Table 1. Chemotherapeutic agents associated with CIHF and their molecular targets, modified from (3).

Class	Agent	Molecular mechanism	Incidence of CIHF in %
TKIs based on monoclonal antibodies	Bevacizumab	VEGF-A inhibition	2–4
	Trastuzumab	Inhibition of HER2/HER2 dimerization by binding of extracellular subdomain IV	Up to 27 when combined with anthracyclines
	Ado-trastuzumab emtansine	Trastuzumab conjugated to cytotoxic tubulin inhibitor emtansine	1.8
	Pertuzumab	Inhibition of HER2/HER3 dimerization by binding of extracellular subdomain II	4.5–14.5
Small molecule TKIs	Sunitinib	Several VEGFR, PDGF-R, GCSF-R, c-KIT, RET, FLT3, AMPK	1–27
	Sorafenib	VEGFR-2 and -3, PDGF-R, c-Kit, Raf kinase family	1.9–11
	Lapatinib	HER2 and HER1/EGFR	0.9–4.9
	Dasatinib	Bcr-abl, c-KIT, Src, ephrins	8–9
	Dabrafenib	B-Raf	Up to 10
	Imatinib	Bcr-abl, PDGF-R, M-CSF-R	<1
	Nilotinib	Bcr-abl, c-KIT	<1
	Ponatinib	BCR-abl, FGF-R, VEGFR-2, PDGF-R, FLT3	3–15
	Trametinib	MEK1 and MEK2	Up to 10
Proteasome inhibitors	Bortezomib	Reversible inhibition of the 20S proteasome	2–5
	Carfilzomib	Irreversible inhibition of the 20S proteasome	7

PDGF-R, platelet-derived growth factor receptor; GCSF-R, granulocyte colony-stimulating factor receptor; c-KIT, mast/stem cell growth factor receptor; FGF-R, fibroblast growth factor receptor; FLT3, Fms like tyrosine kinase 3; AMPK, adenosine monophosphate-activated protein kinase; Src, proto-oncogene tyrosine-protein kinase; Ephrins, Eph family receptor ligands; Bcr-abl, kinase product of the Philadelphia translocation; MEK, mitogen-activated protein kinase; M-CSF-R, macrophage colony-stimulating factor receptor.