OP-3633
OP-3633 is a potent and selective steroidal glucocorticoid receptor (GR) antagonist with an IC50 of 29 nM, with inhibition of GR transcriptional activity. OP-3633 exhibits low progesterone receptor (PR) agonism and androgen receptor (AR) antagonism.
For research use only. We do not sell to patients.
- CAS No.: 2102494-14-2
- Formula: C30H39NO2
- Molecular Weight:445.64
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
IC50: 29 nM (GR)[1]
Cellular Effect
|
Cell Line
|
Type | Value | Description | References |
|---|---|---|---|---|
| CHO-K1 | IC50 |
1135 nM
Compound: 15; OP-3633
|
Antagonist activity at human progesterone receptor expressed in CHO-K1 cells harboring firefly luciferase gene after 20 hrs by One-Glo luciferase reporter gene assay
Antagonist activity at human progesterone receptor expressed in CHO-K1 cells harboring firefly luciferase gene after 20 hrs by One-Glo luciferase reporter gene assay
|
[PMID: 31274313] |
| CHO-K1 | IC50 |
16 nM
Compound: 15; OP-3633
|
Antagonist activity at human glucocorticoid receptor expressed in CHO-K1 cells assessed as inhibition of glucocorticoid receptor-dexamethasone coactivator protein-protein interaction incubated for 24 hrs by bioluminescence assay
Antagonist activity at human glucocorticoid receptor expressed in CHO-K1 cells assessed as inhibition of glucocorticoid receptor-dexamethasone coactivator protein-protein interaction incubated for 24 hrs by bioluminescence assay
|
[PMID: 31274313] |
| CHO-K1 | IC50 |
29 nM
Compound: 15; OP-3633
|
Antagonist activity at human glucocorticoid receptor expressed in CHO-K1 cells harboring firefly luciferase gene after 20 hrs by One-Glo luciferase reporter gene assay
Antagonist activity at human glucocorticoid receptor expressed in CHO-K1 cells harboring firefly luciferase gene after 20 hrs by One-Glo luciferase reporter gene assay
|
[PMID: 31274313] |
| LNCaP | EC50 |
>2500 nM
Compound: 15; OP-3633
|
Agonist activity at human androgen receptor in human LNCAP cells harboring firefly luciferase gene after 20 hrs by One-Glo luciferase reporter gene assay
Agonist activity at human androgen receptor in human LNCAP cells harboring firefly luciferase gene after 20 hrs by One-Glo luciferase reporter gene assay
|
[PMID: 31274313] |
| LNCaP | IC50 |
912 nM
Compound: 15; OP-3633
|
Antagonist activity at human androgen receptor in human LNCAP cells harboring firefly luciferase gene after 20 hrs by One-Glo luciferase reporter gene assay
Antagonist activity at human androgen receptor in human LNCAP cells harboring firefly luciferase gene after 20 hrs by One-Glo luciferase reporter gene assay
|
[PMID: 31274313] |
In Vitro
OP-3633 exhibits low progesterone receptor (PR) agonism with an EC50 higher than 2500 nM[1].
OP-3633 exhibits low androgen receptor (PR) antagonism, with an IC50 of 1135 nM[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. 2102494-14-2
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Molecular Weight 445.64
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Formula C30H39NO2
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SMILES
O=C1CC[C@]2(C)[C@@]3([H])[C@@H](C4=CC=C(N(C)C)C=C4)C[C@]5(C)[C@@](C#CC)(O)CC[C@@]5([H])[C@]3([H])CCC2=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.
Protocols
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Dual Luciferin reporter gene assay
Luciferin reporter gene assay is a reporting system to detect the activity of Firefly Luciferase using luciferin as a substrate, which is often used in the research of miRNA target gene verification and promoter transcriptive activity regulation. Dual luciferase usually refers to Firefly luciferase and Renilla luciferase.
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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)