Stigmast-5-en-3-ol
Stigmast-5-en-3-ol induces cancer cell apoptosis and inhibits proliferation by increasing the production of Bax, Caspase-9, p53, and PARP cleavage and reducing Bcl-xl expression. Stigmast-5-en-3-ol exhibits potent inhibitory activity against glucoamylase and α-amylase and possesses high antioxidant activity. Stigmast-5-en-3-ol can be used in the research of diseases such as leukemia, breast cancer, type 2 diabetes, and obesity.
For research use only. We do not sell to patients.
- CAS No.: 5779-62-4
- Formula: C29H50O
- Molecular Weight:414.71
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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Biological Activity
Description
IC50 & Target
[1]|
Caspase-9 |
Bax |
Bcl-xL |
In Vitro
Stigmast-5-en-3-ol (Compound DGEH21-3-2) (12.5-50 μg/mL, 24 h) shows cytotoxic effects against HL-60 and MCF-7 cells, with IC50 s of 37.82 and 45.17 μg/mL respectively[1].
Stigmast-5-en-3-ol (12.5-50 μg/mL, 24 h) induces apoptosis, increases DNA damage, increases production of Bax, Caspase-9, p53 and PARP cleavage, and decreased Bcl-xl levels in HL-60 and MCF-7 cells[1].
Stigmast-5-en-3-ol (Compound 24R) (2-10 μg/mL, 30 min) exhibits potent inhibitory activity against glucoamylase and α-amylase with IC50 s of 5.8 and 7.198 µg/mL respectively, shows high radical activity[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:HL-60 and MCF-7 cells
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Concentration:12.5, 25, 50 μg/mL
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Incubation Time:24 h
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Result:Increased the number of apoptotic bodies and dose-dependently increased the sub-G1 apoptotic cell population, resulting in a sub-G1 apoptotic cell population of 66.30% in HL-60 cells and 60.05% in MCF-7 cells at 50 μg/ml.
Increased production of Bax, Caspase-9, and PARP cleavage, and decreased Bcl-xl levels.
Dose-dependent increased p53 expression in MCF-7 cells.
Chemical Information
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CAS No. 5779-62-4
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Molecular Weight 414.71
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Formula C29H50O
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SMILES
C[C@@]12[C@](CC[C@]2([H])[C@H](C)CC[C@@H](CC)C(C)C)([H])[C@@]3([H])[C@@](CC1)([H])[C@@]4(C(CC(CC4)O)=CC3)C
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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