Tekturna- uses and side effects

Tekturna (aliskiren)
Potential health benefits on cancers and research finds 2007

Novartis' Tekturna (aliskiren) tablets was approved on March 6,
2007 for the treatment of high blood pressure, or hypertension.
Tekturna, a new molecular entity (NME), is the first high blood
pressure drug approved by FDA that inhibits renin, a kidney
enzyme associated with the regulation of blood pressure. Tekturna
acts at the beginning of the blood pressure regulation process,
while other available high blood pressure medications act at later
stages.

High blood pressure is often considered as the silent killer,
because it usually has no symptoms until it causes major damage
to the body organs, such as stroke, heart attack, kidney failure,
heart failure and death.

The effectiveness of Tekturna in lowering blood pressure has been
demonstrated in six placebo-controlled eight-week clinical trials,
which studied more than 2,000 patients with mild to moderate
hypertension. The effect was maintained for up to one year.
Tekturna was effective across all demographic subgroups, [1,4] but
African American patients tended to have smaller reductions in
blood pressure than Caucasians and Asians, as is generally true
for drugs that affect the renin-angiotensin system, a component of
blood pressure regulation.

Tekturna by itself demonstrates effective blood lowering in a
number of studies. Tekturna can also be used in combination with
a thiazide diuretic (hydrochlorothiazide), an angiotensin-converting
enzyme inhibitor (ramipril) or a calcium channel blocker
(amlodipine), a diuretic, further reductions in blood pressure were
achieved. [3]

What are the side effects and drug interaction of Tekturna?

Aliskiren is a novel, orally active direct renin inhibitor that lowers
blood pressure alone and in combination with existing
antihypertensive agents. As aliskiren does not affect cytochrome
P450 enzyme activities, is minimally metabolised, and is not
extensively protein bound, the potential for drug interactions is
predicted to be low. [5]

In studies of healthy male volunteers aged 18-45 years, mean AUC
and t1/2 for aliskiren were not significantly changed by the intake
of lovastatin, atenolol or celecoxib.

Aliskiren mean Cmax was not affected by either lovastatin or
atenolol, although a non-significant 36% increase was observed
with celecoxib. Modest, non-significant increases in aliskiren
systemic availability followed coadministration with cimetidine.

Tekturna was evaluated for safety in more than 6,460 patients,
including 1,740 who were treated longer than six months, and more
than 1,250 for over one year. Side effects were usually mild and
brief. The most common side effect experienced by patients taking
Tekturna was diarrhea. Diarrhea was reported by approximately 2
percent of patients on the higher of the two approved doses,
compared with approximately 1 percent on placebo. Rarely,
patients taking Tekturna developed an allergic reaction with
swelling of the face, lips or tongue and difficulty breathing, as has
been seen with other drugs for high blood pressure that act directly
on the renin-angiotensin system.

The most commonly reported adverse events were headache,
dizziness and gastrointestinal symptoms (all mild in severity), which
were similar in frequency during antihypertensive drug treatment
alone and in combination with aliskiren except for an increase in
dizziness during treatment with the combination of aliskiren and
hydrochlorothiazide. [5]

Tekturna and other drugs that act directly on the renin-angiotensin
system should not be used during pregnancy because they can
cause injury and even death to the developing fetus. [1]

According to Brown MJ's review article, of currently available
antihypertensive drugs, only the beta-blockers suppress renin
secretion, unfortunately they also reduce heart rate and cardiac
output. [2] While, calcium channel blockers and diuretics cause a
modest activation of the renin system secondary to the fall in renal
afferent arteriolar pressure and reduction in filtered sodium load.
[2] Aliskiren is the first orally available direct inhibitor that blocks
the renin system at its rate limiting step and is shown to reduce
angiotensin I and II and plasma renin activity. [1-2]

ALL RIGHTS RESERVED ZHION 2007. CONSULT WITH YOUR DOCTOR FOR ANY
QUESTION OR BEFORE TAKING ANY SUPPLEMENT OR MEDICINE. THIS ARTICLE IS
FOR YOUR REFERENCE ONLY.

[1] FDA Approves New Drug Treatment for High Blood Pressure FDA News March 6, 2007.
[2] Brown MJ. Direct renin inhibition a new way of targeting the renin system. J Renin
Angiotensin Aldosterone Syst. 2006 Jan;7(2):S8-S11. [3] Schmieder RE. Aliskiren: a
clinical profile. J Renin Angiotensin Aldosterone Syst. 2006 Jan;7 Suppl 2:S16-20. [4]
Vaidyanathan S, Jermany J, Yeh C, Bizot MN, Camisasca R. Aliskiren, a novel orally
effective renin inhibitor, exhibits similar pharmacokinetics and pharmacodynamics in
Japanese and Caucasian subjects. Br J Clin Pharmacol. 2006 Dec;62(6):690-8. [5]
Vaidyanathan S, et al, Lack of pharmacokinetic interactions of aliskiren, a novel direct
renin inhibitor for the treatment of hypertension, with the antihypertensives amlodipine,
valsartan, hydrochlorothiazide (HCTZ) and ramipril in healthy volunteers. Dieterle W,
Corynen S, Vaidyanathan S, Mann J. Pharmacokinetic interactions of the oral renin
inhibitor aliskiren with lovastatin, atenolol, celecoxib and cimetidine. Int J Clin
Pharmacol Ther. 2005 Nov;43(11):527-35.