SML3953
Istaroxime hydrochloride
≥98% (HPLC)
동의어(들):
Androstane-3,6,17-trione, 3-[O-(2-aminoethyl)oxime], hydrochloride (1:1)
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크기 선택
보기 변경
제품정보 (DICE 배송 시 비용 별도)
실험식(Hill 표기법):
C21H32N2O3·HCl
CAS 번호:
Molecular Weight:
396.95
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
Quality Level
assay
≥98% (HPLC)
form
powder
storage condition
desiccated
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
-10 to -25°C
Biochem/physiol Actions
Positive inotropic agent that inhibits Na + /K + -ATPase and increases activity of Ca 2+ -ATPase at the sarcoplasmic reticulum.
Istaroxime is a positive inotropic agent that inhibits Na + /K + -ATPase and increases activity of Ca 2+ -ATPase at the sarcoplasmic reticulum. It improves cardiac performance in the failing heart. Istaroxime ameliorates calcium dysregulation Zebrafish PLN R14del arrhythmogenic cardiomyopathy model.
Istaroxime is a positive inotropic agent that inhibits Na + /K + -ATPase and increases activity of Ca 2+ -ATPase at the sarcoplasmic reticulum. It improves cardiac performance in the failing heart. Istaroxime ameliorates calcium dysregulation Zebrafish PLN R14del arrhythmogenic cardiomyopathy model.
Disclaimer
Hygroscopic
signalword
Warning
hcodes
pcodes
Hazard Classifications
STOT RE 2
target_organs
Gastro-intestinal system,Heart
저장 등급
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
SERCA2a stimulation by istaroxime improves intracellular Ca2+ handling and diastolic dysfunction in a model of diabetic cardiomyopathy
Cardiovascular Research, 118(4), 1020-1032 (2022)
Istaroxime, a stimulator of sarcoplasmic reticulum calcium adenosine triphosphatase isoform 2a activity, as a novel therapeutic approach to heart failure
The American Journal of Cardiology, 99(2A), 24A-32A (2007)
S M Kamel et al.
Nature communications, 12(1), 7151-7151 (2021-12-11)
The heterozygous Phospholamban p.Arg14del mutation is found in patients with dilated or arrhythmogenic cardiomyopathy. This mutation triggers cardiac contractile dysfunction and arrhythmogenesis by affecting intracellular Ca2+ dynamics. Little is known about the physiological processes preceding induced cardiomyopathy, which is characterized