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GNF-2_Molecular_structure_CAS_778270-11-4)
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GNF-2

Catalog No. G9420 Name Sigma Aldrich
CAS Number 778270-11-4 Website http://www.sigmaaldrich.com
M. F. C18H13F3N4O2 Telephone 1-800-521-8956
M. W. 374.3166296 Fax
Purity ≥98% (HPLC) Email
Storage Chembase ID: 153875

SYNONYMS

IUPAC name
3-(6-{[4-(trifluoromethoxy)phenyl]amino}pyrimidin-4-yl)benzamide
IUPAC Traditional name
3-(6-{[4-(trifluoromethoxy)phenyl]amino}pyrimidin-4-yl)benzamide
Synonyms
3-[6-[[4-(Trifluoromethoxy)phenyl]amino]-4-pyrimidinyl]benzamide

DATABASE IDS

CAS Number 778270-11-4
MDL Number MFCD09265253
PubChem SID 24724498

PROPERTIES

Empirical Formula (Hill Notation) C18H13F3N4O2
Purity ≥98% (HPLC)
Apperance off-white solid
Solubility H2O: <2 mg/mL
Solubility DMSO: ≥5 mg/mL
GHS Pictograms GHS07
GHS Signal Word Warning
GHS Hazard statements H315-H319-H335
European Hazard Symbols Irritant Irritant (Xi)
MSDS Link Download
Personal Protective Equipment dust mask type N95 (US), Eyeshields, Gloves
GHS Precautionary statements P261-P305 + P351 + P338
Risk Statements 36/37/38
Safety Statements 26
Storage Temperature 2-8°C
German water hazard class 3

DETAILS

Description (English)
Biochem/physiol Actions
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.
Description (简体中文)
Biochem/physiol Actions
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.

REFERENCES