Nilotinib

BCR-ABL Inhibitor
DB04868
Approved Indication

For the potential treatment of various leukemias, including chronic myeloid leukemia (CML).

2 Targets
3 Resistance Mutations
8 References
3CS9 Structure Loaded
3D Structure PDB: 3CS9
Switch structure: RCSB ↗
Mechanism of Action

Chronic myelogenous leukaemia (CML) is caused by the BCR-ABL oncogene. Nilotinib inhibits the tyrosine kinase activity of the BCR-ABL protein. Nilotinib fits into the ATP-binding site of the BCR-ABL protein with higher affinity than imatinib, over-riding resistance caused by mutations. The ability of AMN107 to inhibit TEL-platelet-derived growth factor receptor-beta (TEL-PDGFRbeta), which causes chronic myelomonocytic leukaemia, and FIP1-like-1-PDGFRalpha, which causes hypereosinophilic syndrome, suggests potential use of AMN107 for myeloproliferative diseases characterised by these kinase fusions (Stover et al, 2005; Weisberg et al, 2005). AMN107 also inhibits the c-Kit receptor kinase, including the D816V-mutated variant of KIT, at pharmacologically achievable concentrations, supporting potential utility in the treatment of mastocytosis, and gastrointestinal stromal tumours (Weisberg et al, 2005; von Bubnoff et al, 2005; Gleixner et al, 2006).

Resistance Mutations — 3 resistance samples observed in COSMIC
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ABL1
p.T315V p.T334V
KIT
p.N655T 3

Resistance mutations sourced from COSMIC Drug Resistance database. Cyan = on-target · Amber = off-target · numbered badge = PubMed references for that mutation

Details
DrugBank ID DB04868 ↗
Approval Date 2007-10-29
Molecular Weight 529.5158 g/mol
Drug Class BCR-ABL Inhibitor
ATC Codes L01XE08
Synonyms Nilotinibum
SMILES
CC1=CN(C=N1)C1=CC(=CC(NC(=O)C2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)=C1)C(F)(F)F
ADMET Profile
Computing properties…