Nilotinib (AMN-107)

M.Wt: 529.52
Formula: C₂₈H₂₂F₃N₇O
Solubility: DMSO
Purity: >99%
Storage: at -20℃ 2 years
CAS No.: 641571-10-0

Price and Availability of Nilotinib (AMN-107):

Applications & Customer's Feedback of Nilotinib (AMN-107):

Glucosylceramide synthase inhibitor PDMP sensitizes chronic myeloid leukemia T315I mutant to Bcr-Abl inhibitor and cooperatively induces glycogen synthase kinase-3-regulated apoptosis.  ------ Huang WC,Tsai CC,et al. FASEB J. 2011 Oct;25:3661-73.

Biological Activity of Nilotinib (AMN-107):

Chronic myelogenous leukaemia (CML) and Philadelphia chromosome positive (Ph+) acute lymphoblastic leukaemia (ALL) are caused by the BCR-ABL oncogene.
AMN107 inhibited the proliferation of Ba/F3 cells expressing p210- and p190-Bcr-Abl, or K562 and Ku-812F cells with IC50 values <12 nM.
AMN107 was quantitatively via capture ELISA for its effect on cellular Bcr-Abl autophosphorylation activity and on Bcr-Abl-dependent cell proliferation. AMN107,IC50 =20–60 nM.^[1]
The effects of AMN107 were compared with those of imatinib on imatinib-sensitive (KBM5 and KBM7) and imatinib-resistant CML cell lines (KBM5-STI571^R1.0 and KBM7-STI571^R1.0). Compared with the antiproliferative activity of imatinib , AMN107 was 43times more potent in KBM5 (IC50 of 11.3 versus 480.5 nM) and 60 times more potent in KBM7(IC50 of 4.3versus 259.0 nM) cells. IC50 for AMN107 and imatinib were 2,418.3 and 6,361.4 nM, respectively, in KBM5- STI571^R1.0, and 97.2 and 2,497.3nM, respectively, in KBM7-STI571^R1.0 cells.^[2]

References on Nilotinib (AMN-107):

[1] Ellen Weisberg et al. Cancer Cell. 2005 February;17(2):129-141

[2] Mirna Golemovic et al. Clinical Cancer Research.2005 July; 11:4941

MSDS
Batch S103303: H-NMR  HPLC  COA
Batch S103304: H-NMR  HPLC  COA

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