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(S)-nitro-Blebbistatin Sale

(Synonyms: S(-)7Desmethyl8nitro Blebbistatin) 目录号 : GC41739

A more stable form of (–)-blebbistatin

(S)-nitro-Blebbistatin Chemical Structure

Cas No.:856925-75-2

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1mg
¥1,627.00
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5mg
¥6,511.00
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10mg
¥10,262.00
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25mg
¥17,097.00
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产品描述

(S)-nitro-Blebbistatin is a more stable form of (-)-blebbistatin , which is a selective cell-permeable inhibitor of non-muscle myosin II ATPases. (-)-Blebbistatin rapidly and reversibly inhibits Mg-ATPase activity and in vitro motility of non-muscle myosin IIA and IIB for several species (IC50s = 0.5-5 µM), while poorly inhibiting smooth muscle myosin (IC50 = 80 µM). Through these effects, it blocks apoptosis-related bleb formation, directed cell migration, and cytokinesis in vertebrate cells. However, prolonged exposure to blue light (450-490 nm) results in degradation of blebbistatin to an inactive product via cytotoxic intermediates, which may be problematic for its use in fluorescent live cell imaging applications. The addition of a nitro group stabilizes the molecule to circumvent its degradation by prolonged blue light exposure. (S)-nitro-Blebbistatin has the same stereochemistry as the active (-)-blebbistatin enantiomer.

Chemical Properties

Cas No. 856925-75-2 SDF
别名 S(-)7Desmethyl8nitro Blebbistatin
Canonical SMILES O=C1[C@@]2(O)C(N(C3=CC=CC=C3)CC2)=NC4=C1C=CC([N+]([O-])=O)=C4
分子式 C17H13N3O4 分子量 323.3
溶解度 DMF: 16 mg/ml,DMSO: 16 mg/ml,DMSO:PBS(pH7.2) (1:1): 0.5 mg/ml 储存条件 Store at -20°C
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储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
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1 mg 5 mg 10 mg
1 mM 3.0931 mL 15.4655 mL 30.931 mL
5 mM 0.6186 mL 3.0931 mL 6.1862 mL
10 mM 0.3093 mL 1.5466 mL 3.0931 mL
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Research Update

Deciphering cellular signals in adult mouse sinoatrial node cells

iScience 2021 Dec 25;25(1):103693.PMID:35036877DOI:10.1016/j.isci.2021.103693.

Sinoatrial node (SAN) cells are the pacemakers of the heart. This study describes a method for culturing and infection of adult mouse SAN cells with FRET-based biosensors that can be exploited to examine signaling events. SAN cells cultured in media with blebbistatin or (S)-nitro-Blebbistatin retain their morphology, protein distribution, action potential (AP) waveform, and cAMP dynamics for at least 40 h. SAN cells expressing targeted cAMP sensors show distinct β-adrenergic-mediated cAMP pools. Cyclic GMP, protein kinase A, Ca2+/CaM kinase II, and protein kinase D in SAN cells also show unique dynamics to different stimuli. Heart failure SAN cells show a decrease in cAMP and cGMP levels. In summary, a reliable method for maintaining adult mouse SAN cells in culture is presented, which facilitates studies of signaling networks and regulatory mechanisms during physiological and pathological conditions.

Illuminating cell signaling with genetically encoded FRET biosensors in adult mouse cardiomyocytes

J Gen Physiol 2018 Nov 5;150(11):1567-1582.PMID:30242036DOI:10.1085/jgp.201812119.

FRET-based biosensor experiments in adult cardiomyocytes are a powerful way of dissecting the spatiotemporal dynamics of the complicated signaling networks that regulate cardiac health and disease. However, although much information has been gleaned from FRET studies on cardiomyocytes from larger species, experiments on adult cardiomyocytes from mice have been difficult at best. Thus the large variety of genetic mouse models cannot be easily used for this type of study. Here we develop cell culture conditions for adult mouse cardiomyocytes that permit robust expression of adenoviral FRET biosensors and reproducible FRET experimentation. We find that addition of 6.25 µM blebbistatin or 20 µM (S)-nitro-Blebbistatin to a minimal essential medium containing 10 mM HEPES and 0.2% BSA maintains morphology of cardiomyocytes from physiological, pathological, and transgenic mouse models for up to 50 h after adenoviral infection. This provides a 10-15-h time window to perform reproducible FRET readings using a variety of CFP/YFP sensors between 30 and 50 h postinfection. The culture is applicable to cardiomyocytes isolated from transgenic mouse models as well as models with cardiac diseases. Therefore, this study helps scientists to disentangle complicated signaling networks important in health and disease of cardiomyocytes.