AR ligand-48
AR ligand-48 is an AR (Androgen Receptor) inhibitor and a ligand for the target protein for PROTAC (AR). AR ligand-48 can be used to synthesize PROTAC AR Degrader-12 (HY-179433).
For research use only. We do not sell to patients.
- CAS No.: 1318208-88-6
- Formula: C23H28N2O7
- Molecular Weight:444.48
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
|
AR |
Cellular Effect
|
Cell Line
|
Type | Value | Description | References |
|---|---|---|---|---|
| LNCaP | IC50 |
40 nM
Compound: 5
|
Inhibition of full length AR/PELP1 (unknown origin) interaction expressed in human LNCaP cells preincubated for 2 hrs followed by DHT addition measured after 24 hrs by Western blot analysis
Inhibition of full length AR/PELP1 (unknown origin) interaction expressed in human LNCaP cells preincubated for 2 hrs followed by DHT addition measured after 24 hrs by Western blot analysis
|
[PMID: 27503683] |
In Vitro
AR PROTAC contains two different ligands connected by a linker; one is an E3 ligase ligand ((S,S,S)-AHPC-Me) (Compound D2) (HY-112078), and the other is for Ligands of AR target protein (AR ligand-48) (HY-179442). PROTAC exploits the intracellular ubiquitin-proteasome system to selectively degrade target proteins[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
-
CAS No. 1318208-88-6
-
Molecular Weight 444.48
-
Formula C23H28N2O7
-
SMILES
COC(C1=CC(OCC(C)C)=C(C=C1)NC(C2=CC(OCC(C)C)=C(C=C2)[N+]([O-])=O)=O)=O
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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)