1. GPCR/G Protein
    Neuronal Signaling
  2. Adrenergic Receptor
  3. Dabuzalgron

Dabuzalgron (Synonyms: Ro 115-1240)

Cat. No.: HY-117071 Purity: 98.72%
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Dabuzalgron (Ro 115-1240) is an orally active and selective α-1A adrenergic receptor agonist for the treatment of urinary incontinence. Dabuzalgron protects against Doxorubicin-induced cardiotoxicity by preserving mitochondrial function.

For research use only. We do not sell to patients.

Dabuzalgron Chemical Structure

Dabuzalgron Chemical Structure

CAS No. : 219311-44-1

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10 mM * 1 mL in DMSO USD 171 In-stock
Estimated Time of Arrival: December 31
5 mg USD 155 In-stock
Estimated Time of Arrival: December 31
10 mg USD 280 In-stock
Estimated Time of Arrival: December 31
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Based on 1 publication(s) in Google Scholar

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Description

Dabuzalgron (Ro 115-1240) is an orally active and selective α-1A adrenergic receptor agonist for the treatment of urinary incontinence. Dabuzalgron protects against Doxorubicin-induced cardiotoxicity by preserving mitochondrial function[1].

IC50 & Target

α-1A adrenergic receptor[1]

In Vitro

Dabuzalgron treatment increases ERK phosphorylation in a dose-dependent fashion with an EC50 of 4.8 μM. ERK1/2 activation contributes to the cardioprotective effects of Dabuzalgron[1].
Dabuzalgron (10 μM; 4 hours) protects NRVMs from cell death due to Doxorubicin (DOX)[1].
Activation of the α1A-AR with Dabuzalgron (10 μM; 4 hours) mitigates the detrimental effects of DOX on mitochondrial membrane potential and abrogates the activation of important elements of the apoptotic response to mitochondrial damage[1].

Western Blot Analysis[1]

Cell Line: Neonatal rat ventricular myocytes (NRVMs)
Concentration: 0.1 μM, 1 μM, 10 μM and 100 μM
Incubation Time: 15 minutes
Result: Increased ERK phosphorylation in a dose-dependent fashion with an EC50 of 4.8 μM.
In Vivo

Dabuzalgron (10 μg/kg; oral gavage; twice daily; for 7 days; C57Bl6J wild-type or α1A-AR knockout mice) treatment protects against DOX cardiotoxicity by activating the α1A-AR. Dabuzalgron protects against the reduction in transcripts related to mitochondrial function, up-regulates PGC1α, preserves ATP content, and reduces oxidative stress in the hearts of mice treated with DOX[1].

Animal Model: Male C57Bl6J wild-type (WT) or α1A-AR knockout (AKO) mice (8-12-week-old) injected with Doxorubicin (DOX)[1]
Dosage: 10 μg/kg
Administration: Oral gavage; twice daily; for 7 days
Result: Preserved contractile function and reduced fibrosis after DOX administration. AKO mice treated with DOX had worse survival and more profoundly impaired contractile function than WT mice. Protected against the reduction in transcripts related to mitochondrial function, preserved ATP content, and reduced oxidative stress in the hearts of mice treated with DOX.
Molecular Weight

317.79

Formula

C₁₂H₁₆ClN₃O₃S

CAS No.

219311-44-1

SMILES

CS(=O)(NC1=C(Cl)C=CC(OCC2=NCCN2)=C1C)=O

Shipping

Room temperature in continental US; may vary elsewhere.

Storage
Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
References
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Keywords:

DabuzalgronRo 115-1240Adrenergic ReceptorBeta ReceptorCelldeathapoptosismitochondrialmembranepotentialurinaryincontinenceInhibitorinhibitorinhibit

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