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


GNF-2 is an allosteric inhibitor of Bcr-abl tyrosine kinase activity (IC50 = 267 nM); inhibits proliferation and induces apoptosis in Bcr-abl-expressing cells. Selective for Bcr-abl over a panel of serine, threonine and tyrosine kinases. Non-ATP-competitive.

Product information

CAS Number: 778270-11-4

Molecular Weight: 374.32

Formula: C18H13F3N4O2

Chemical Name: 3-(6-{[4-(trifluoromethoxy)phenyl]amino}pyrimidin-4-yl)benzamide

Smiles: NC(=O)C1=CC(=CC=C1)C1=CC(NC2C=CC(=CC=2)OC(F)(F)F)=NC=N1


InChi: 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)

Technical Data

Appearance: Solid Power

Purity: ≥98% (or refer to the Certificate of Analysis)

Solubility: DMSO: ≥ 45 mg/mL

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis

Storage Condition: Dry, dark and -20 oC for 1 year or refer to the Certificate of Analysis.

Shelf Life: ≥12 months if stored properly.

Stock Solution Storage: 0 - 4 oC for 1 month or refer to the Certificate of Analysis.

Drug Formulation: To be determined.

HS Tariff Code: 382200

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. 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.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.

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.


  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.

Products are for research use only. Not for human use.

Payment & Security

PayPal Venmo

Your payment information is processed securely. We do not store credit card details nor have access to your credit card information.

Estimate shipping

You may also like

Recently viewed