NNC-112
NNC-112 is a dopamine D1 receptor antagonist with a Ki of 0.18 nM for rat D1R and a Ki of 18 nM for 5-HT2. NNC-112 competitively inhibits [3H]SCH 23390 binding and blocks dopamine-stimulated adenylate cyclase. NNC-112 blocks D1 receptor-mediated rotational behavior in 6-OHDA-lesioned rats. NNC-112 can serve as a C11-labeled radioligand ([11C] NNC 112) for positron emission tomography imaging. NNC-112 can be used for research on schizophrenia and hypertension.
For research use only. We do not sell to patients.
- CAS No.: 125341-24-4
- Formula: C19H18ClNO2
- Molecular Weight:327.81
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[2]|
D1 Receptor 0.18 nM (Ki) |
5-HT2A Receptor 18 nM (Ki) |
In Vitro
NNC-112 (60 min) is a highly potent inhibitor of the binding of [3H]SCH 23390 to rat striatal dopamine D1 receptors, with a KI of 0.18 nM[2].
NNC-112 (20 min) exhibits low affinity for rat striatal dopamine D2 receptors, with a KI of 898 nM[2].
NNC-112 exhibits moderate affinity for 5-HT2 receptors with a KI of 18 nM[2].
NNC-112 (15 min) is a potent competitive inhibitor of dopamine-stimulated adenylate cyclase in rat striatal tissue, with a KI of 2.8 nM[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
NNC-112 (s.c.; 0.5 h before the agonist) selectively antagonizes D1 receptor-mediated rotational behavior in 6-OHDA (HY-B1081A)-lesioned rats with an ED50 of 0.08 mg/kg, without affecting D2-mediated rotation[2].
Pretreatment with NNC-112 (2-2.5 mg/kg; i.v.) produces 77% blockade of [11C]NNC 112 binding in the rat renal cortex, indicating that the PET signal is predominantly driven by specific D1-like receptor binding[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley rats[4]
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Dosage:2 mg/kg; 2.5 mg/kg
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Administration:i.v.; single pretreatment bolus
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Result:Reached an average of 0.083% injected dose per mL of tissue at 35 min in the left renal cortex, corresponding to a blocking percentage of 77%.
Chemical Information
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CAS No. 125341-24-4
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Molecular Weight 327.81
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Formula C19H18ClNO2
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SMILES
CN1C[C@@H](C=2C(=CC(Cl)=C(O)C2)CC1)C3=C4C(=CC=C3)C=CO4
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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)
NNC-112 Related Classifications
HY-165450 Related Classifications
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