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219311-44-1

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219311-44-1 Structure

219311-44-1 Structure
IdentificationBack Directory
[Name]

Dabuzalgron
[CAS]

219311-44-1
[Synonyms]

Dabuzalgron
Ro 115-1240
N-[6-chloro-3-(4,5-dihydro-1H-imidazol-2-ylmethoxy)-2-methyl-phenyl]me thanesulfonamide
MethanesulfonaMide, N-[6-chloro-3-[(4,5-dihydro-1H-iMidazol-2-yl)Methoxy]-2-Methylphenyl]-
[Molecular Formula]

C12H16ClN3O3S
[MDL Number]

MFCD13195546
[MOL File]

219311-44-1.mol
[Molecular Weight]

317.79
Chemical PropertiesBack Directory
[density ]

1.46
[storage temp. ]

Store at -20°C
[solubility ]

DMSO: 26 mg/mL (81.82 mM)
[form ]

Solid
[color ]

White to off-white
Safety DataBack Directory
[Symbol(GHS) ]

Exclamation Mark (GHS07)
GHS07
[Signal word ]

Warning
[Hazard statements ]

H302-H315-H319-H335
[Precautionary statements ]

P261-P280-P301+P312-P302+P352-P305+P351+P338
Hazard InformationBack Directory
[Uses]

Treatment of stress urinary incontinence.
[Definition]

ChEBI: Dabuzalgron is a sulfonamide that is N-phenylmethanesulfonamide which carries a chloro group at position 2, 4,5-dihydro-1H-imidazol-2-ylmethoxy group at position 5, and a methyl group at position 6. Its is a selective alpha-adrenoceptor agonist that is used in the treatment of urinary incontinence. It has a role as an alpha-adrenergic agonist. It is a member of monochlorobenzenes, an aromatic ether, a sulfonamide and a member of imidazoles.
[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.
[storage]

Store at -20°C
Spectrum DetailBack Directory
[Spectrum Detail]

Dabuzalgron(219311-44-1)1HNMR
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