Valsartan

Systematic (IUPAC) name
(S)-3-methyl-2-[N-({4-[2-(2H-1,2,3,4-tetrazol-5-yl)phenyl]phenyl}methyl)pentanamido]butanoic acid
Identifiers
CAS number	137862-53-4
ATC code	C09CA03
PubChem	60846
DrugBank	APRD00133
Chemical data
Formula	C24H29N5O3
Mol. mass	435.519 g/mol
SMILES	eMolecules & PubChem
Pharmacokinetic data
Bioavailability	25%
Protein binding	95%
Metabolism	?
Half life	6 hours
Excretion	Renal 30%, biliary 70%
Therapeutic considerations
Pregnancy cat.	D
Legal status	℞ Prescription only
Routes	oral
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Valsartan is an angiotensin II receptor antagonist (more commonly called an "ARB", which stands for angiotensin receptor blocker), with particularly high affinity for the type I (AT₁) angiotensin receptor. In the U.S., valsartan is indicated for treatment of high blood pressure, congestive heart failure (CHF), or post-myocardial infarction (MI).^{[citation needed]}

Valsartan is marketed by Novartis under the trade name Diovan. In India, it is marketed by CIPLA under the trade name Valtan and by Torrent Pharmaceuticals under the trade name Valzaar. In 2005, Diovan was prescribed more than 12 million times in the United States. Global sales approx $6.0bn.^{[citation needed]} Patent expires in 2012.^{[citation needed]}

A study released by the Journal of Clinical Investigation in 2007 found some efficacy in the use of valsartan in the treatment and prevention of Alzheimer's Disease although such use is considered to be highly experimental.^[1]

[edit] Administration

Oral tablets, containing 40 mg (scored), 80 mg, 160 mg or 320 mg of valsartan. Usual dosage ranges from 40–320 mg daily.

In some markets available as a hard gelatin capsule, containing 40 mg, 80 mg, or 160 mg of valsartan.

Diovan HCT contains a combination of valsartan and hydrochlorothiazide but, unlike Diovan, is only indicated for hypertension, not for CHF or post-MI.^{[citation needed]}

[edit] Myocardial infarction controversy

Whether angiotensin receptor blockers may or may not increase the risk of myocardial infarction was announced in the BMJ^[2] and was debated in 2006 in the medical journal of the American Heart Association.^[3][4] To date^[when?], there is no consensus on whether ARBs have a tendency to increase MI, but there is also no substantive evidence to indicate that ARBs are able to reduce MI.

In the VALUE trial, the angiotensin II receptor blocker valsartan produced a statistically significant 19% (p=0.02) relative increase in the prespecified secondary end point of myocardial infarction (fatal and non-fatal) compared with amlodipine.^[5]

The CHARM-alternative trial showed a significant +52% (p=0.025) increase in myocardial infarction with candesartan (versus placebo) despite a reduction in blood pressure.^[6]

Indeed, as a consequence of AT1 blockade, ARBs increase Angiotensin II levels several-fold above baseline by uncoupling a negative-feedback loop. Increased levels of circulating Angiotensin II result in unopposed stimulation of the AT2 receptors, which are, in addition upregulated. Unfortunately, recent data suggest that AT2 receptor stimulation may be less beneficial than previously proposed and may even be harmful under certain circumstances through mediation of growth promotion, fibrosis, and hypertrophy, as well as proatherogenic and proinflammatory effects.^[7][8][9]

[edit] Side effects

Most commonly, headache and dizziness. Sensitivity to sun light and bright artificial light.

There is a case report of a stillbirth in which valsartan is implicated.^[10]

[edit] See also

Angiotensin Receptor Blockers: Drug discovery and development

[edit] References

[edit] External links

• PubMed:Valsartan
• Official Diovan Site