Agastinol
Agastinol is a naturally sourced caspase-3 inhibitor. Agastinol inhibits the expression of caspase-3 and apoptosis induced by Etoposide (HY-13629) in human leukemia U937 cells. Agastinol can be used in leukemia-related research.
For research use only. We do not sell to patients.
- CAS No.: 413615-33-5
- Formula: C27H28O8
- Molecular Weight:480.51
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Caspase Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
Caspase 3 15.2 μg/mL (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| U-937 | IC50 |
15.2 μg/mL
Compound: 1, agastinol
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Inhibition of etoposide-induced caspase 3 induction in human U937 cells after 7 hrs
Inhibition of etoposide-induced caspase 3 induction in human U937 cells after 7 hrs
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[PMID: 11908994] |
In Vitro
Agastinol (compound 1) inhibits the expression of caspase-3 in human leukemia U937 cells induced by Etoposide (HY-13629), with an IC50 of 15.2 μg/mL[1][2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 413615-33-5
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Molecular Weight 480.51
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Formula C27H28O8
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SMILES
C(OC(=O)C1=CC=C(O)C=C1)[C@H]2[C@@H](OC[C@H]2CC3=CC(OC)=C(O)C=C3)C4=CC(OC)=C(O)C=C4
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Structure Classification
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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
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)