title: Bcr-Abl tyrosine kinase inhibitors: a patent review.
abstract: BACKGROUND
  Breakpoint cluster region Abelson (Bcr-Abl) tyrosine kinase (TK) is a constitutively activated cytoplasmic TK and is the underlying cause of chronic myeloid leukemia (CML). To date, imatinib represents the frontline treatment for CML therapy. The development of resistance has prompted the search for novel Bcr-Abl inhibitors.
  
  
  METHODS
  This review presents a short overview of drugs already approved for CML therapy and of the compounds that are in clinical trials. The body of the article deals with Bcr-Abl inhibitors patented since 2008, focusing on their chemical features.
  
  
  CONCLUSIONS
  The search for Bcr-Abl inhibitors is very active. We believe that a number of patented compounds could enter clinical trials and some could be approved for CML therapy in the next few years. Overall, Bcr-Abl inhibitors constitute a very appealing research field that can be expected to expand further.
authors: Università degli Studi di Genova, Dipartimento di Farmacia , Viale Benedetto XV 3, I-16132, Genova , Italy +0039 010 3538362 ; schensil@unige.it.
authors: Andrea
authors: A
authors: Desogus
authors: Silvia
authors: S
authors: Schenone
authors: Chiara
authors: C
authors: Brullo
authors: Cristina
authors: C
authors: Tintori
authors: Francesca
authors: F
authors: Musumeci
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D015195:Drug Design; D019008:Drug Resistance, Neoplasm; D016044:Fusion Proteins, bcr-abl / Q000037:antagonists & inhibitors* / Q000378:metabolism; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000201:enzymology; D010330:Patents as Topic; D047428:Protein Kinase Inhibitors / Q000494:pharmacology*
chemical_list: D000970:Antineoplastic Agents; D047428:Protein Kinase Inhibitors; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl
keywords: T315I; breakpoint cluster region Abl tyrosine kinase; chronic myeloid leukemia; inhibitors; mutation; tyrosine kinase