Table 2.

First phase I clinical trials in 56 patients

Treatment	Mechanism of action	Patients	%	Investigator, year
XL-184	VEGFR2 and Met TKI	18	32	Salgia et al., 2008 (28)
Tipifarnib + sorafenib	FTI + VEGFR2, VEGFR3, PDGFR-β, Raf-1, FLT3 TKI	13	23	Chintala et al., 2008 (29)
RTA 402 CDDO-Me	NF-κB and STAT3 inhibition	6	11	Hong et al., 2008 (30)
Azacitidine + valproic acid	DNA hypomethylation	4	7	Braiteh et al., 2008 (31)
Patupilone	Microtubule stabilization	2	4	Kurzrock et al., 2007 (32)
MK-2461	c-Met TKI	2	4	Camacho et al., 2008 (33)
Other		11a	20

FLT3, fms-like tyrosine kinase 3; FTI, farnesyltransferase inhibitor; Met, hepatocyte growth factor/scatter factor receptor; NF-κB, nuclear factor κβ; PDGFR-β, platelet-derived growth factor receptor-β; STAT3, signal transducer and activator of transcription-3; TKI, tyrosine kinase inhibitor; VEGFR2, vascular endothelial growth factor receptor 2; VEGFR3, vascular endothelial growth factor receptor 3. 

^aOne patient each was treated with salirasib (Ras inhibitor); sunitinib, paclitaxel, and carboplatin; AZD 4877 (kinesin spindle protein inhibitor); PXD 101 (histone deacetylase inhibitor); bevacizumab plus sorafenib; nab-rapamycin (albumin-bound mammalian target of rapamycin kinase inhibitor); E7107 (spliceosome inhibitor); valproic acid plus sunitinib; liposomal doxorubicin, bortezomib (proteasome inhibitor), and gemcitabine; hepatic arterial infusion of paclitaxel; and KX2-391 (Src kinase inhibitor).