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GNF 7 is a potent Bcr-Abl inhibitor (IC50 values are 61 and 133 nM for T315I and wild-type Bcr-Abl, respectively), inhibiting a range of clinically relevant Bcr-Abl mutants such as T315I, G250E, E255V, F317L and M351T. GNF 7 is also a Ras signaling inhibitor as well as inhibiting Ack1 and germinal center kinase (GCK). GNF 7 induces cell cycle arrest and apoptosis in leukemia cells harboring NRAS mutations, and shows growth inhibitory activity in human colon cancer cells. It prolongs survival in a leukemia cell xenotransplantation model in mice and is orally bioavailable.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
The following data is based on the product molecular weight 547.53. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|0.5 mM||3.65 mL||18.26 mL||36.53 mL|
|2.5 mM||0.73 mL||3.65 mL||7.31 mL|
|5 mM||0.37 mL||1.83 mL||3.65 mL|
|25 mM||0.07 mL||0.37 mL||0.73 mL|
References are publications that support the biological activity of the product.
Nonami et al (2015) Identification of novel therapeutic targets in acute leukemias with NRAS mutations using a pharmacologic approach. Blood 125 3133 PMID: 25833960
Choi et al (2010) A type-II kinase inhibitor capable of inhibiting the T315I "gatekeeper" mutant of Bcr-Abl. J.Med.Chem 53 5439 PMID: 20604564
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Keywords: GNF 7, GNF 7 supplier, GNF7, RAS, inhibitors, inhibits, Ack1, germinal, centre, kinases, GCK, leukemia, TNK2, Bcr-Abl, GNF-7, Ras, GTPases, Abl, Kinase, 5607, Tocris Bioscience
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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Written by Kirsten L. Bryant, Adrienne D. Cox and Channing J. Der, this review provides a comprehensive overview of RAS protein function and RAS mutations in cancer. Key signaling pathways are highlighted and therapeutic vulnerabilities are explored. This review also includes a detailed section on RAS drug discovery and targeting synthetic lethal interactors of mutant RAS. Compounds available from Tocris are listed.
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.
Adapted from the 2015 Cancer Product Guide Edition 3, this poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.