News from the Bench
Discover what’s going on at CST, receive our latest application notes and tips, read our science features, and learn about our products.
Our U.S. Offices Are Closed
Our U.S. offices are closed in observance of Thanksgiving. We will reopen on Monday, December 1st.
Thank you for your patience.
To Purchase # 12209S
|$ 0. 00|
Find answers on our FAQs page.
PTM information and tools available.
Western blot analysis of extracts from K-562 cells, untreated (-) or treated (+) with Nilotinib (1000 nM, 24 hr), using PathScan® Bcr/Abl Activity Assay: Phospho-c-Abl, Phospho-Stat5, and Phospho-CrkL Multiplex Western Detection Cocktail #5300 to detect inhibition of phospho-Bcr-Abl, phospho-Stat5, and phospho-CrkL.Learn more about how we get our images
Gallery: Nilotinib #12209
Nilotinib is supplied as a lyophilized powder. For a 5 mM stock, reconstitute the 5 mg in 1.89 ml DMSO. Working concentrations and length of treatment can vary depending on the desired effect, but it is typically used at 10-1000 nM for 2-72 hr. Nilotinib is soluble in DMSO at 50 mg/ml; very poorly soluble in ethanol and water with maximum solubility in water at ~10-20 µM.Storage: Store lyophilized or in solution at -20ºC, desiccated. Protect from light. In lyophilized form, the chemical is stable for 24 months. Once in solution, use within 3 months to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.
Nilotinib (AMN-107) is a novel tyrosine kinase inhibitor that potently inhibits Bcr-Abl. Nilotinib is more effective than imatinib at decreasing the proliferation and viability in cells expressing wild-type Bcr-Abl and is active against many imatinib-resistant Bcr-Abl mutants, with the exception of T315I (1-4). Nilotinib has been shown to inhibit Abl activity in cells expressing wild-type Abl and imatinib-resistant mutant Abl, with ~20-fold greater potency than imatinib. Nilotinib is similarly effective at inhibiting Abl autophosphorylation (3). Research studies have demonstrated that nilotinib treatment of Bcr-Abl-expressing K-562 cells attenuates Stat5 and CrkL phosphorylation, decreases Bcl-xL and c-Myc expression, induces p27 and Bim expression, and induces PARP cleavage. Many of these effects are enhanced by cotreatment with the histone deacetylase inhibitor LBH589 (5).
For Research Use Only. Not For Use In Diagnostic Procedures. Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc. PathScan® is a trademark of Cell Signaling Technology, Inc.