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Merck
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217699

Sigma-Aldrich

RO-3306

≥95% (HPLC), solid, Cdk1 inhibitor, Calbiochem®

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别名:
Cdk1 Inhibitor IV, RO-3306
经验公式(希尔记法):
C18H13N3OS2
分子量:
351.45
UNSPSC代码:
12352200
NACRES:
NA.77

product name

Cdk1 Inhibitor IV, RO-3306, RO-3306 is a cell-permeable, potent and ATP-competitive inhibitor of Cdk1 (Ki = 35 nM and 110 nM for Cdk1/B1 and Cdk1/A, respectively).

质量水平

检测方案

≥95% (HPLC)

形式

solid

制造商/商品名称

Calbiochem®

储存条件

OK to freeze
protect from light

颜色

brown

溶解性

DMSO: 10 mg/mL

运输

ambient

储存温度

2-8°C

一般描述

A cell-permeable quinolinyl thiazolinone compound that acts as a potent and ATP-competitive inhibitor of Cdk1 (Ki = 35 nM and 110 nM for Cdk1/B1 and Cdk1/A, respectively). It affects Cdk2/E, PKCδ, and SGK only at much higher concentrations (Ki = 340, 318, and 497 nM, respectively), and shows little effect against Cdk4/D and six other commonly studied kinases (Ki ≥ 2 µM). Short-term treatment for up to 20 hrs results in fully reversible G2/M cell cycle arrest, while prolonged treament (>48 hrs) results in apoptotic cell death in proliferating cancer cells, but not in nontumorigenic epithelial cell lines. Also available as a 10 mM solution in DMSO (Cat. No. 217721).

生化/生理作用

Cell permeable: yes
Primary Target
Cdk1
Product competes with ATP.
Reversible: no
Target Ki: 35 nM and 110 nM for Cdk1/B1 and Cdk1/A, respectively

包装

Packaged under inert gas

警告

Toxicity: Irritant (B)

重悬

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

其他说明

Vassilev, L.T., et al. 2006. Proc. Natl. Acad. Sci. USA103, 10660.

法律信息

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable


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Journal of cellular biochemistry, 115(4), 763-771 (2014-01-24)
Genistein, an isoflavone abundantly present in soybeans, possesses anticancer properties and induces growth inhibition including cell cycle arrest and apoptosis. Although abnormal cell division, such as defects in chromosome segregation and spindle formation, and polyploidization have been described, the mechanisms
Pia-Amata Leimbacher et al.
Molecular cell, 74(3), 571-583 (2019-03-23)
In mitosis, cells inactivate DNA double-strand break (DSB) repair pathways to preserve genome stability. However, some early signaling events still occur, such as recruitment of the scaffold protein MDC1 to phosphorylated histone H2AX at DSBs. Yet, it remains unclear whether
Beate Vajen et al.
International journal of molecular sciences, 23(9) (2022-05-15)
Chromosomal instability (CIN) can be a driver of tumorigenesis but is also a promising therapeutic target for cancer associated with poor prognosis such as triple negative breast cancer (TNBC). The treatment of TNBC cells with defects in DNA repair genes
Ryan P Barnes et al.
Nature structural & molecular biology, 29(7), 639-652 (2022-07-01)
Oxidative stress is a primary cause of cellular senescence and contributes to the etiology of numerous human diseases. Oxidative damage to telomeric DNA has been proposed to cause premature senescence by accelerating telomere shortening. Here, we tested this model directly
Olivier Brison et al.
Nature structural & molecular biology, 30(4), 539-550 (2023-04-07)
Genome integrity requires replication to be completed before chromosome segregation. The DNA-replication checkpoint (DRC) contributes to this coordination by inhibiting CDK1, which delays mitotic onset. Under-replication of common fragile sites (CFSs), however, escapes surveillance, resulting in mitotic chromosome breaks. Here

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