A β1 adrenergic receptor antagonist
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Celiprolol (hydrochloride)

Item No. 16715

Product Insert (PDF)Safety Data Sheet (SDS) (PDF)
Technical Information
Formal Name
N'-[3-acetyl-4-[3-[(1,1-dimethylethyl)amino]-2-hydroxypropoxy]phenyl]-N,N-diethyl-urea, monohydrochloride
CAS Number
57470-78-7
Synonyms
  • Corliprol
  • NSC 324509
Molecular Formula
C20H33N3O4 • HCl
Formula Weight
416.0
Purity
≥98%
Formulation
A crystalline solid
Solubility(Learn about Variance in Solubility)
DMF: 10 mg/mlDMSO: 10 mg/mlEthanol: 2 mg/mlPBS (pH 7.2): 5 mg/ml
λmax
234, 328 nm
SMILES
CC(C1=C(OCC(CNC(C)(C)C)O)C=CC(NC(N(CC)CC)=O)=C1)=O.Cl
InChi Code
InChI=1S/C20H33N3O4.ClH/c1-7-23(8-2)19(26)22-15-9-10-18(17(11-15)14(3)24)27-13-16(25)12-21-20(4,5)6;/h9-11,16,21,25H,7-8,12-13H2,1-6H3,(H,22,26);1H
InChi Key
VKJHTUVLJYWAEY-UHFFFAOYSA-N
Shipping & Storage Information
Storage
-20°C
Shipping
Room temperature in continental US; may vary elsewhere
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    1 mg

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    5 mg

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    10 mg

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    25 mg

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    Product Description

    Celiprolol is a β1 adrenergic receptor antagonist and a β2 adrenergic receptor partial agonist that has been shown to relax human arteries and veins with ED50 values of 40-50 µM in vitro.1 At 1-10 mg/kg/h, celiprolol can reduce myocardial infarct size and increase nitric oxide (NO) production in a rabbit model of myocardial ischemia.2 Furthermore, 100 mg/kg/d celiprolol has been reported to stimulate expression and activate phosphorylation of endothelial NO synthase in rat cardiac myocytes.3

    WARNING This product is not for human or veterinary use.

    References & Product Citations
    Product Description References

    1. Hoffman, D.L. Mitochondria and cellular homeostatis: Beyond ATP synthesis. Mitochondrial Health 2014, 1-2 (2014).

    2. Chen, X., Minatoguchi, S., Arai, M., et al. Celiprolol, a selective β1-blocker, reduces the infarct size through production of nitric oxide in a rabbit model of myocardial infarction. Circ. J. 71(4), 574-579 (2007).

    3. Liao, Y., Asakura, M., Takashima, S., et al. Celiprolol, a vasodilatory β-blocker, inhibits pressure overload-induced cardiac hypertrophy and prevents the transition to heart failure via nitric oxide-dependent mechanisms in mice. Circulation 110(6), 692-699 (2004).