Intensive efforts have been spent to discover therapeutic, non-peptide and 
orally effective hypertensive drugs. One drug that emerged from this effort is 
aliskiren, a direct human renin inhibitor that blocks the conversion of 
angiotensinogen to angiotensin I (Ang I). In contrast to other antihypertensive 
agents, aliskiren decreases plasma renin activity (PRA). In healthy human 
subjects, doses of between 40 and 640 mg of aliskiren exert a dose-dependent 
reduction in PRA and Ang I and Ang II levels. The bioavailability of aliskiren 
is low (2%), peak plasma concentrations are reached within one to three hours 
and the binding with plasma proteins achieves approximately 47-51%. Aliskiren is 
slightly metabolized (20%) by CYP3A4. The most common adverse events include 
diarrhea, headache, back pain and gastrointestinal disorders. Aliskiren is well 
tolerated, and may be used alone or in combination with other antihypertensive 
agents. Aliskiren belongs to a new class of agents that effectively and 
specifically inhibit the RAS. This drug functions through a novel mechanism of 
action and has the potential to become a true alternative to angiotensin 
converting enzyme inhibitors and angiotensin receptor blockers in the therapy of 
hypertension and other cardiovascular and renal disorders.