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Merck
모든 사진(1)

주요 문서

SML0774

Sigma-Aldrich

SR 3677

≥98% (HPLC)

동의어(들):

N-[2-[2-(Dimethylamino)ethoxy]-4-(1H-pyrazol-4-yl)phenyl]-2,3-dihydro-1,4-benzodioxin-2-carboxamide., SR-3677, SR3677

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About This Item

실험식(Hill 표기법):
C22H24N4O4
CAS Number:
Molecular Weight:
408.45
UNSPSC 코드:
12352200

분석

≥98% (HPLC)

양식

powder

색상

white to light brown

solubility

DMSO: 15 mg/mL, clear

저장 온도

2-8°C

InChI

1S/C22H24N4O4/c1-26(2)9-10-28-20-11-15(16-12-23-24-13-16)7-8-17(20)25-22(27)21-14-29-18-5-3-4-6-19(18)30-21/h3-8,11-13,21H,9-10,14H2,1-2H3,(H,23,24)(H,25,27)

InChI key

OQWZIAVXCYIZNN-UHFFFAOYSA-N

애플리케이션

SR 3677 has been used as Rho-associated kinase (ROCK) inhibitor in cardiac reprogramming.[1]

생화학적/생리학적 작용

SR-3677 is a very potent, selective ROCK inhibitor, with higher potency against ROCK II (IC50 = 3 nM) than ROCK I (IC50 = 56 nM). In a kinase screening panel, SR-3677 was shown to only have activity against three other kinases (PKA, MRCK and Akt1) all with IC50 values over 1 μM. The compound has nM potency in cell based assays, and is efficacious in an ex-vivo model for increasing aqueous humor outflow in porcine eyes.
SR-3677 is a very potent, selective ROCK inhibitor.
SR3677 decreases amyloid precursor protein (sAPPβ) and amyloid-β (Aβ) in a dose-dependent manner. In 5XFAD mouse brain, SR3677 represses the enzymatic activity of β-site APP cleaving enzyme 1 (BACE1). SR3677 has the ability to change the endocytic supply of BACE1 and induce APP traffic to lysosomes.[2]

특징 및 장점

This compound is featured on the PKA & PKG and PKB/Akt pages of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

픽토그램

Exclamation mark

신호어

Warning

유해 및 위험 성명서

Hazard Classifications

Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

표적 기관

Respiratory system

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


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시험 성적서(COA)

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문서 라이브러리 방문

Jeremy H Herskowitz et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 33(49), 19086-19098 (2013-12-07)
Alzheimer's disease (AD) is the leading cause of dementia and has no cure. Genetic, cell biological, and biochemical studies suggest that reducing amyloid-β (Aβ) production may serve as a rational therapeutic avenue to delay or prevent AD progression. Inhibition of
Yuanbiao Zhao et al.
Nature communications, 6, 8243-8243 (2015-09-12)
Direct reprogramming of fibroblasts into cardiomyocytes by forced expression of cardiomyogenic factors, GMT (GATA4, Mef2C, Tbx5) or GHMT (GATA4, Hand2, Mef2C, Tbx5), has recently been demonstrated, suggesting a novel therapeutic strategy for cardiac repair. However, current approaches are inefficient. Here

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