Apoptosis inducer 63
Apoptosis inducer 63 is an Apoptosis inducer. Apoptosis inducer 63 induces apoptosis and interferes with cell cycle progression through G2/M phase arrest and subsequent G1 phase accumulation. Apoptosis inducer 63 exhibits anticancer activity against colorectal cancer, lung cancer, and epithelioid carcinoma. Apoptosis inducer 63 can be used for research on colorectal cancer.
For research use only. We do not sell to patients.
- CAS No.: 872984-72-0
- Formula: C23H21N5O4
- Molecular Weight:431.44
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| A-431 | CC50 |
3.71 μM
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Cytotoxicity against human epidermoid carcinoma A-431 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Cytotoxicity against human epidermoid carcinoma A-431 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
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42570380 |
| BJ | CC50 |
11.58 μM
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Cytotoxicity against normal human epidermoid fibroblast BJ cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Cytotoxicity against normal human epidermoid fibroblast BJ cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
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42570380 |
| A549 | CC50 |
9.21 μM
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Cytotoxicity against human lung carcinoma A-549 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Cytotoxicity against human lung carcinoma A-549 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
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42570380 |
| NCI-H1299 | CC50 |
10.36 μM
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Cytotoxicity against human p53-deficient lung carcinoma NCI-H1299 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Cytotoxicity against human p53-deficient lung carcinoma NCI-H1299 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
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42570380 |
| MRC5 | CC50 |
10.79 μM
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Cytotoxicity against normal human lung fibroblast MRC-5 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Cytotoxicity against normal human lung fibroblast MRC-5 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
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42570380 |
| HCT-116 | CC50 |
8.8 μM
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Cytotoxicity against human colorectal carcinoma HCT116 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Cytotoxicity against human colorectal carcinoma HCT116 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
|
42570380 |
| HCT-116 | CC50 |
10.22 μM
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Cytotoxicity against human colorectal carcinoma HCT116 p53−/− cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Cytotoxicity against human colorectal carcinoma HCT116 p53−/− cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
|
42570380 |
In Vitro
Apoptosis inducer 63 (Compound 28) (0.32-160 μM; 72 h) exhibits highly potent growth inhibitory activity against A-431 cells with a CC50 of 3.71 μM[1].
Apoptosis inducer 63 (0.32-160 μM; 72 h) exhibits highly potent growth inhibitory activity against A-549 cells with a CC50 of 9.21 μM[1].
Apoptosis inducer 63 (0.32-160 μM; 72 h) exhibits highly potent growth inhibition against HCT116 cells, with a CC50 of 8.8 μM[1].
Apoptosis inducer 63 (5-40 μM; 96 h) induces apoptosis in both HCT116 and HCT116 p53−/− colorectal cancer cells, and at lower concentrations, the proportion of apoptotic cells is slightly higher in the p53-deficient cell line[1].
Apoptosis inducer 63 (20 μM) interferes with cell cycle progression in HCT116 and HCT116 p53−/− cells by inducing G2/M phase arrest and subsequent G1 phase accumulation, independent of p53 status[1].
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:HCT116 and HCT116 p53−/−
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Concentration:5-40 μM
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Incubation Time:96 h
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Result:Detected a substantial number of apoptotic cells in untreated samples, which increased significantly following treatment with 40 μM.
Detected a significantly higher proportion of apoptotic cells in the p53−/− line after treatment with 10 μM for 2-3 days and with 20 μM for 1-3 days.
Chemical Information
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CAS No. 872984-72-0
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Molecular Weight 431.44
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Formula C23H21N5O4
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SMILES
OC[C@@H]1[C@@H](O)[C@@H](O)[C@H](N2C=NC3=C2N=CN=C3NC4=CC=C5C(CC6=C5C=CC=C6)=C4)O1
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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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Detection of 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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Flow cytometric DNA-content cell-cycle staining
Flow cytometric DNA-content cell-cycle staining measures the fluorescence intensity of DNA-bound fluorochromes in single cells or nuclei to estimate DNA content distributions, allowing assignment of populations to G0/G1, S, and G2/M phases by DNA histogram deconvolution. Propidium iodide (PI) intercalates into DNA, and PI fluorescence is proportional to cellular DNA content when staining is performed under conditions that make DNA accessible and minimize non-DNA signal. Cells with G2/M DNA content are expected to show approximately twice the fluorescence intensity of G0/G1 cells, while S-phase cells occupy intermediate fluorescence values. PI-based DNA-content analysis can also detect cells with fractional DNA content, often reported as sub-G1, when DNA fragmentation and extraction during staining reduce retained DNA signal in apoptotic cells. DAPI is an alternative DNA fluorochrome for univariate DNA-content analysis, while bivariate approaches combining DNA content with proliferation
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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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BrdU Incorporation Assay
Bromodeoxyuridine (BrdU) incorporation assay is based on the principle that BrdU, a thymidine analog, is incorporated into newly synthesized DNA during the S phase of the cell cycle, thereby serving as a marker of DNA replication and cellular proliferation. Incorporated BrdU can be detected using anti-BrdU antibodies following DNA denaturation, enabling visualization or quantification of proliferating cells through immunochemical detection methods such as immunofluorescence or immunohistochemistry.
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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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Protocol for Cell Cycle
Cell-cycle analysis by flow cytometry measures DNA content in single cells to estimate the fraction of cells in G0/G1, S, and G2/M phases. Propidium iodide intercalates into DNA, and after RNA removal with RNase, fluorescence intensity reflects cellular DNA content: 2N cells are assigned to G0/G1, cells between 2N and 4N to S phase, and 4N cells to G2/M. DNA-content analysis alone cannot reliably separate G0 from G1 or G2 from M. Ki-67 can distinguish quiescent G0 cells from cycling cells, EdU or BrdU incorporation marks active DNA synthesis in S phase, and phospho-histone H3 staining identifies mitotic cells within the 4N population.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)