BRD4 ligand 17
BRD4 ligand 17 is the target protein ligand of BRD4 RIMTAC-1 (HY-187390). BRD4 RIMTAC-1 is a BRD4 PROTAC degrader based on RIPK1-mediated targeted chimeric (RIMTAC) technology, which can be used for research on cancer and inflammation-related diseases.
For research use only. We do not sell to patients.
- CAS No.: 1629730-92-2
- Formula: C23H25ClN6OS
- Molecular Weight:469.00
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
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BRD4 |
In Vitro
PROTACs contain two different ligands connected by a linker; one is a ligand for an E3 ubiquitin ligase and the other is for the target protein. PROTACs exploit 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
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CAS No. 1629730-92-2
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Molecular Weight 469.00
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Formula C23H25ClN6OS
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SMILES
CC1=NN=C2N1C3=C(C(C)=C(C)S3)C(C4=CC=C(Cl)C=C4)=N[C@H]2CC(N5CCNCC5)=O
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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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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)