达布扎琼

生物活性靶点体外研究体内研究达布扎琼试剂级价格

达布扎琼

CAS号:219311-44-1
英文名:Dabuzalgron
中文名:达布扎琼
CBNumber:CB31261458
分子式:C12H16ClN3O3S
分子量:317.79
MOL File:219311-44-1.mol

达布扎琼化学性质

密度 :1.46
储存条件 :Store at -20°C
溶解度 :DMSO: 26 mg/mL (81.82 mM)
形态 :Solid
颜色 :White to off-white

达布扎琼性质、用途与生产工艺

生物活性 Dabuzalgron (Ro 115-1240) 是一种口服活性的，选择性的 α-1A 肾上腺素能受体激动剂，动物模型中，用于缓解尿失禁。Dabuzalgron 可通过维持线粒体功能来预防由阿霉素引起的心脏毒性。
靶点

α-1A adrenergic receptor

体外研究

Dabuzalgron treatment increases ERK phosphorylation in a dose-dependent fashion with an EC ₅₀ 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 EC ₅₀ of 4.8 μM.

体内研究

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.