Merck
すべての画像(1)

資料

G9420

Sigma-Aldrich

GNF-2

≥98% (HPLC), solid

すべての画像(1)
別名:
3-[6-[[4-(Trifluoromethoxy)phenyl]amino]-4-pyrimidinyl]benzamide
Empirical Formula (Hill Notation):
C18H13F3N4O2
CAS番号:
778270-11-4
分子量:
374.32
MDL番号:
MFCD09265253
PubChem Substance ID:
24724498
NACRES:
NA.77

品質水準

100

アッセイ

≥98% (HPLC)

形状

solid

色

off-white

溶解性

H2O: <2 mg/mL
DMSO: ≥5 mg/mL

保管温度

2-8°C

SMILES string

NC(=O)c1cccc(c1)-c2cc(Nc3ccc(OC(F)(F)F)cc3)ncn2

InChI

1S/C18H13F3N4O2/c19-18(20,21)27-14-6-4-13(5-7-14)25-16-9-15(23-10-24-16)11-2-1-3-12(8-11)17(22)26/h1-10H,(H2,22,26)(H,23,24,25)

InChI key

WEVYNIUIFUYDGI-UHFFFAOYSA-N

類似品目との比較

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当該品目
197221SML0511SML1990
GNF-2 &#8805;98% (HPLC), solid

Sigma-Aldrich

G9420

GNF-2

Bcr-abl Inhibitor The Bcr-abl Inhibitor, also referenced under CAS 778270-11-4, controls the biological activity of Bcr-abl. This small molecule/inhibitor is primarily used for Phosphorylation &amp; Dephosphorylation applications.

Sigma-Aldrich

197221

Bcr-abl Inhibitor

GNF-5 &#8805;98% (HPLC)

Sigma-Aldrich

SML0511

GNF-5

GW806742X &#8805;98% (HPLC)

Sigma-Aldrich

SML1990

GW806742X

form

solid

form

solid

form

powder

form

powder

color

off-white

color

white

color

white to beige

color

white to beige

solubility

H2O: <2 mg/mL, DMSO: ≥5 mg/mL

solubility

DMSO: 10 mg/mL, ethanol: 2 mg/mL

solubility

DMSO: 10 mg/mL (clear solution)

solubility

DMSO: 2 mg/mL, clear

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

2-8°C

生物化学的／生理学的作用

GNF-2 belongs to a new class of Bcr-abl inhibitors. GNF-2 appears to bind to the myristoyl binding pocket, an allosteric site distant from the active site, stabilizing the inactive form of the kinase. It inhibits Bcr-abl phosphorylation with an IC50 of 267 nM, but does not inhibit a panel of 63 other kinases, including native c-Abl, and shows complete lack of toxicity towards cells not expressing Bcr-Abl. GNF-2 shows great potential for a new class of inhibitor to study Bcr-abl activity and to treat resistant Chronic myelogenous leukemia (CML), which is caused the Bcr-Abl oncoprotein.

特徴および利点

This compound is a featured product for Kinase Phosphatase Biology research. Click here to discover more featured Kinase Phosphatase Biology products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
This compound is featured on the Abl page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

保管分類コード

11 - Combustible Solids

WGK

WGK 3

個人用保護具 (PPE)

dust mask type N95 (US), Eyeshields, Gloves

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  • もしTO09019TOなどのロット番号を見つけた場合は、最初の2文字を除いたロット番号09019TOを入力します。

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Melissanne de Wispelaere et al.
Cell chemical biology, 25(8), 1006-1016 (2018-06-26)
Viral envelope proteins are required for productive viral entry and initiation of infection. Although the humoral immune system provides ample evidence for targeting envelope proteins as an antiviral strategy, there are few pharmacological interventions that have this mode of action.
Inhibitors of Bcr-abl... breaking new ground again.
Jeffrey F Ohren et al.
Nature chemical biology, 2(2), 63-64 (2006-01-20)
Francisco J Adrián et al.
Nature chemical biology, 2(2), 95-102 (2006-01-18)
Chronic myelogenous leukemia (CML) is a myeloproliferative disorder characterized at the molecular level by the expression of Bcr-abl, a 210-kDa fusion protein with deregulated tyrosine kinase activity. Encouraged by the clinical validation of Bcr-abl as the target for the treatment
So-Youn Kim et al.
Cell death and differentiation, 26(3), 502-515 (2018-07-11)
Platinum-based chemotherapies can result in ovarian insufficiency by reducing the ovarian reserve, a reduction believed to result from apoptosis of immature oocytes via activation/phosphorylation of TAp63α by multiple kinases including CHEK2, CK1, and ABL1. Here we demonstrate that cisplatin (CDDP)
Haibin Tong et al.
Journal of cellular biochemistry, 119(3), 2806-2817 (2017-10-24)
The excessive recruitment and improper activation of polymorphonuclear neutrophils (PMNs) often induces serious injury of host tissues, leading to inflammatory disorders. Therefore, to understand the molecular mechanism on neutrophil recruitment possesses essential pathological and physiological importance. In this study, we
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