ROCK2-IN-20
ROCK2-IN-20 is a selective ROCK2 inhibitor with an IC50 value of 12 nM. ROCK2-IN-20 can be used for research on multiple sclerosis, pulmonary arterial hypertension, and glaucoma.
For research use only. We do not sell to patients.
- CAS No.: 1219722-56-1
- Formula: C19H20N4O2
- Molecular Weight:336.40
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
ROCK2 12 nM (IC50) |
PKA 610 nM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| A7R5 | IC50 |
59 nM
Compound: 12o
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Inhibition of ROCK-mediated myosin light chain bisphosphorylation in rat A7R5 cells after 1 hr by fluorescence assay in presence of L-alpha-lysophosphatidic acid
Inhibition of ROCK-mediated myosin light chain bisphosphorylation in rat A7R5 cells after 1 hr by fluorescence assay in presence of L-alpha-lysophosphatidic acid
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[PMID: 23570561] |
In Vitro
Chemical Information
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CAS No. 1219722-56-1
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Molecular Weight 336.40
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Formula C19H20N4O2
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SMILES
O=C(NC=1C=CC(=CC1)C=2C=NNC2)N(CC=3C=CC=CC3)CCO
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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 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)