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经验公式(希尔记法):
C19H27N3O5S2
化学文摘社编号:
分子量:
441.56
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
产品名称
多非利特, ≥98% (HPLC)
SMILES string
CN(CCOc1ccc(NS(C)(=O)=O)cc1)CCc2ccc(NS(C)(=O)=O)cc2
InChI
1S/C19H27N3O5S2/c1-22(13-12-16-4-6-17(7-5-16)20-28(2,23)24)14-15-27-19-10-8-18(9-11-19)21-29(3,25)26/h4-11,20-21H,12-15H2,1-3H3
InChI key
IXTMWRCNAAVVAI-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
color
white to off-white
solubility
DMSO: >20 mg/mL
storage temp.
room temp
Quality Level
Gene Information
human ... KCNH2(3757)
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signalword
Danger
hcodes
Hazard Classifications
Aquatic Chronic 2 - Repr. 1B - STOT RE 2
存储类别
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
flash_point_f
Not applicable
flash_point_c
Not applicable
João F S Carvalho et al.
Journal of medicinal chemistry, 56(7), 2828-2840 (2013-03-12)
Drug-induced blockade of the human ether-a-go-go-related gene K(+) channel (hERG) represents one of the major antitarget concerns in pharmaceutical industry. SAR studies of this ion channel have shed light on the structural requirements for hERG interaction but most importantly may
Oleg E Osadchii
Cardiovascular drugs and therapy, 26(6), 489-500 (2012-08-25)
Dofetilide is class III antiarrhythmic agent which prolongs cardiac action potential duration because of selective inhibition of I (Kr), the rapid component of the delayed rectifier K(+) current. Although clinical studies reported on proarrhythmic risk associated with dofetilide treatment, the
R Al-Dashti et al.
The Canadian journal of cardiology, 17(1), 63-67 (2001-02-15)
Dofetilide is a new, pure class III antiarrhythmic agent that prolongs the refractory period and action potential duration without having beta-blocking or calcium channel-blocking properties, making it unique among established class III agents. Dofetilide is effective in converting atrial and
C Torp-Pedersen et al.
Expert opinion on investigational drugs, 9(11), 2695-2704 (2000-11-04)
Dofetilide is a class III anti-arrhythmic drug that has been approved for the treatment of atrial fibrillation. Two clinical studies, which enrolled 996 patients, demonstrated pharmacological conversion to sinus rhythm to occur in 30% of patients. Following pharmacological or electrical
Zhiyi Yu et al.
Toxicology and applied pharmacology, 274(1), 78-86 (2013-11-10)
Drugs that block the cardiac K(+) channel encoded by the human ether-à-go-go gene (hERG) have been associated with QT interval prolongation leading to proarrhythmia, and in some cases, sudden cardiac death. Because of special structural features of the hERG K(+)
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