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GNF-2 CAS NO.778270-11-4
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- Min.Order: 100 Gram
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≥98.0%(100-500)Gram≥98.0%(1000-5000)Gram
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Keywords
- GNF-2
- GNF-2;Bcr-abl Inhibitor;3-[6-[[4-(Trifluoromethoxy)phenyl]amino]-4-pyrimidinyl]benzamide;Benzamide, 3-[6-[[4-(trifluoromethoxy)phenyl]amino]-4-pyrimidinyl]-;3-[6-[[4-(Trifluoromethoxy)phenyl]amino]-4-
- 778270-11-4
Quick Details
- ProName: GNF-2
- CasNo: 778270-11-4
- Molecular Formula: C18H13F3N4O2
- Appearance: Almost white crystalline powder
- Application: CAS：778270-11-4； GNF-2;Bcr-abl Inhibi...
- DeliveryTime: 3 months
- PackAge: 100g,500g,1kg,25kg
- Port: shang hai
- ProductionCapacity: 1000 Gram/Week
- Purity: 98%
- Storage: Dry seal
- Transportation: shipping
- LimitNum: 100 Gram
Superiority
We are committed to provide excellence in researching, manufacturing and drug discovery process.
Our research team of scientists consists of western-trained Ph.D.s with experience and capabilities in drug R&D methodologies and medicinal chemistry.
Details
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
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].