Catalog No. size PriceQuantity
M102-2S 2mg solid $79
M102-10S 10mg solid $324


Product Information
Storage: Powder -20oC 3 years 4oC 2 years In solvent -80oC 6 months -20oC 1 month
Chemical Name: 3-(6-((4-(trifluoromethoxy)phenyl)amino)pyrimidin-4-yl)benzamide InChi Key: WEVYNIUIFUYDGI-UHFFFAOYSA-N
Solubility: DMSO: ≥ 45 mg/mL
CAS#: 778270-11-4
Purity: >98%
Formula: C18H13F3N4O2
Molecular Weight: 374.32


Biological Activity:

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-Abl 

How to use:

in 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].


[1]. Adrián FJ, et al. Allosteric inhibitors of Bcr-abl-dependent cell proliferation. Nat Chem Biol. 2006 Feb;2(2):95-102.
[2]. Khateb M, et al. Overcoming Bcr-Abl T315I mutation by combination of GNF-2 and ATP competitors in an Abl-independent mechanism. BMC Cancer. 2012 Nov 27;12:563.
[3]. Mian AA, et al. Allosteric inhibition enhances the efficacy of ABL kinase inhibitors to target unmutated BCR-ABL and BCR-ABL-T315I.BMC Cancer. 2012 Sep 17;12:411.
[4]. Kim HJ, et al. The tyrosine kinase inhibitor GNF-2 suppresses osteoclast formation and activity. J Leukoc Biol. 2013 Oct 15.
[5]. Huang WC, et al. Glucosylceramide synthase inhibitor PDMP sensitizes chronic myeloid leukemia T315I mutant to Bcr-Abl inhibitor and cooperatively induces glycogen synthase kinase-3-regulated apoptosis. FASEB J. 2011 Oct;25(10):3661-73.

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