TABLE 1.

Currently available ABL-inhibiting TKIs, their known cardiovascular-associated toxicity, and the possible underlying mechanisms.

TKI gen	Drug	Cardiovascular toxicity	Involved mechanisms
1st	Imatinib	Potential benefit on metabolic and cardiovascular function	NA
2nd	Nilotinib	Arterial hypertension, ischemic events	Increased P-selectin, sICAM-1, sVCAM-1, TNF-alpha, IL-6, PAR-1-mediated alpha granule release, endogenous thrombin levels (in vitro and in vivo), inhibition of endothelial cell proliferation, increased glucose levels, glomerular impairment, mast cell disruption (impaired tissue repair)
2nd	Dasatinib	Pulmonary arterial hypertension	Hypoxic pulmonary vasoconstriction responses reduction (possible)
2nd	Bosutinib	Potentially none	NA
3rd	Ponatinib	Peripheral arterial obstructive disease, other ischemic events	Not known. Hypothetically similar to nilotinib. Dose dependent.