targets; Ergosterol affected the β-catenin signaling pathway by inhibiting AKT/GSK-3β/β-catenin axis; Ergosterol downregulated β-catenin activity; Fig. 2b, 3a–c, 4c,d; matching Methods.

AKT Ser473 phosphorylation: Western blot time course; total AKT and β-actin controls. Mean ± SD, three independent experiments. — Fig. 3a and caption; Results: Ergosterol affected the β-catenin signaling pathway by inhibiting AKT/GSK-3β/β-catenin axis; Western blot analysis

Nuclear β-catenin localization at 20 μM, 24 h: Confocal immunofluorescence with Hoechst nuclear stain and Pearson correlation analysis. Mean ± SD, three independent experiments; no exact bar values inferred. — Fig. 2b and caption; Methods: Immunofluorescence

β-Catenin transcriptional reporter at 20 μM, 24 h: Explicit labels in Fig. 4d. Renilla normalization; wild-type TOP and mutant FOP controls. Bars show mean ± SD of three independent experiments; numerical SD not supplied as labels. — Fig. 4d and caption; Methods: Dual luciferase activity

Nuclear β-catenin response under wild-type β-catenin overexpression: Confocal immunofluorescence; empty-vector and β-catenin-expression conditions. Do not interpret as rescue of cell survival. — Fig. 4c and caption; Results: Ergosterol downregulated β-catenin activity; Methods: Transient transfection

Specifications

Manufacturer Adooq Bioscience
CAS Number 57-87-4
Formula C28H44O
Molecular Weight 396.6
SMILES
C[C@H](/C=C/[C@H](C)C(C)C)[C@H]1CC[C@@H]2[C@@]1(CC[C@H]3C2=CC=C4[C@@]3(CC[C@@H](C4)O)C)C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 0.01 mg/mL (0.02 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Sunita Nilkhet, Wudtipong Vongthip, Pattawika Lertpatipanpong, et al. Ergosterol inhibits the proliferation of breast cancer cells by suppressing AKT/GSK-3beta/beta-catenin pathway Scientific Reports (2024). PMID: 39179606 DOI: 10.1038/s41598-024-70516-1 Source material

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