dALK-3
dALK-3 is an EML4-ALK inhibitor with an IC50 of 13.1 nM against the human target. dALK-3 induces proteasomal degradation of EML4-ALK through components of the ubiquitin-proteasome system. dALK-3 exhibits antiproliferative activity against cancer cells. dALK-3 can be used in research related to non-small cell lung cancer.
For research use only. We do not sell to patients.
- Formula: C39H45ClN7O5P
- Molecular Weight:758.25
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| NCI-H3122 | GI50 |
0.004 μM
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Antiproliferative activity against human H3122 non-small-cell lung cancer cells with EML4-ALK fusion incubated for 72 hrs assessed by CellTiter-Glo assay.
Antiproliferative activity against human H3122 non-small-cell lung cancer cells with EML4-ALK fusion incubated for 72 hrs assessed by CellTiter-Glo assay.
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39681169 |
| NCI-H3122 | GI50 |
0.002 μM
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Antiproliferative activity against RNF126-depleted human H3122 non-small-cell lung cancer cells with EML4-ALK fusion incubated for 72 hrs assessed by CellTiter-Glo assay.
Antiproliferative activity against RNF126-depleted human H3122 non-small-cell lung cancer cells with EML4-ALK fusion incubated for 72 hrs assessed by CellTiter-Glo assay.
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39681169 |
| NCI-H3122 | DC50 |
0.182 μM
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Dose-dependent degradation of EML4-ALK protein in human H3122 non-small-cell lung cancer cells with EML4-ALK fusion measured via western blotting.
Dose-dependent degradation of EML4-ALK protein in human H3122 non-small-cell lung cancer cells with EML4-ALK fusion measured via western blotting.
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39681169 |
In Vitro
dALK-3 (1-10 μM; 8 h) induces dose-dependent proteasomal degradation of EML4-ALK in H3122 cells with a DC50 of 0.182 μM, and inhibits ALK downstream signaling pathways including STAT3 and AKT[1].
dALK-3 (1 μM; 24 h)-induced EML4-ALK degradation in H3122 cells depends on the proteasome pathway[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:H3122 non-small-cell lung cancer cells with EML4-ALK fusion
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Concentration:1, 3, 10 μM
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Incubation Time:8 h
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Result:Induced dose-dependent degradation of EML4-ALK protein, achieving 82% degradation at 10 μM after 8 h.
Exhibited a DC50 of 0.182 μM and a Dₘₐₓ of 78.2% for ALK degradation.
Reduced p-ALK levels, and at 1 μM, inhibited p-STAT3 more effectively than brigatinib, while inhibiting p-AKT to a similar extent as brigatinib.
Chemical Information
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Molecular Weight 758.25
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Formula C39H45ClN7O5P
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SMILES
ClC1=C(NC2=CC=CC=C2P(C)(C)=O)N=C(NC3=C(OC)C=C(N4CCC(N5CCN(C(/C=C/C(C6=CC=C(OC)C=C6)=O)=O)CC5)CC4)C=C3)N=C1
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
dALK-3 Related Classifications
HY-170592 Related Classifications
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