Olmesartan (OL) is the pharmacologically active metabolite of Olmesartan 
medoxomil (OM), an FDA-approved angiotensin II receptor antagonist for 
administrating cardiovascular diseases. The drug has been found to have 
potential effects on diverse protein kinase signaling involved in the 
pathogenesis of atherosclerosis, either by directly inhibiting the hub kinases 
or by indirectly modulating marginal members in the signaling pathways. In the 
present study, we computationally model the kinase-chemical Interaction Profile 
between six OL-related chemicals (i.e. OL, OM, Valsartan [VL], Losartan [LS], 
Candesartan [CD] and Telmisartan [TL]) and 23 human protein kinases in 
atherosclerosis. The profile is analyzed systematically at molecular level to 
identify unexpected kinase targets for OL. There is a good consistence between 
co-citation frequency and affinity scoring for the chemical association with 
kinase candidates; the OL and its analogs VL and LS exhibit a similar binding 
profile to the atherosclerosis kinase spectrum. It is suggested that the 
Ser/Thr-specific kinases PI3Kα and ROCK1 are potential druggable targets of OL 
for atherosclerosis therapy. As a paradigm, kinase assays reveal that the 
inhibitory potency of OL and Y-27632 (positive control) on ROCK1 is determined 
at micromolar level, while the OM (negative control) possesses no detectable 
activity for the kinase.