Valsartan

Identification

Summary

Valsartan is an angiotensin-receptor blocker used to manage hypertension alone or in combination with other antihypertensive agents and to manage heart failure in patients who are intolerant to ACE inhibitors.

Brand Names

Dafiro, Diovan, Diovan Hct, Entresto, Exforge, Exforge Hct

Generic Name

Valsartan

DrugBank Accession Number

DB00177

Background

Valsartan belongs to the angiotensin II receptor blocker (ARB) family of drugs, which also includes telmisartan, candesartan, losartan, olmesartan, and irbesartan. ARBs selectively bind to angiotensin receptor 1 (AT1) and prevent the protein angiotensin II from binding and exerting its hypertensive effects, which include vasoconstriction, stimulation and synthesis of aldosterone and ADH, cardiac stimulation, and renal reabsorption of sodium, among others. Overall, valsartan's physiologic effects lead to reduced blood pressure, lower aldosterone levels, reduced cardiac activity, and increased excretion of sodium.

Valsartan also affects the renin-angiotensin aldosterone system (RAAS), which plays an important role in hemostasis and regulation of kidney, vascular, and cardiac functions. Pharmacological blockade of RAAS via AT1 receptor blockade inhibits negative regulatory feedback within RAAS, which is a contributing factor to the pathogenesis and progression of cardiovascular disease, heart failure, and renal disease. In particular, heart failure is associated with chronic activation of RAAS, leading to inappropriate fluid retention, vasoconstriction, and ultimately a further decline in left ventricular function. ARBs have been shown to have a protective effect on the heart by improving cardiac function, reducing afterload, increasing cardiac output and preventing ventricular hypertrophy and remodelling.⁵

By comparison, the angiotensin-converting enzyme inhibitor (ACEI) class of medications (which includes drugs such as ramipril, lisinopril, and perindopril) inhibit the conversion of angiotensin I to angiotensin II through inhibition of the ACE enzyme. However, this does not prevent the formation of all angiotensin II within the body. The angiotensin II receptor blocker (ARB) family of drugs unique in that it blocks all angiotensin II activity, regardless of where or how it was synthesized.

Valsartan is commonly used for the management of hypertension, heart failure, and Type 2 Diabetes-associated nephropathy, particularly in patients who are unable to tolerate ACE inhibitors. ARBs such as valsartan have been shown in a number of large-scale clinical outcomes trials to improve cardiovascular outcomes including reducing risk of myocardial infarction, stroke, the progression of heart failure, and hospitalization.^{1,9,10,11,12,13,14,15} Valsartan also slows the progression of diabetic nephropathy due to its renoprotective effects.^6,7,8 Improvements in chronic kidney disease with valsartan include both clinically and statistically significant decreases in urinary albumin and protein excretion in patients diagnosed with type 2 diabetes and in nondiabetic patients diagnosed with chronic kidney disease.^1,10

Valsartan was initially approved in 1996 in Europe for the treatment of hypertension in adults. Shortly after, in 1997, this drug was approved in the United States.¹ Valsartan is generally well-tolerated with a side-effect profile superior to that of other antihypertensive drugs.^3,4

Type

Small Molecule

Groups

Approved, Investigational

Structure

Similar Structures

Weight: Average: 435.5188
Monoisotopic: 435.227039819
Chemical Formula: C₂₄H₂₉N₅O₃

Synonyms

(S)-N-Valeryl-N-{[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]-methyl}-valine
N-(P-(O-1H-Tetrazol-5-ylphenyl)benzyl)-N-valeryl-L-valine
N-pentanoyl-N-{[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]methyl}-L-valine
Valsartan

External IDs

CGP 48933
CGP-48933

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Pharmacology

Indication

Valsartan is indicated for the treatment of hypertension to reduce the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions. It is also indicated for the treatment of heart failure (NYHA class II-IV) and for left ventricular dysfunction or failure after myocardial infarction when the use of an angiotensin-converting enzyme inhibitor (ACEI) is not appropriate.^29,18

It is also used in combination with sacubitril.²¹

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Associated Conditions

Indication Type	Indication	Combined Product Details	Approval Level	Age Group	Patient Characteristics
Used in combination to prevent	Cardiovascular death	Combination Product in combination with: Sacubitril (DB09292)	••••••••••••	•••••	••••••• ••••• ••••••• •••• ••••••• •••••••• •••••••• ••••• ••••• ••••••
Prevention of	Cardiovascular mortality		••••••••••••	•••••	•••• ••••••••••• •••••••••••• •••• ••••••••••• •••••••• •••••••••••
Management of	Diabetic nephropathy		••• •••••		•••• • •••••••• ••••••••
Used in combination to treat	Heart failure	Combination Product in combination with: Sacubitril (DB09292)	••••••••••••	•••••••••
Used in combination to treat	High blood pressure (hypertension)	Combination Product in combination with: Aliskiren (DB09026)	••••••••••••

Contraindications & Blackbox Warnings

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Pharmacodynamics

Valsartan inhibits the pressor effects of angiotensin II with oral doses of 80 mg inhibiting the pressor effect by about 80% at peak with approximately 30% inhibition persisting for 24 hours. Removal of the negative feedback of angiotensin II causes a 2- to 3-fold rise in plasma renin and consequent rise in angiotensin II plasma concentration in hypertensive patients. Minimal decreases in plasma aldosterone were observed after administration of valsartan.

In multiple-dose studies in hypertensive patients, valsartan had no notable effects on total cholesterol, fasting triglycerides, fasting serum glucose, or uric acid.¹⁸

Hypotension

Excessive hypotension was rarely seen (0.1%) in patients with uncomplicated hypertension treated with valsartan alone. In patients with an activated renin-angiotensin system, such as volume- and/or salt-depleted patients receiving high doses of diuretics, symptomatic hypotension may occur. This condition should be corrected prior to administration of valsartan, or the treatment should start under close medical supervision.

Caution should be observed when initiating therapy in patients with heart failure. Patients with heart failure given valsartan commonly have some reduction in blood pressure, but discontinuation of therapy because of continuing symptomatic hypotension usually is not necessary when dosing instructions are followed. In controlled trials in heart failure patients, the incidence of hypotension in valsartan-treated patients was 5.5% compared to 1.8% in placebo-treated patients.

If excessive hypotension occurs, the patient should be placed in the supine position and, if necessary, given an intravenous infusion of normal saline. A transient hypotensive response is not a contraindication to further treatment, which usually can be continued without difficulty once the blood pressure has stabilized.¹⁸

Impaired Renal Function

Changes in renal function including acute renal failure can be caused by drugs that inhibit the renin-angiotensin system and by diuretics. Patients whose renal function may depend in part on the activity of the renin-angiotensin system (e.g., patients with renal artery stenosis, chronic kidney disease, severe congestive heart failure, or volume depletion) may be at particular risk of developing acute renal failure on valsartan. Monitor renal function periodically in these patients. Consider withholding or discontinuing therapy in patients who develop a clinically significant decrease in renal function on valsartan.¹⁸

Hyperkalemia

Some patients with heart failure have developed increases in potassium. These effects are usually minor and transient, and they are more likely to occur in patients with pre-existing renal impairment. Dosage reduction and/or discontinuation of valsartan may be required.¹⁸

Mechanism of action

Valsartan belongs to the angiotensin II receptor blocker (ARB) family of drugs, which selectively bind to angiotensin receptor 1 (AT1) and prevent angiotensin II from binding and exerting its hypertensive effects. These include vasoconstriction, stimulation and synthesis of aldosterone and ADH, cardiac stimulation, and renal reabsorption of sodium among others. Overall, valsartan's physiologic effects lead to reduced blood pressure, lower aldosterone levels, reduced cardiac activity, and increased excretion of sodium.

Valsartan also affects the renin-angiotensin aldosterone system (RAAS), which plays an important role in hemostasis and regulation of kidney, vascular, and cardiac functions. Pharmacological blockade of RAAS via AT1 receptor blockade inhibits negative regulatory feedback within RAAS which is a contributing factor to the pathogenesis and progression of cardiovascular disease, heart failure, and renal disease. In particular, heart failure is associated with chronic activation of RAAS, leading to inappropriate fluid retention, vasoconstriction, and ultimately a further decline in left ventricular function. ARBs have been shown to have a protective effect on the heart by improving cardiac function, reducing afterload, increasing cardiac output and prevent ventricular hypertrophy.⁵

The angiotensin-converting enzyme inhibitor (ACEI) class of medications (which includes drugs such as ramipril, lisinopril, and perindopril) inhibits the conversion of angiotensin I to angiotensin II by inhibiting the ACE enzyme but does not prevent the formation of all angiotensin II. ARB activity is unique in that it blocks all angiotensin II activity, regardless of where or how it was synthesized.

Valsartan is commonly used for the management of hypertension, heart failure, and type 2 diabetes-associated nephropathy, particularly in patients who are unable to tolerate ACE inhibitors. ARBs such as valsartan have been shown in a number of large-scale clinical outcomes trials to improve cardiovascular outcomes including reducing risk of myocardial infarction, stroke, the progression of heart failure, and hospitalization.^{1,9,10,11,12,13,14,15} Valsartan also slows the progression of diabetic nephropathy due to its renoprotective effects.^6,7,8 Improvements in chronic kidney disease with valsartan include both clinically and statistically significant decreases in urinary albumin and protein excretion in patients diagnosed with type 2 diabetes and in nondiabetic patients diagnosed with chronic kidney disease.^1,10

Valsartan also binds to the AT2 receptor, however AT2 is not known to be associated with cardiovascular homeostasis like AT1. Valsartan has about 20,000-fold higher affinity for the AT1 receptor than for the AT2 receptor. The increased plasma levels of angiotensin II following AT1 receptor blockade with valsartan may stimulate the unblocked AT2 receptor.¹⁸

Target	Actions	Organism
AType-1 angiotensin II receptor	antagonist	Humans

Absorption

After one oral dose, the antihypertensive activity of valsartan begins within approximately 2 hours and peaks within 4-6 hours in most patients.²⁴ Food decreases the exposure to orally administered valsartan by approximately 40% and peak plasma concentration by approximately 50%. AUC and Cmax values of valsartan generally increase linearly with increasing dose over the therapeutic dose range. Valsartan does not accumulate appreciably in plasma following repetitive administration.¹⁸

Volume of distribution

The steady-state volume of distribution of valsartan after intravenous administration is small (17 L), indicating that valsartan does not distribute into tissues extensively.²⁴

Protein binding

Valsartan is highly bound to serum proteins (95%), mainly serum albumin.¹⁸

Metabolism

Valsartan undergoes minimal liver metabolism and is not biotransformed to a high degree, as only approximately 20% of a single dose is recovered as metabolites.^1,24 The primary metabolite, accounting for about 9% of dose, is valeryl 4-hydroxy valsartan. In vitro metabolism studies involving recombinant CYP 450 enzymes indicated that the CYP 2C9 isoenzyme is responsible for the formation of valeryl-4-hydroxy valsartan. Valsartan does not inhibit CYP 450 isozymes at clinically relevant concentrations. CYP 450 mediated drug interaction between valsartan and coadministered drugs are unlikely because of the low extent of metabolism.¹⁸

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Valsartan
- Valeryl-4-hydroxyvalsartan

Route of elimination

Valsartan, when administered as an oral solution, is primarily recovered in feces (about 83% of dose) and urine (about 13% of dose). The recovery is mainly as unchanged drug, with only about 20% of dose recovered as metabolites.¹⁸

Half-life

After intravenous (IV) administration, valsartan demonstrates bi-exponential decay kinetics, with an average elimination half-life of about 6 hours.¹⁸

Clearance

Following intravenous administration, plasma clearance of valsartan is approximately 2 L/hour and its renal clearance is 0.62 L/hour (about 30% of total clearance).¹⁸

Adverse Effects

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Toxicity

Approximate LD50 >2000 mg/kg (Gavage, rat) ²⁴

Reproductive Toxicology Studies

No teratogenic effects were seen when valsartan was given to pregnant mice and rats at oral doses up to 600 mg/kg/day and to pregnant rabbits at oral doses reaching up to 10 mg/kg/day. Despite this, marked decreases in fetal weight, pup birth weight, pup survival rate, and delays in developmental milestones were noted in studies in which parental rats were treated with valsartan at oral, maternally toxic doses of 600 mg/kg/day during the organogenesis period or during late gestation and lactation.¹⁸

Pregnancy

When used in pregnancy, drugs that act directly on the renin-angiotensin system (RAAS) can cause injury and death to the developing fetus. When pregnancy is detected, valsartan should be discontinued as soon as possible.¹⁸

Pathways

Pathway	Category
Valsartan Action Pathway	Drug action

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Not Available

Interactions

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This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.

Drug	Interaction
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Abaloparatide	The risk or severity of adverse effects can be increased when Valsartan is combined with Abaloparatide.
Abatacept	The metabolism of Valsartan can be increased when combined with Abatacept.
Abrocitinib	The metabolism of Abrocitinib can be decreased when combined with Valsartan.
Acebutolol	Valsartan may increase the hypotensive activities of Acebutolol.
Aceclofenac	The risk or severity of renal failure, hyperkalemia, and hypertension can be increased when Valsartan is combined with Aceclofenac.

Food Interactions

Take with or without food. Co-administration with food slightly alters pharmacokinetics, but not to a clinically significant extent.

Products

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Product Images

Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End
Act Valsartan	Tablet	320 mg	Oral	Actavis Pharma Company	2011-02-16	2019-08-14
Act Valsartan	Tablet	40 mg	Oral	Actavis Pharma Company	2011-02-16	2019-08-14
Act Valsartan	Tablet	160 mg	Oral	Actavis Pharma Company	2011-02-16	2019-08-14
Act Valsartan	Tablet	80 mg	Oral	Actavis Pharma Company	2011-02-16	2019-08-14
Diovan	Tablet	80 mg/1	Oral	Aphena Pharma Solutions Tennessee, Inc.	2001-07-01	Not applicable

Generic Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End
Apo-valsartan	Tablet	40 mg	Oral	Apotex Corporation	2012-07-12	Not applicable
Apo-valsartan	Tablet	160 mg	Oral	Apotex Corporation	2012-07-12	Not applicable
Apo-valsartan	Tablet	80 mg	Oral	Apotex Corporation	2012-07-12	Not applicable
Apo-valsartan	Tablet	320 mg	Oral	Apotex Corporation	2012-07-12	Not applicable
Auro-valsartan	Tablet	40 mg	Oral	Auro Pharma Inc	2014-02-06	Not applicable

Mixture Products

Name	Ingredients	Dosage	Route	Labeller	Marketing Start	Marketing End
ALENCAL VALS 2.5/160MG TABLETAS RECUBIERTAS	Valsartan (160 mg) + Levamlodipine (2.5 mg)	Tablet, coated	Oral	CLARIPACK S.A.	2015-01-23	2020-08-05
ALENCAL VALS 2.5/320 MG TABLETAS RECUBIERTAS	Valsartan (320 mg) + Levamlodipine (2.5 mg)	Tablet, coated	Oral	COLOMPACK S.A.	2017-03-16	Not applicable
AMLO VALSACOR 10/160MG FTA	Valsartan (160 mg) + Amlodipine (10 mg)	Tablet, film coated	Oral		2018-10-01	Not applicable
AMLO VALSACOR 10/160MG FTA	Valsartan (160 mg) + Amlodipine (10 mg)	Tablet, film coated	Oral		2018-10-01	Not applicable
AMLO VALSACOR 10/160MG FTA	Valsartan (160 mg) + Amlodipine (10 mg)	Tablet, film coated	Oral		2018-10-01	Not applicable

Chemical Identifiers

UNII: 80M03YXJ7I
CAS number: 137862-53-4
InChI Key: ACWBQPMHZXGDFX-QFIPXVFZSA-N
InChI: InChI=1S/C24H29N5O3/c1-4-5-10-21(30)29(22(16(2)3)24(31)32)15-17-11-13-18(14-12-17)19-8-6-7-9-20(19)23-25-27-28-26-23/h6-9,11-14,16,22H,4-5,10,15H2,1-3H3,(H,31,32)(H,25,26,27,28)/t22-/m0/s1
IUPAC Name: (2S)-3-methyl-2-(N-{[2'-(2H-1,2,3,4-tetrazol-5-yl)-[1,1'-biphenyl]-4-yl]methyl}pentanamido)butanoic acid
SMILES: CCCCC(=O)N(CC1=CC=C(C=C1)C1=CC=CC=C1C1=NNN=N1)[C@@H](C(C)C)C(O)=O

References

Synthesis Reference

Zvi Harel, Igor Rukhman, "Process for the preparation of valsartan." U.S. Patent US20050010053, issued January 13, 2005.

US20050010053

General References

Black HR, Bailey J, Zappe D, Samuel R: Valsartan: more than a decade of experience. Drugs. 2009;69(17):2393-414. doi: 10.2165/11319460-000000000-00000. [Article]
Fogari R, Zoppi A: A drug safety evaluation of valsartan. Expert Opin Drug Saf. 2011 Mar;10(2):295-303. doi: 10.1517/14740338.2011.543416. Epub 2010 Dec 11. [Article]
McInnes GT: Clinical advantage of valsartan. Cardiology. 1999;91 Suppl 1:14-8. doi: 10.1159/000047283. [Article]
Chiolero A, Burnier M: Pharmacology of valsartan, an angiotensin II receptor antagonist. Expert Opin Investig Drugs. 1998 Nov;7(11):1915-25. doi: 10.1517/13543784.7.11.1915 . [Article]
Akazawa H, Yabumoto C, Yano M, Kudo-Sakamoto Y, Komuro I: ARB and cardioprotection. Cardiovasc Drugs Ther. 2013 Apr;27(2):155-60. doi: 10.1007/s10557-012-6392-2. [Article]
Zhou G, Cheung AK, Liu X, Huang Y: Valsartan slows the progression of diabetic nephropathy in db/db mice via a reduction in podocyte injury, and renal oxidative stress and inflammation. Clin Sci (Lond). 2014 May;126(10):707-20. doi: 10.1042/CS20130223. [Article]
Suzuki K, Souda S, Ikarashi T, Kaneko S, Nakagawa O, Aizawa Y: Renoprotective effects of low-dose valsartan in type 2 diabetic patients with diabetic nephropathy. Diabetes Res Clin Pract. 2002 Sep;57(3):179-83. [Article]
Currie G, Bethel MA, Holzhauer B, Haffner SM, Holman RR, McMurray JJV: Effect of valsartan on kidney outcomes in people with impaired glucose tolerance. Diabetes Obes Metab. 2017 Jun;19(6):791-799. doi: 10.1111/dom.12877. Epub 2017 Mar 17. [Article]
Ezekowitz JA, O'Meara E, McDonald MA, Abrams H, Chan M, Ducharme A, Giannetti N, Grzeslo A, Hamilton PG, Heckman GA, Howlett JG, Koshman SL, Lepage S, McKelvie RS, Moe GW, Rajda M, Swiggum E, Virani SA, Zieroth S, Al-Hesayen A, Cohen-Solal A, D'Astous M, De S, Estrella-Holder E, Fremes S, Green L, Haddad H, Harkness K, Hernandez AF, Kouz S, LeBlanc MH, Masoudi FA, Ross HJ, Roussin A, Sussex B: 2017 Comprehensive Update of the Canadian Cardiovascular Society Guidelines for the Management of Heart Failure. Can J Cardiol. 2017 Nov;33(11):1342-1433. doi: 10.1016/j.cjca.2017.08.022. Epub 2017 Sep 6. [Article]
Leung AA, Daskalopoulou SS, Dasgupta K, McBrien K, Butalia S, Zarnke KB, Nerenberg K, Harris KC, Nakhla M, Cloutier L, Gelfer M, Lamarre-Cliche M, Milot A, Bolli P, Tremblay G, McLean D, Tran KC, Tobe SW, Ruzicka M, Burns KD, Vallee M, Prasad GVR, Gryn SE, Feldman RD, Selby P, Pipe A, Schiffrin EL, McFarlane PA, Oh P, Hegele RA, Khara M, Wilson TW, Penner SB, Burgess E, Sivapalan P, Herman RJ, Bacon SL, Rabkin SW, Gilbert RE, Campbell TS, Grover S, Honos G, Lindsay P, Hill MD, Coutts SB, Gubitz G, Campbell NRC, Moe GW, Howlett JG, Boulanger JM, Prebtani A, Kline G, Leiter LA, Jones C, Cote AM, Woo V, Kaczorowski J, Trudeau L, Tsuyuki RT, Hiremath S, Drouin D, Lavoie KL, Hamet P, Gregoire JC, Lewanczuk R, Dresser GK, Sharma M, Reid D, Lear SA, Moullec G, Gupta M, Magee LA, Logan AG, Dionne J, Fournier A, Benoit G, Feber J, Poirier L, Padwal RS, Rabi DM: Hypertension Canada's 2017 Guidelines for Diagnosis, Risk Assessment, Prevention, and Treatment of Hypertension in Adults. Can J Cardiol. 2017 May;33(5):557-576. doi: 10.1016/j.cjca.2017.03.005. Epub 2017 Mar 10. [Article]
Lee VC, Rhew DC, Dylan M, Badamgarav E, Braunstein GD, Weingarten SR: Meta-analysis: angiotensin-receptor blockers in chronic heart failure and high-risk acute myocardial infarction. Ann Intern Med. 2004 Nov 2;141(9):693-704. doi: 10.7326/0003-4819-141-9-200411020-00011. [Article]
Brenner BM, Cooper ME, de Zeeuw D, Keane WF, Mitch WE, Parving HH, Remuzzi G, Snapinn SM, Zhang Z, Shahinfar S: Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med. 2001 Sep 20;345(12):861-9. doi: 10.1056/NEJMoa011161. [Article]
Yusuf S, Teo KK, Pogue J, Dyal L, Copland I, Schumacher H, Dagenais G, Sleight P, Anderson C: Telmisartan, ramipril, or both in patients at high risk for vascular events. N Engl J Med. 2008 Apr 10;358(15):1547-59. doi: 10.1056/NEJMoa0801317. Epub 2008 Mar 31. [Article]
Pfeffer MA, McMurray JJ, Velazquez EJ, Rouleau JL, Kober L, Maggioni AP, Solomon SD, Swedberg K, Van de Werf F, White H, Leimberger JD, Henis M, Edwards S, Zelenkofske S, Sellers MA, Califf RM: Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both. N Engl J Med. 2003 Nov 13;349(20):1893-906. doi: 10.1056/NEJMoa032292. Epub 2003 Nov 10. [Article]
O'Gara PT, Kushner FG, Ascheim DD, Casey DE Jr, Chung MK, de Lemos JA, Ettinger SM, Fang JC, Fesmire FM, Franklin BA, Granger CB, Krumholz HM, Linderbaum JA, Morrow DA, Newby LK, Ornato JP, Ou N, Radford MJ, Tamis-Holland JE, Tommaso CL, Tracy CM, Woo YJ, Zhao DX: 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013 Jan 29;61(4):e78-e140. doi: 10.1016/j.jacc.2012.11.019. Epub 2012 Dec 17. [Article]
Nakashima A, Kawashita H, Masuda N, Saxer C, Niina M, Nagae Y, Iwasaki K: Identification of cytochrome P450 forms involved in the 4-hydroxylation of valsartan, a potent and specific angiotensin II receptor antagonist, in human liver microsomes. Xenobiotica. 2005 Jun;35(6):589-602. [Article]
Bader, M. (2004). Renin-angiotensin-aldosterone system. In Encyclopedic reference of molecular pharmacology (pp. 810-814). Berlin: Springer. [ISBN:9783540298328]
FDA Approved Drug Products: Diovan (valsartan) oral tablets [Link]
FDA Approved Drug Products: EXFORGE (amlodipine and valsartan) tablets [Link]
FDA Approved Drug Products: DIOVAN HCT (valsartan and hydrochlorothiazide) tablets [Link]
FDA Approved Drug Products: ENTRESTO (sacubitril and valsartan) tablets [Link]
FDA Approved Drug Products: EXFORGE HCT (amlodipine, valsartan, and hydrochlorothiazide) tablets [Link]
FDA Approved Drug Products: Valturna (aliskiren and valsartan) tablets [Link]
Health Canada Product Monograph: Valsartan-HCTZ (valsartan/hydrochlorothiazide) tablets for oral use [Link]
NZ Data Sheet, Valsartan and sacubitril [File]
Valsartan and Sacubitril FDA label [File]
Valsartan and Amlodipine FDA label [File]
Valsartan and Nevibolol FDA label [File]
Health Canada Monograph - Valsartan [File]

External Links

Human Metabolome Database: HMDB0014323
KEGG Drug: D00400
PubChem Compound: 60846
PubChem Substance: 46509000
ChemSpider: 54833
BindingDB: 50049186
RxNav: 69749
ChEBI: 9927
ChEMBL: CHEMBL1069
ZINC: ZINC000003875259
Therapeutic Targets Database: DAP000363
PharmGKB: PA451848
Guide to Pharmacology: GtP Drug Page
PDBe Ligand: U35
RxList: RxList Drug Page
Drugs.com: Drugs.com Drug Page
Wikipedia: Valsartan

PDB Entries

7bm1 / 8dqt / 8egu

MSDS

Download (24 KB)

Clinical Trials

Clinical Trials Learn More" title="About Clinical Trials" id="clinical-trials-info" class="drug-info-popup" href="javascript:void(0);">

Phase	Status	Purpose	Conditions	Count
4	Active Not Recruiting	Basic Science	Hypertension	1
4	Active Not Recruiting	Prevention	Blood Pressures / Impaired Glucose Tolerance / Obesity	1
4	Active Not Recruiting	Treatment	Chagas Disease / Heart Failure	1
4	Active Not Recruiting	Treatment	Heart Failure	1
4	Completed	Basic Science	Type 2 Diabetes Mellitus	1

Pharmacoeconomics

Manufacturers

Novartis pharmaceuticals corp
Novartis Corporation

Packagers

Advanced Pharmaceutical Services Inc.
AQ Pharmaceuticals Inc.
A-S Medication Solutions LLC
Bryant Ranch Prepack
Cardinal Health
Dispensing Solutions
Diversified Healthcare Services Inc.
Doctor Reddys Laboratories Ltd.
Heartland Repack Services LLC
Lake Erie Medical and Surgical Supply
Murfreesboro Pharmaceutical Nursing Supply
Novartis AG
Nucare Pharmaceuticals Inc.
PD-Rx Pharmaceuticals Inc.
Physicians Total Care Inc.
Prepackage Specialists
Prepak Systems Inc.
Promex Medical Inc.
Resource Optimization and Innovation LLC
Southwood Pharmaceuticals
Stat Rx Usa
Vangard Labs Inc.

Dosage Forms

Form	Route	Strength
Tablet, film coated	Oral	12.5 mg
Tablet, coated	Oral
Capsule	Oral	160 mg/1
Capsule	Oral	80 mg/1
Tablet	Oral	160 mg/1
Tablet	Oral	320 mg
Tablet	Oral	320 mg/1
Tablet	Oral	40 mg
Tablet	Oral	40 mg/1
Tablet	Oral	80 mg/1
Tablet, film coated	Oral
Capsule	Oral	160 mg
Tablet	Oral	160 mg
Solution	Oral
Tablet, coated	Oral	320 mg
Tablet, coated	Oral	40 mg
Capsule	Oral	80 mg
Tablet	Oral	80 mg
Tablet, film coated	Oral
Tablet, film coated	Oral	40.00 mg
Tablet, delayed release	Oral	320 mg
Tablet, delayed release	Oral	100 mg
Tablet, film coated	Oral	200 mg
Tablet, film coated	Oral	50 mg
Tablet, film coated	Oral	10.00 mg
Tablet, film coated	Oral	5.00 mg
Tablet, film coated	Oral	160.00 mg
Tablet	Oral	80.000 mg
Tablet	Oral	160.000 mg
Tablet, coated	Oral	100 mg
Tablet, coated	Oral	200 mg
Tablet, coated	Oral	50 mg
Tablet	Oral	40.00 mg
Solution	Oral	4 mg/1mL
Capsule	Oral
Tablet, film coated	Oral	40 MG
Tablet, film coated	Oral	80.00 mg
Solution	Oral	3 MG/ML
Tablet, coated	Oral	8000000 mg
Tablet, coated	Oral	5 mg
Tablet, coated	Oral	160 mg/1
Tablet, coated	Oral	320 mg/1
Tablet, coated	Oral	40 mg/1
Tablet, coated	Oral	80 mg/1
Tablet, film coated	Oral	160 mg/1
Tablet, film coated	Oral	320 mg/1
Tablet, film coated	Oral	40 mg/1
Tablet, film coated	Oral	80 mg/1
Capsule, coated	Oral	160 mg
Tablet, film coated	Oral	120 MG
Tablet	Oral
Capsule	Oral	40 MG
Tablet	Oral
Capsule, coated	Oral
Capsule, coated	Oral	80 mg
Tablet	Oral	160.000 mg
Capsule, coated	Oral	40 mg
Tablet	Oral	80.00 mg
Capsule, liquid filled	Oral	160 mg
Capsule, liquid filled	Oral	80 mg
Capsule, liquid filled	Oral
Tablet	Oral	40.000 mg
Tablet, film coated	Oral	320 mg
Tablet, film coated	Oral	80 mg
Tablet, coated	Oral	160 mg
Tablet, coated	Oral	80 mg
Tablet, film coated	Oral	160 mg

Prices

Unit description	Cost	Unit
Diovan hct 320-25 mg tablet	4.63USD	tablet
Diovan hct 320-12.5 mg tablet	4.1USD	tablet
Diovan hct 160-25 mg tablet	3.66USD	tablet
Diovan hct 160-12.5 mg tablet	3.27USD	tablet
Diovan 320 mg tablet	3.17USD	tablet
Diovan hct 80-12.5 mg tablet	3.0USD	tablet
Diovan 160 mg tablet	2.42USD	tablet
Diovan 80 mg tablet	2.33USD	tablet
Diovan 40 mg tablet	2.32USD	tablet

DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)
US5399578	No	1995-03-21	2012-03-21
CA2259148	No	2009-09-29	2017-06-18
CA2036427	No	1998-12-29	2011-02-15
US6294197	Yes	2001-09-25	2017-12-18
US5559111	Yes	1996-09-24	2019-01-21
US6395728	No	2002-05-28	2019-07-08
US5972990	Yes	1999-10-26	2017-04-26
US8168616	No	2012-05-01	2026-07-03
US8101599	No	2012-01-24	2023-05-16
US8475839	Yes	2013-07-02	2023-11-16
US8796331	Yes	2014-08-05	2023-07-14
US8101659	Yes	2012-01-24	2023-07-14
US7468390	Yes	2008-12-23	2024-05-27
US8404744	Yes	2013-03-26	2023-07-14
US8877938	Yes	2014-11-04	2027-11-27
US7803838	No	2010-09-28	2026-08-29
US7838552	No	2010-11-23	2027-10-04
US9388134	Yes	2016-07-12	2027-05-08
US9517226	No	2016-12-13	2033-08-22
US9937143	No	2018-04-10	2033-08-22
US11058667	No	2021-07-13	2036-05-09
US11135192	No	2021-10-05	2033-08-22

Properties

State

Solid

Experimental Properties

Property	Value	Source
melting point (°C)	116-117 °C	https://www.chemicalbook.com/ChemicalProductProperty_US_CB6182539.aspx
boiling point (°C)	83-88	https://www.trc-canada.com/product-detail/?V095750
water solubility	soluble in ethanol, DMSO, and dimethyl formamide at 30 mg/mL	https://www.caymanchem.com/pdfs/14178.pdf
logP	1.499	http://www.japsonline.com/admin/php/uploads/54_pdf.pdf
pKa	4.73	http://www.japsonline.com/admin/php/uploads/54_pdf.pdf

Predicted Properties

Property	Value	Source
Water Solubility	0.0234 mg/mL	ALOGPS
logP	3.68	ALOGPS
logP	5.27	Chemaxon
logS	-4.3	ALOGPS
pKa (Strongest Acidic)	4.35	Chemaxon
pKa (Strongest Basic)	-0.64	Chemaxon
Physiological Charge	-2	Chemaxon
Hydrogen Acceptor Count	6	Chemaxon
Hydrogen Donor Count	2	Chemaxon
Polar Surface Area	112.07 Å²	Chemaxon
Rotatable Bond Count	10	Chemaxon
Refractivity	134.77 m³·mol^-1	Chemaxon
Polarizability	47.27 Å³	Chemaxon
Number of Rings	3	Chemaxon
Bioavailability	1	Chemaxon
Rule of Five	No	Chemaxon
Ghose Filter	No	Chemaxon
Veber's Rule	No	Chemaxon
MDDR-like Rule	Yes	Chemaxon

Predicted ADMET Features

Property	Value	Probability
Human Intestinal Absorption	+	0.9956
Blood Brain Barrier	-	0.8032
Caco-2 permeable	-	0.6912
P-glycoprotein substrate	Substrate	0.685
P-glycoprotein inhibitor I	Non-inhibitor	0.5548
P-glycoprotein inhibitor II	Non-inhibitor	0.5966
Renal organic cation transporter	Non-inhibitor	0.8646
CYP450 2C9 substrate	Non-substrate	0.7722
CYP450 2D6 substrate	Non-substrate	0.9116
CYP450 3A4 substrate	Non-substrate	0.5073
CYP450 1A2 substrate	Non-inhibitor	0.8707
CYP450 2C9 inhibitor	Non-inhibitor	0.5398
CYP450 2D6 inhibitor	Non-inhibitor	0.8816
CYP450 2C19 inhibitor	Inhibitor	0.5539
CYP450 3A4 inhibitor	Non-inhibitor	0.5521
CYP450 inhibitory promiscuity	High CYP Inhibitory Promiscuity	0.5618
Ames test	Non AMES toxic	0.6384
Carcinogenicity	Non-carcinogens	0.645
Biodegradation	Not ready biodegradable	1.0
Rat acute toxicity	2.6518 LD50, mol/kg	Not applicable
hERG inhibition (predictor I)	Weak inhibitor	0.9766
hERG inhibition (predictor II)	Non-inhibitor	0.7388

ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Spectra

Mass Spec (NIST)

Not Available

Spectra

Spectrum	Spectrum Type	Splash Key
Predicted GC-MS Spectrum - GC-MS	Predicted GC-MS	splash10-000i-3094000000-1a2b93c2e5e760118ffd
LC-MS/MS Spectrum - LC-ESI-qTof , Positive	LC-MS/MS	splash10-0a4i-0122900000-e2d5ae1b4433254a8ebe
LC-MS/MS Spectrum - LC-ESI-qTof , Positive	LC-MS/MS	splash10-0a4u-1492000000-bc19c44b1bd382b3180f
LC-MS/MS Spectrum - LC-ESI-QTOF , negative	LC-MS/MS	splash10-001i-0000900000-45397dbc5403f1111d85
LC-MS/MS Spectrum - LC-ESI-QTOF , negative	LC-MS/MS	splash10-003r-0303900000-1056988fef13dc9becc8
LC-MS/MS Spectrum - LC-ESI-QTOF , negative	LC-MS/MS	splash10-004i-0900000000-65d8dfbf9280fcea77fb
LC-MS/MS Spectrum - LC-ESI-QTOF , negative	LC-MS/MS	splash10-004i-0900000000-77a9588a3e936c9d2e28
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0udi-0009000000-160f82ad0952fc9b3350
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-001i-0000900000-d7bf9d8976f47e44ab4a
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0fb9-0915000000-1f5a4e134cd8450810e7
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-004i-0900000000-19095db3835430e9fe16
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-004i-0900000000-00e9b9924b37c4db7a8d
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-004i-0900000000-fb8741bb91ee87d8245e
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-001i-0000900000-be5ab1c8cde8851235e3
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0fb9-0915000000-08501c181e1066f2aa0a
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-004i-0900000000-6cabcfa5948837eddb2e
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-004i-0900000000-d0aedd0bab06b374571a
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-004i-0901000000-a4572421f0a393f299a1
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0udi-0009000000-0f743f9e78dce83f2414
LC-MS/MS Spectrum - LC-ESI-QFT , negative	LC-MS/MS	splash10-003r-0912600000-feeef5a05d8ef569460d
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-000i-0022900000-07c84eac301d580a8bea
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0a4u-0190000000-8a48f701b19b54e7ebf9
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0a4u-0190000000-34257438319cae238dcb
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0a4i-0590000000-403ef14fce06289de8e7
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0a59-0960000000-d4e79af5b474f613f6e9
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-052u-0093000000-ee050d1727838e542ce7
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-066r-0013900000-27f31e9591de9c0d036b
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0a4u-0096600000-2c9e5fef1cb7e2e64e67
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0a4u-0091000000-0bff344a92ee0cc41b8f
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0a4i-0390000000-fa2f74ef15c1a6b93838
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0a59-0960000000-ca847cc390cd0e68c6b6
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0pec-0920000000-5c29e64b37c8cde1c7ba
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0ziu-0910000000-08f3eecf83a71f4fb485
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0a4u-0096600000-598ea56da3433ecd4bab
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0a4u-0091000000-0aaf7a6567cb3745cb23
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0a4i-0490000000-4b8d8ce6d0a486599b71
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0a59-0950000000-6cd1be141d3f05844a75
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0pec-0920000000-053a50818908a33699b3
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0ziu-0910000000-c10b0879c877503826c5
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-066r-0013900000-af025bf00303b40b6d48
MS/MS Spectrum - , positive	LC-MS/MS	splash10-0a4i-0122900000-e2d5ae1b4433254a8ebe
MS/MS Spectrum - , positive	LC-MS/MS	splash10-0a4u-1492000000-bc19c44b1bd382b3180f
MS/MS Spectrum - , positive	LC-MS/MS	splash10-0a4i-0012900000-1b87098801f65211057a
MS/MS Spectrum - , positive	LC-MS/MS	splash10-0a4u-0392000000-5823d4f7c41e4fd6208b
LC-MS/MS Spectrum - LC-ESI-QFT , positive	LC-MS/MS	splash10-0a4u-0391100000-8997765a9ed3c9424c07
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	splash10-000i-0023900000-1dae1ce9ac868fdcade9
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	splash10-001i-9215700000-815ee4d14af5206c0bc4
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	splash10-052r-0194300000-c2aa9fc85c2c4cbb2bf8
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0f89-2279100000-5beb7025f951a3aad1c4
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0a4r-1192100000-fa11726b318fb267d297
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0002-4290000000-86b7e66cc4c3d641a5fc
Predicted 1H NMR Spectrum	1D NMR	Not Applicable
Predicted 13C NMR Spectrum	1D NMR	Not Applicable

Chromatographic Properties

Collision Cross Sections (CCS)

Adduct	CCS Value (Å²)	Source type	Source
[M-H]-	228.4427286	predicted	DarkChem Lite v0.1.0
[M-H]-	202.3463	predicted	DeepCCS 1.0 (2019)
[M+H]+	228.1296286	predicted	DarkChem Lite v0.1.0
[M+H]+	204.74187	predicted	DeepCCS 1.0 (2019)
[M+Na]+	229.2696286	predicted	DarkChem Lite v0.1.0
[M+Na]+	211.3199	predicted	DeepCCS 1.0 (2019)

Targets

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Property	Measurement	pH	Temperature (°C)	References
Ki (nM)	4700	N/A	N/A	A27343

Details1. Type-1 angiotensin II receptor

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Antagonist

General Function: Protein heterodimerization activity
Specific Function: Receptor for angiotensin II. Mediates its action by association with G proteins that activate a phosphatidylinositol-calcium second messenger system.
Gene Name: AGTR1
Uniprot ID: P30556
Uniprot Name: Type-1 angiotensin II receptor
Molecular Weight: 41060.53 Da

References

Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [Article]
Azizi M, Menard J, Bissery A, Guyenne TT, Bura-Riviere A, Vaidyanathan S, Camisasca RP: Pharmacologic demonstration of the synergistic effects of a combination of the renin inhibitor aliskiren and the AT1 receptor antagonist valsartan on the angiotensin II-renin feedback interruption. J Am Soc Nephrol. 2004 Dec;15(12):3126-33. [Article]
Criscione L, de Gasparo M, Buhlmayer P, Whitebread S, Ramjoue HP, Wood J: Pharmacological profile of valsartan: a potent, orally active, nonpeptide antagonist of the angiotensin II AT1-receptor subtype. Br J Pharmacol. 1993 Oct;110(2):761-71. [Article]
Shargorodsky M, Leibovitz E, Lubimov L, Gavish D, Zimlichman R: Prolonged treatment with the AT1 receptor blocker, valsartan, increases small and large artery compliance in uncomplicated essential hypertension. Am J Hypertens. 2002 Dec;15(12):1087-91. [Article]
de Gasparo M, Whitebread S: Binding of valsartan to mammalian angiotensin AT1 receptors. Regul Pept. 1995 Nov 10;59(3):303-11. [Article]
Siragy HM, El-Kersh MA, De Gasparo M, Webb RL, Carey RM: Differences in AT2 -receptor stimulation between AT1 -receptor blockers valsartan and losartan quantified by renal interstitial fluid cGMP. J Hypertens. 2002 Jun;20(6):1157-63. [Article]
Ulutas Z, Ermis N, Ozhan O, Parlakpinar H, Vardi N, Ates B, Colak C: The Protective Effects of Compound 21 and Valsartan in Isoproterenol-Induced Myocardial Injury in Rats. Cardiovasc Toxicol. 2021 Jan;21(1):17-28. doi: 10.1007/s12012-020-09590-6. Epub 2020 Jul 9. [Article]
Stanfield, Cindy L.;Germann, William J. (2009). Principles of Human Physiology (3rd ed.). Benjamin-Cummings Publishing Company. [ISBN:978-0321556660]
Valsartan HCT monograph [File]

Enzymes

Details1. Cytochrome P450 2C9

Kind: Protein
Organism: Humans
Pharmacological action: Unknown
Actions: Substrate

General Function: Steroid hydroxylase activity
Specific Function: Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally un...
Gene Name: CYP2C9
Uniprot ID: P11712
Uniprot Name: Cytochrome P450 2C9
Molecular Weight: 55627.365 Da

References

Nakashima A, Kawashita H, Masuda N, Saxer C, Niina M, Nagae Y, Iwasaki K: Identification of cytochrome P450 forms involved in the 4-hydroxylation of valsartan, a potent and specific angiotensin II receptor antagonist, in human liver microsomes. Xenobiotica. 2005 Jun;35(6):589-602. [Article]
Kamiyama E, Yoshigae Y, Kasuya A, Takei M, Kurihara A, Ikeda T: Inhibitory effects of angiotensin receptor blockers on CYP2C9 activity in human liver microsomes. Drug Metab Pharmacokinet. 2007 Aug;22(4):267-75. [Article]
Cabaleiro T, Roman M, Ochoa D, Talegon M, Prieto-Perez R, Wojnicz A, Lopez-Rodriguez R, Novalbos J, Abad-Santos F: Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers. Drug Metab Dispos. 2013 Jan;41(1):224-9. doi: 10.1124/dmd.112.046292. Epub 2012 Nov 1. [Article]
Guo G, Zhao Y, Chai J, Hao D, Song F: Effectiveness evaluation of cardiovascular drugs based on CYP2C9 target protein. Pak J Pharm Sci. 2015 Jul;28(4 Suppl):1545-9. [Article]

Transporters

Details1. Solute carrier organic anion transporter family member 1B3

Kind: Protein
Organism: Humans
Pharmacological action: Unknown
Actions: Substrate

General Function: Sodium-independent organic anion transmembrane transporter activity
Specific Function: Mediates the Na(+)-independent uptake of organic anions such as 17-beta-glucuronosyl estradiol, taurocholate, triiodothyronine (T3), leukotriene C4, dehydroepiandrosterone sulfate (DHEAS), methotre...
Gene Name: SLCO1B3
Uniprot ID: Q9NPD5
Uniprot Name: Solute carrier organic anion transporter family member 1B3
Molecular Weight: 77402.175 Da

References

Poirier A, Cascais AC, Funk C, Lave T: Prediction of pharmacokinetic profile of valsartan in human based on in vitro uptake transport data. J Pharmacokinet Pharmacodyn. 2009 Dec;36(6):585-611. doi: 10.1007/s10928-009-9139-3. Epub 2009 Nov 20. [Article]
Poirier A, Cascais AC, Funk C, Lave T: Prediction of pharmacokinetic profile of valsartan in humans based on in vitro uptake-transport data. Chem Biodivers. 2009 Nov;6(11):1975-87. doi: 10.1002/cbdv.200900116. [Article]
Hanna I, Alexander N, Crouthamel MH, Davis J, Natrillo A, Tran P, Vapurcuyan A, Zhu B: Transport properties of valsartan, sacubitril and its active metabolite (LBQ657) as determinants of disposition. Xenobiotica. 2018 Mar;48(3):300-313. doi: 10.1080/00498254.2017.1295171. Epub 2017 Mar 10. [Article]
Alam K, Crowe A, Wang X, Zhang P, Ding K, Li L, Yue W: Regulation of Organic Anion Transporting Polypeptides (OATP) 1B1- and OATP1B3-Mediated Transport: An Updated Review in the Context of OATP-Mediated Drug-Drug Interactions. Int J Mol Sci. 2018 Mar 14;19(3). pii: ijms19030855. doi: 10.3390/ijms19030855. [Article]

Details2. Solute carrier organic anion transporter family member 1B1

Kind: Protein
Organism: Humans
Pharmacological action: Unknown
Actions: Substrate
Inhibitor

General Function: Sodium-independent organic anion transmembrane transporter activity
Specific Function: Mediates the Na(+)-independent uptake of organic anions such as pravastatin, taurocholate, methotrexate, dehydroepiandrosterone sulfate, 17-beta-glucuronosyl estradiol, estrone sulfate, prostagland...
Gene Name: SLCO1B1
Uniprot ID: Q9Y6L6
Uniprot Name: Solute carrier organic anion transporter family member 1B1
Molecular Weight: 76447.99 Da

References

Poirier A, Cascais AC, Funk C, Lave T: Prediction of pharmacokinetic profile of valsartan in human based on in vitro uptake transport data. J Pharmacokinet Pharmacodyn. 2009 Dec;36(6):585-611. doi: 10.1007/s10928-009-9139-3. Epub 2009 Nov 20. [Article]
Poirier A, Cascais AC, Funk C, Lave T: Prediction of pharmacokinetic profile of valsartan in humans based on in vitro uptake-transport data. Chem Biodivers. 2009 Nov;6(11):1975-87. doi: 10.1002/cbdv.200900116. [Article]
Karlgren M, Ahlin G, Bergstrom CA, Svensson R, Palm J, Artursson P: In vitro and in silico strategies to identify OATP1B1 inhibitors and predict clinical drug-drug interactions. Pharm Res. 2012 Feb;29(2):411-26. doi: 10.1007/s11095-011-0564-9. Epub 2011 Aug 23. [Article]
Alam K, Crowe A, Wang X, Zhang P, Ding K, Li L, Yue W: Regulation of Organic Anion Transporting Polypeptides (OATP) 1B1- and OATP1B3-Mediated Transport: An Updated Review in the Context of OATP-Mediated Drug-Drug Interactions. Int J Mol Sci. 2018 Mar 14;19(3). pii: ijms19030855. doi: 10.3390/ijms19030855. [Article]
Hanna I, Alexander N, Crouthamel MH, Davis J, Natrillo A, Tran P, Vapurcuyan A, Zhu B: Transport properties of valsartan, sacubitril and its active metabolite (LBQ657) as determinants of disposition. Xenobiotica. 2018 Mar;48(3):300-313. doi: 10.1080/00498254.2017.1295171. Epub 2017 Mar 10. [Article]
Valsartan Canadian Monograph [File]

Details3. Canalicular multispecific organic anion transporter 1

Kind: Protein
Organism: Humans
Pharmacological action: Unknown
Actions: Substrate

General Function: Organic anion transmembrane transporter activity
Specific Function: Mediates hepatobiliary excretion of numerous organic anions. May function as a cellular cisplatin transporter.
Gene Name: ABCC2
Uniprot ID: Q92887
Uniprot Name: Canalicular multispecific organic anion transporter 1
Molecular Weight: 174205.64 Da

References

Yamashiro W, Maeda K, Hirouchi M, Adachi Y, Hu Z, Sugiyama Y: Involvement of transporters in the hepatic uptake and biliary excretion of valsartan, a selective antagonist of the angiotensin II AT1-receptor, in humans. Drug Metab Dispos. 2006 Jul;34(7):1247-54. doi: 10.1124/dmd.105.008938. Epub 2006 Apr 19. [Article]
Hanna I, Alexander N, Crouthamel MH, Davis J, Natrillo A, Tran P, Vapurcuyan A, Zhu B: Transport properties of valsartan, sacubitril and its active metabolite (LBQ657) as determinants of disposition. Xenobiotica. 2018 Mar;48(3):300-313. doi: 10.1080/00498254.2017.1295171. Epub 2017 Mar 10. [Article]
Valsartan HCT Canadian Monograph [File]

Drug created at June 13, 2005 13:24 / Updated at February 20, 2024 23:55

Valsartan

Identification

Structure for Valsartan (DB00177)

Pharmacology

Interactions

Products

Categories

Chemical Identifiers

References

Clinical Trials

Pharmacoeconomics

Properties

Spectra

Collision Cross Sections (CCS)

Targets

References

Enzymes

References

Transporters

References

References

References