Table 1.

TK fusion inhibitors

Target process	Molecule	TK fusion	Current status	Resistance	Reference
ATP competition	Imatinib, nilotinib, dasatinib	X-ABL, X-PDGFRA and X-PDGFRB	Approved	Mutations	[11, 13]
	DCC-2036	BCR-ABL	Mouse model	†	[12]
	Crisotinib (PF02341066)	EML4-ALK	Clinical trial	Mutations	[5]
	CH5424802	EML4-ALK	Mouse model	†	[109]
	Dovitinib (TKI258)	X-FGFR1	In vitro*		[110, 111]
	Tasocitinib (CP690550) and Ruxolitinib (INCB018424)	X-JAK2	In vitro*	Mutations	[69]
Oligomerization	Helix-2	BCR-ABL	In vitro	†	[40]
Conformation	GNF-2, GNF-5 (allosteric inhibitors)	BCR-ABL	Mouse model	Mutations‡	[62]
Expression and chaperones	Tanespimycin (17-AAG)	BCR-ABL	In vitro		[25, 112, 113]
	Alvespimycin (17-DMAG)	BCR-ABL	In vitro*		[104]
	EC141	BCR-ABL	In vitro		[114]
	Novobiocin	BCR-ABL	In vitro		[115]
	Ascorbate + menadione	BCR-ABL	In vitro		[105]
	siRNA	BCR-ABL	In vitro	†	[25, 26]

^*Clinical trials are ongoing for other indications.

^†Active against mutants that are resistant to conventional ATP competitors.

^‡The combination of GNF-2 with helix-2 or nilotinib is active against resistant mutations.