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| __NOTOC__ | | __NOTOC__ |
| {{Azilsartan kamedoxomil}}
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| '''''For patient information about Azilsartan kamedoxomil, click [[Azilsartan kamedoxomil (patient information)|here]].'''''
| | ===[[Azilsartan kamedoxomil|Azilsartan Kamedoxomil (Edarbi)]]=== |
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| {{SB}} EDARBI<sup>®</sup>
| | ===[[Azilsartan kamedoxomil and chlorthalidone|Azilsartan Kamedoxomil and Chlorthalidone (Edarbyclor)]]=== |
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| ==Overview== | | ==Overview== |
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| '''Azilsartan''' ([[International Nonproprietary Name|INN]], codenamed TAK-536) is an [[angiotensin II receptor antagonist]] used in the treatment of hypertension that was developed by [[Takeda Pharmaceutical Company|Takeda]].
| | Azilsartan is a selective AT1 subtype [[angiotensin]] II receptor antagonist used in treatment of [[hypertension]] to lower blood pressure. Common adverse reactions include [[hypotension]]/[[orthostatic hypotension]]. |
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| It is marketed in tablet form under the trade name '''Edarbi''' as the [[prodrug]] '''azilsartan medoxomil''' (INN, codenamed TAK-491). On 25 February 2011, the [[Food and Drug Administration (United States)|U.S. Food and Drug Administration]] (FDA) approved azilsartan medoxomil for the treatment of high blood pressure in adults.<ref>{{cite press release |url=http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm244722.htm |title=FDA approves Edarbi to treat high blood pressure | publisher = [[Food and Drug Administration (United States)|U.S. Food and Drug Administration]] (FDA) | date = February 25, 2011 |accessdate=2011-03-01}}</ref> On March 8, 2012, [[Health Canada]] approved the drug for mild to moderate essential hypertension. <ref>[http://www.hc-sc.gc.ca/dhp-mps/prodpharma/sbd-smd/drug-med/nd_ad_2012_edarbi_145305-eng.php Notice of Decision for EDARBI]</ref>
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| ==Category== | | ==Category== |
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| Category:Angiotensin II receptor antagonists;Benzimidazoles;Carbamates;Ethers;Cardiovascular Drugs
| | Angiotensin 2 Receptor Blocker |
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| ==FDA Package Insert==
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| ''' [[Azilsartan kamedoxomil indications and usage|Indications and Usage]]'''
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| '''| [[Azilsartan kamedoxomil dosage and administration|Dosage and Administration]]'''
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| '''| [[Azilsartan kamedoxomil dosage forms and strengths|Dosage Forms and Strengths]]'''
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| '''| [[Azilsartan kamedoxomil contraindications|Contraindications]]'''
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| '''| [[Azilsartan kamedoxomil warnings and precautions|Warnings and Precautions]]'''
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| '''| [[Azilsartan kamedoxomil adverse reactions|Adverse Reactions]]'''
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| '''| [[Azilsartan kamedoxomil drug interactions|Drug Interactions]]'''
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| '''| [[Azilsartan kamedoxomil use in specific populations|Use in Specific Populations]]'''
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| '''| [[Azilsartan kamedoxomil overdosage|Overdosage]]'''
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| '''| [[Azilsartan kamedoxomil description|Description]]'''
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| '''| [[Azilsartan kamedoxomil clinical pharmacology|Clinical Pharmacology]]'''
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| '''| [[Azilsartan kamedoxomil nonclinical toxicology|Nonclinical Toxicology]]'''
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| '''| [[Azilsartan kamedoxomil clinical studies|Clinical Studies]]'''
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| '''| [[Azilsartan kamedoxomil how supplied storage and handling|How Supplied/Storage and Handling]]'''
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| '''| [[Azilsartan kamedoxomil patient counseling information|Patient Counseling Information]]'''
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| '''| [[Azilsartan kamedoxomil labels and packages|Labels and Packages]]'''
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| ==Mechanism of Action==
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| Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzymes (ACE, kinase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Azilsartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in many tissues, such as vascular smooth muscle and the adrenal gland. Its action is, therefore, independent of the pathway for angiotensin II synthesis.
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| An AT2 receptor is also found in many tissues, but this receptor is not known to be associated with cardiovascular homeostasis. Azilsartan has more than a 10,000-fold greater affinity for the AT1 receptor than for the AT2 receptor.
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| Blockade of the renin-angiotensin system with ACE inhibitors, which inhibit the biosynthesis of angiotensin II from angiotensin I, is widely used in the treatment of hypertension. ACE inhibitors also inhibit the degradation of bradykinin, a reaction catalyzed by ACE. Because azilsartan does not inhibit ACE (kinase II), it should not affect bradykinin levels. Whether this difference has clinical relevance is not yet known. Azilsartan does not bind to or block other receptors or ion channels known to be important in cardiovascular regulation.
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| Blockade of the angiotensin II receptor inhibits the negative regulatory feedback of angiotensin II on renin secretion, but the resulting increased plasma renin activity and angiotensin II circulating levels do not overcome the effect of azilsartan on blood pressure.
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| ==References==
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| {{Reflist}}
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| [[Category:Angiotensin II receptor antagonists]]
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| [[Category:Benzimidazoles]]
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| [[Category:Carbamates]]
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| [[Category:Ethers]]
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| [[Category:Cardiovascular Drugs]]
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| [[Category:Drugs]]
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