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Merck
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重要文件

324879

Sigma-Aldrich

CCT020312

≥98% (HPLC), solid, EIF2AK3 activator, Calbiochem®

同義詞:

EIF2AK3活化剂,CCT020312, 6-溴-3-[5-(4-溴-苯基)-1-(3-二乙氨基-丙酰基)-4,5-二氢-1H-吡唑-3-基]-4-苯基-1H-喹啉-2-酮,PERK活化剂,CCT020312

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About This Item

經驗公式(希爾表示法):
C31H30Br2N4O2
CAS號碼:
分子量::
650.40
MDL號碼:
分類程式碼代碼:
12352200
NACRES:
NA.77
暫時無法取得訂價和供貨情況

產品名稱

EIF2AK3活化剂,CCT020312, The EIF2AK3 Activator, CCT020312 modulates the biological activity of EIF2AK3.

品質等級

化驗

≥98% (HPLC)

形狀

solid

製造商/商標名

Calbiochem®

儲存條件

OK to freeze
protect from light

顏色

yellow-white

溶解度

DMSO: 50 mg/mL

運輸包裝

ambient

儲存溫度

−20°C

SMILES 字串

O=C1C(C2=NN(C(CCN(CC)CC)=O)C(C3=CC=C(Br)C=C3)C2)=C(C4=CC=CC=C4)C5=CC(Br)=CC=C5N1

一般說明

一种二氢吡唑衍生物,作为真核翻译起始因子2-α激酶3(eIF2AK3/PERK)的选择性激活剂,并增加HT29和MCF7细胞中EIF2A在Ser51位点的磷酸化。不抑制细胞周期蛋白依赖性激酶的活性,但引起细胞周期蛋白D表达的快速丧失。还显示阻断HT29细胞中的Rb蛋白磷酸化(EC50 = 4.2 µM)。据报道,可使紫杉烷诱导的EIF2A磷酸化缺陷的癌症细胞对紫杉醇治疗敏感。即使去除细胞增殖(GI50 = 3.1 µM),也能诱导长期抑制细胞增殖。

包裝

用惰性气体包装

警告

毒性:标准处理(A)

重構

复溶后,等分并冷冻保存(-20°C)。储备溶液在-20°C下可稳定保存至多3个月。

其他說明

Stockwell, S. R., et al. 2011.Plos One In press.

法律資訊

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

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 2

閃點(°F)

Not applicable

閃點(°C)

Not applicable


分析證明 (COA)

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PKR-like kinase (PERK) plays a significant role in inducing angiogenesis in various cancer types including glioblastoma. By proteomics analysis of the conditioned medium from a glioblastoma cell line treated with a PERK inhibitor, we showed that peptidylglycine α-amidating monooxygenase (PAM)
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Delirium is the most common postoperative complication in older patients after prolonged anesthesia and surgery and is associated with accelerated cognitive decline and dementia. The neuronal pathogenesis of postoperative delirium is largely unknown. The unfolded protein response (UPR) is an
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Human cancers often contain genetic alterations that disable G1/S checkpoint control and loss of this checkpoint is thought to critically contribute to cancer generation by permitting inappropriate proliferation and distorting fate-driven cell cycle exit. The identification of cell permeable small

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