PF-06842874
PF-06842874 is a CDK4/Cyclin D1 and CDK6/Cyclin D3 inhibitor (Ki values are 62 and 130 nM, respectively). PF-06842874 can be used in the research of pulmonary arterial hypertension and cancer.
For research use only. We do not sell to patients.
- CAS No.: 2516247-98-4
- Formula: C21H27N3O4
- Molecular Weight:385.46
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
CDK4/cyclinD1 62 nM (Ki) |
cdk6/cyclin D3 130 nM (Ki) |
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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CAS No. 2516247-98-4
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Molecular Weight 385.46
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Formula C21H27N3O4
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SMILES
O=C1N(C2CCCC2)C3=CC(N[C@H]4[C@@H](COCC4)O)=NC=C3C(C)=C1C(C)=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 Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)