Dabuzalgron

Research use only, not for human use.

Dabuzalgron is an orally active selective alpha-1A adrenergic receptor agonist used to treat urinary incontinence. Dabuzaron prevents cardiotoxicity caused by doxorubicin by maintaining mitochondrial function.Dabuzaron treatment increased ERK phosphorylation in a dose-dependent manner with an EC50 of 4.8 μM.

Dabuzalgron is an orally active selective alpha-1A adrenergic receptor agonist used to treat urinary incontinence. Dabuzaron prevents cardiotoxicity caused by doxorubicin by maintaining mitochondrial function.Dabuzaron treatment increased ERK phosphorylation in a dose-dependent manner with an EC50 of 4.8 μM. ERK1 / 2 activation helps Dabuzaron's cardioprotection. Dabuzaron (10 μM; 4 hours) protects NRVM from cell death caused by doxorubicin (DOX). Dabuzaren (10 μM; 4 hours) activation of α1A-AR alleviates the harmful effects of DOX on mitochondrial membrane potential and eliminates the activation of important elements of the apoptotic response to mitochondrial damage.Dabuzaron (10μg / kg; oral tube; twice daily; 7 consecutive days; C57B16J wild-type or α1A-AR gene knockout mice) treatment can prevent DOX cardiotoxicity by activating α1A-AR. Dabuzaron prevents mitochondrial function-related transcript reduction, up-regulates PGC1α, retains ATP content, and reduces oxidative stress in DOX-treated mouse hearts.

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.Dabuzalgron (10 μM; 4 hours) protects NRVMs from cell death due to Doxorubicin (DOX).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. Western Blot Analysis 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.

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. Animal Model:Male C57Bl6J wild-type (WT) or α1A-AR knockout (AKO) mice (8-12-week-old) injected with Doxorubicin (DOX) 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.

Ro 115-1240

Angiogenesis

Adrenergic Receptor

α1A-adrenergic receptor

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219311-44-1

317.79

C12H16ClN3O3S

>98% (HPLC)

DMSO:25 mg/mL(78.67 mM)

Cc1c(OCC2=NCCN2)ccc(Cl)c1NS(C)(=O)=O

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(-20℃)

With Ice Pack

≥ 2 years