GNF-2

Cas No.:	778270-11-4
Chemical Name:	Benzamide,3-[6-[[4-(trifluoromethoxy)phenyl]amino]-4-pyrimidinyl]-
Synonyms:	Benzamide,3-[6-[[4-(trifluoromethoxy)phenyl]amino]-4-pyrimidinyl]-;GNF-2;3-(6-((4-(Trifluoromethoxy)phenyl)amino)pyrimidin-4-yl)benzamide;3-[6-[4-(trifluoromethoxy)anilino]pyrimidin-4-yl]benzamide;Gnf 2;3k5v;Bcr-abl Inhibitor;3-[6-[[4-(Trifluoromethoxy)phenyl]amino]-4-pyrimidinyl]benzamide
SMILES:	O=C(C1=CC=CC(C2=CC(NC3=CC=C(OC(F)(F)F)C=C3)=NC=N2)=C1)N
Formula:	C18H13F3N4O2
M.Wt:	374.317
Sotrage:	2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO

Description:

GNF-2 is a highly selective non-ATP competitive inhibitor of oncogenic Bcr-Abl activity (IC50 = 0.14 μM).IC50 value: 0.14 uM [1]Target: Bcr-Ablin vitro: Ba/F3 cells harboring native or T315I mutated Bcr-Abl constructs were treated with GNF-2 and AKIs. We monitored the effect of GNF-2 with AKIs on the proliferation and clonigenicity of the different Ba/F3 cells. In addition, we monitored the auto-phosphorylation activity of Bcr-Abl and JAK2 in cells treated with GNF-2 and AKIs [2]. GNF-2 increased the effects of AKIs on unmutated BCR/ABL. Interestingly, the combination of Dasatinib and GNF-2 overcame resistance of BCR/ABL-T315I in all models used in a synergistic manner [3].GNF-2 dose-dependently inhibited the proliferation of osteoclast precursors through the suppression of the M-CSFR c-Fms. In addition, GNF-2 accelerated osteoclast apoptosis by inducing caspase-3 and Bim expression. Furthermore, GNF-2 interfered with actin cytoskeletal organization and subsequently blocked the bone-resorbing activity of mature osteoclasts [4].in vivo: Combining PDMP and GNF-2 eliminated transplanted-CML-T315I-mutants in vivo and dose dependently sensitized primary cells from CML T315I patients to GNF-2-induced proliferation inhibition and apoptosis[5].