CRT0093964
CRT0093964 is an isoform-selective non-carboxylate inhibitor of AKR1C3 (IC50=0.11 μM) with no activity against AKR1C1, AKR1C2, AKR1C4, COX-1, and COX-2.CRT0093964 can be used for the research of leukemia, hormone-related cancers, colon cancer.
For research use only. We do not sell to patients.
- CAS No.: 700856-05-9
- Formula: C15H20ClN3O2
- Molecular Weight:309.79
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All 17β-HSD Isoforms
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Biological Activity
Description
IC50 & Target
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AKR1C3 0.11 μM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HCT-116 | IC50 |
0.018 μM
Compound: 24
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Inhibition of AKR1C3 (unknown origin) expressed in human HCT116 cells assessed as formation of PR-104H from PR-104A preincubated for 2 hrs
Inhibition of AKR1C3 (unknown origin) expressed in human HCT116 cells assessed as formation of PR-104H from PR-104A preincubated for 2 hrs
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[PMID: 24411201] |
In Vitro
CRT0093964 (0.1 nM-100 μM; 1 h) potently and selectively inhibits purified recombinant AKR1C3 with an IC50 of 0.11 μM; in contrast, this compound shows no inhibitory effect on AKR1C1, AKR1C2 or AKR1C4 at concentrations up to 30 μM[1].
CRT0093964 (1 nM-3 μM; 2 h pre-treatment) inhibits AKR1C3-dependent metabolism of PR-104A (HY-16405) in AKR1C3-overexpressing HCT-116 cells, with an IC50 of 0.018 μM, and exhibits higher potency in cellular assays than in purified enzyme assays[1].
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. 700856-05-9
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Molecular Weight 309.79
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Formula C15H20ClN3O2
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SMILES
O=C(N1CCOCC1)N2CCN(C3=CC=C(Cl)C=C3)CC2
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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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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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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)