Dabuzalgron

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.

Product information

CAS Number: 219311-44-1

Molecular Weight: 317.79

Formula: C12H16ClN3O3S

Synonym:

Ro 115-1240

Chemical Name: N-{6-chloro-3-[(4, 5-dihydro-1H-imidazol-2-yl)methoxy]-2-methylphenyl}methanesulfonamide

Smiles: CC1C(NS(C)(=O)=O)=C(Cl)C=CC=1OCC1NCCN=1

InChiKey: FOYWMEJSRSBQGB-UHFFFAOYSA-N

InChi: InChI=1S/C12H16ClN3O3S/c1-8-10(19-7-11-14-5-6-15-11)4-3-9(13)12(8)16-20(2,17)18/h3-4,16H,5-7H2,1-2H3,(H,14,15)

Technical Data

Appearance: Solid Power

Purity: ≥98% (or refer to the Certificate of Analysis)

Solubility: DMSO : 26 mg/mL (81.82 mM; Need ultrasonic)

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis

Storage Condition: Dry, dark and -20 ^oC for 1 year or refer to the Certificate of Analysis.

Shelf Life: ≥360 days if stored properly.

Stock Solution Storage: 0 - 4 ^oC for 1 month or refer to the Certificate of Analysis.

Drug Formulation: To be determined

HS Tariff Code: 382200

How to use

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. 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.

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.

References:

1. Beak J, et al. An Oral Selective Alpha-1A Adrenergic Receptor Agonist Prevents Doxorubicin Cardiotoxicity. JACC Basic Transl Sci. 2017 Feb;2(1):39-53.

Products are for research use only. Not for human use.