28-Deoxonimbolide
28-Deoxonimbolide is a Nimbin (HY-N3187) type limonoid, that can be isolated from Azadirachta indica seed extracts. 28-Deoxonimbolide shows anticancer activity. 28-Deoxonimbolide induces apoptotic cell death in HL60 cells via both the mitochondrial- and the death receptor-mediated pathways.
For research use only. We do not sell to patients.
- CAS No.: 126005-94-5
- Formula: C27H32O6
- Molecular Weight:452.54
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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
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Caspase-8 |
Caspase-9 |
Caspase-3 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| A549 | IC50 |
9.3 μM
Compound: 28
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Cytotoxicity against human A549 cells assessed as cell viability after 48 hrs by MTT assay
Cytotoxicity against human A549 cells assessed as cell viability after 48 hrs by MTT assay
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[PMID: 21381696] |
| AZ-521 cell line | IC50 |
2.4 μM
Compound: 28
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Cytotoxicity against human AZ-521 cells assessed as cell viability after 48 hrs by MTT assay
Cytotoxicity against human AZ-521 cells assessed as cell viability after 48 hrs by MTT assay
|
[PMID: 21381696] |
| BC1 cell line | ED50 |
1.34 μg/mL
Compound: 2
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Cytotoxicity against human BC1 cells after 72 hrs
Cytotoxicity against human BC1 cells after 72 hrs
|
[PMID: 2614419] |
| Col2 | ED50 |
1.81 μg/mL
Compound: 2
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Cytotoxicity against human Col2 cells after 72 hrs
Cytotoxicity against human Col2 cells after 72 hrs
|
[PMID: 2614419] |
| HL-60 | IC50 |
2.7 μM
Compound: 28
|
Cytotoxicity against human HL60 cells assessed as cell viability after 48 hrs by MTT assay
Cytotoxicity against human HL60 cells assessed as cell viability after 48 hrs by MTT assay
|
[PMID: 21381696] |
| HT-1080 | ED50 |
1.04 μg/mL
Compound: 2
|
Cytotoxicity against human HT1080 cells after 48 hrs
Cytotoxicity against human HT1080 cells after 48 hrs
|
[PMID: 2614419] |
| KB | ED50 |
1.3 μg/mL
Compound: 2
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Cytotoxicity against human KB cells after 72 hrs
Cytotoxicity against human KB cells after 72 hrs
|
[PMID: 2614419] |
| Lu1 | ED50 |
0.84 μg/mL
Compound: 2
|
Cytotoxicity against human Lu1 cells
Cytotoxicity against human Lu1 cells
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[PMID: 2614419] |
| P388 | ED50 |
0.66 μg/mL
Compound: 2
|
Cytotoxicity against mouse P388 cells after 48 hrs
Cytotoxicity against mouse P388 cells after 48 hrs
|
[PMID: 2614419] |
| SK-BR-3 | IC50 |
1.7 μM
Compound: 28
|
Cytotoxicity against human SK-BR-3 cells assessed as cell viability after 48 hrs by MTT assay
Cytotoxicity against human SK-BR-3 cells assessed as cell viability after 48 hrs by MTT assay
|
[PMID: 21381696] |
| SK-MEL-2 | ED50 |
2.05 μg/mL
Compound: 2
|
Cytotoxicity against human SK-MEL-2 cells after 72 hrs
Cytotoxicity against human SK-MEL-2 cells after 72 hrs
|
[PMID: 2614419] |
In Vitro
28-Deoxonimbolide (1-100 μM, 48 h) exhibits potent cytotoxic activity against HL60 (leukemia), A549 (lung), AZ521 (stomach), SK-BR-3 (breast), CRL1579 (melanoma), and RPMI1788 (normal lymphocyte) cells[1].
28-Deoxonimbolide (30 μM, 0-24 h) induces apoptosis in HL60 cells[1].
28-Deoxonimbolide (30 μM, 0-24 h) increases the levels of cleaved caspases-8, -9, and -3[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:HL60, A549, AZ521, SK-BR-3, CRL1579 cells, RPMI1788
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Concentration:1-100 μM
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Incubation Time:48 h
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Result:Exhibited potent cytotoxic activity against HL60 (leukemia), A549 (lung), AZ521 (stomach), SK-BR-3 (breast), and CRL1579 (melanoma) cells, with IC50 values of 2.7 μM, 9.3 μM, 2.4 μM, 1.7 μM, 14.2 μM, and 2.7 μM, respectively.
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Cell Line:HL60 cells
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Concentration:30 μM
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Incubation Time:8 and 24 h
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Result:Induced early apoptosis in HL60 cells. The ratio of early apoptotic cells was increased after 8 h (10.9% vs 6.1% of negative control) and 24 h (18.7% vs 3.5% of negative control), and that of late apoptotic cells (upper right) was increased after 24 h (28.1% vs 2.9% of negative control).
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Cell Line:HL60 cells
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Concentration:30 μM
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Incubation Time:8 and 24 h
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Result:Diminished the levels of procaspases-8, -9, and -3, and then increased the levels of cleaved caspases-8, -9, and -3.
Chemical Information
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CAS No. 126005-94-5
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Molecular Weight 452.54
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Formula C27H32O6
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SMILES
O=C(OC)C[C@@H]([C@]1(C)C2=C(C)[C@H](C3=COC=C3)C[C@@]2([H])O[C@]1([H])[C@@](OC4)([H])[C@@]5([H])[C@@]4(C)C=C6)[C@@]5(C)C6=O
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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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Detection of Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
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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)