Enalapril - Revision history

Alexander Berchansky at 13:03, 10 January 2024

Alexander Berchansky — Wed, 10 Jan 2024 13:03:32 GMT

←Older revision		Revision as of 13:03, 10 January 2024
Line 1:		Line 1:
-	<~~applet~~ load="" size=~~"430" color~~=~~"" frame="true" spin="on" Scene ="Enalapril/Enal/1" align="~~right" caption="Enalaprilat, the metabolite of Enalapril, also known as Vasotec"/>	+	<StructureSection load='' size='340' side='right' caption='Enalaprilat, the metabolite of Enalapril, also known as Vasotec' scene='Enalapril/Enal/1'>
	===Better Known as: Vasotec===		===Better Known as: Vasotec===
	* Marketed By: Merck & Co.<br />		* Marketed By: Merck & Co.<br />
Line 11:		Line 11:
	===Mechanism of Action===		===Mechanism of Action===
	Angiotensin II has been implicated in cardiac, renal and vascular diseases. <ref>PMID:17083068</ref> Bradykinin, a small peptide that counterbalance the effects of Angiotensin II by acting as a strong vasodilator upon binding AT2, is degraded by the same ACE-1 enzyme. Since ACE-1 is the primary producer of Angiotensin II and degrader of Bradykinins, inhibition of ACE-1 has proven an effective treatment for Hypertension and Congestive Heart Failure. Enalapril is quickly metabolized into Enalaprilat, the more active metabolite of Enalapril predominantly by the Hepatic enzyme CYP3A4. Enalaprilat binds to the active site of <scene name='Enalapril/Ace/1'>Angiotensin-Converting Enzyme</scene>, preventing ACE-1 from binding and converting Angiotensin I into Angiotensin II. <scene name='Enalapril/Enalalprilat/2'>Enalaprilat is bound </scene>to ACE-1 via electrostatic interactions with His 353, Ala 354 (Backbone oxygen), Glue 384, Lys 511, His 513, Tyr 520 and Tyr 523 along with the zinc cation. <ref>PMID:15236580</ref>		Angiotensin II has been implicated in cardiac, renal and vascular diseases. <ref>PMID:17083068</ref> Bradykinin, a small peptide that counterbalance the effects of Angiotensin II by acting as a strong vasodilator upon binding AT2, is degraded by the same ACE-1 enzyme. Since ACE-1 is the primary producer of Angiotensin II and degrader of Bradykinins, inhibition of ACE-1 has proven an effective treatment for Hypertension and Congestive Heart Failure. Enalapril is quickly metabolized into Enalaprilat, the more active metabolite of Enalapril predominantly by the Hepatic enzyme CYP3A4. Enalaprilat binds to the active site of <scene name='Enalapril/Ace/1'>Angiotensin-Converting Enzyme</scene>, preventing ACE-1 from binding and converting Angiotensin I into Angiotensin II. <scene name='Enalapril/Enalalprilat/2'>Enalaprilat is bound </scene>to ACE-1 via electrostatic interactions with His 353, Ala 354 (Backbone oxygen), Glue 384, Lys 511, His 513, Tyr 520 and Tyr 523 along with the zinc cation. <ref>PMID:15236580</ref>
-		+	</StructureSection>
	===Pharmacokinetics===		===Pharmacokinetics===
	<table style="background: cellspacing="0px" align="" cellpadding="0px" width="42%">		<table style="background: cellspacing="0px" align="" cellpadding="0px" width="42%">

David Canner at 09:17, 10 December 2010

David Canner — Fri, 10 Dec 2010 09:17:48 GMT

←Older revision		Revision as of 09:17, 10 December 2010
Line 1:		Line 1:
-	<applet load="" size="~~480~~" color="" frame="true" spin="on" Scene ="Enalapril/Enal/1" align="right" caption="Enalaprilat, the metabolite of Enalapril, also known as Vasotec"/>	+	<applet load="" size="430" color="" frame="true" spin="on" Scene ="Enalapril/Enal/1" align="right" caption="Enalaprilat, the metabolite of Enalapril, also known as Vasotec"/>
	===Better Known as: Vasotec===		===Better Known as: Vasotec===
	* Marketed By: Merck & Co.<br />		* Marketed By: Merck & Co.<br />
Line 13:		Line 13:

	===Pharmacokinetics===		===Pharmacokinetics===
-	~~{\| class~~="~~wikitable~~" ~~border~~="1" width="50%" style="~~text~~-align:~~center"~~	+	<table style="background: cellspacing="0px" align="" cellpadding="0px" width="42%">
-	\|-	+	<tr>
-	~~! colspan="8" align="center"\| ACE~~-~~Inhibitor [[Pharmacokinetics]] Comparison at Equivalent Dosages <ref>PMID~~: ~~7867683</ref~~><~~ref>DOI~~: ~~10.1111/j.1365-2710.2005.00646.x</ref><ref>PMID~~: ~~16075412</ref~~>~~<ref>PMID~~:~~7527101</ref>~~	+	<td style="width:100%; vertical-align:top;border-width:0px; border-style:inset">
-	\|-	+	<div style="height:100%; width: 100%">
-	~~! Parameter~~	+	{{:ACE Inhibitor Pharmacokinetics}}
-	~~! [[Captopril]]~~	+	</div>
-	~~! [[Lisinopril]]~~	+	</td>
-	~~! [[Ramipril]]~~	+	</tr>
-	~~! [[Enalapril]]~~	+	</table>
-	~~! [[Benazepril]]~~	+
-	~~! [[Perindopril]]~~	+
-	~~! [[Trandolapril]]~~	+
-	\|-	+
-	~~! [[Pharmacokinetics#Tmax\|T<sub>max~~</~~sub~~>~~]] (hr)~~	+
-	~~! .98~~	+
-	~~! 6.5~~	+
-	~~! .67~~	+
-	~~! 1.06~~	+
-	~~! .5~~	+
-	~~! .75~~	+
-	~~! .72~~	+
-	\|-	+
-	~~! [[Pharmacokinetics#Cmax\|C<sub>max~~</~~sub~~>~~]] (ng/ml)~~	+
-	~~! 1210~~	+
-	~~! 79~~	+
-	~~! 16.4~~	+
-	~~! 314~~	+
-	~~! 149~~	+
-	~~! 105~~	+
-	~~! 1.68~~	+
-	\|-	+
-	~~! [[Pharmacokinetics#Bioavailability_.28F.29\|Bioavailability]] (%)~~	+
-	~~! 72~~	+
-	~~! 25~~	+
-	~~! 28~~	+
-	~~! 60~~	+
-	~~! 97~~	+
-	~~! 24~~	+
-	~~! 10~~	+
-	\|-	+
-	~~! [[Pharmacokinetics#Protein_Binding\|Protein Binding]] (%)~~	+
-	~~! 97~~	+
-	~~! 0~~	+
-	~~! 73~~	+
-	~~! 20~~	+
-	~~! 97~~	+
-	~~! 20~~	+
-	~~! 80~~	+
-	\|-	+
-	~~! [[Pharmacokinetics#Half_Life_.28T1.2F2.29\|T~~<~~sub>1~~/~~2</sub~~>~~]] (hr)~~	+
-	~~! .56~~	+
-	~~! 10.1~~	+
-	~~! 1.93~~	+
-	~~! 1.6~~	+
-	~~! 10~~	+
-	~~! .9~~	+
-	~~! .68~~	+
-	\|-	+
-	~~! [[Pharmacokinetics#Area_Under_the_Curve_.28AUC.29\|AUC]] (ng/ml/hr)~~	+
-	~~! 1673~~	+
-	~~! 1016~~	+
-	~~! 21.9~~	+
-	~~! 450~~	+
-	~~! 140~~	+
-	~~! 182~~	+
-	~~! 1.86~~	+
-	\|-	+
-	~~! [[Pharmacokinetics#Inhibitory_Concentration_.28IC50.29\|IC<sub>50~~</~~sub~~>~~]] (nM)~~	+
-	~~! 1.1~~	+
-	~~! 5.5~~	+
-	~~! 5.0~~	+
-	~~! 5.4~~	+
-	~~! 1.7~~	+
-	~~! 2.4~~	+
-	~~! 2.5~~	+
-	\|-	+
-	~~! Dosage (mg)~~	+
-	~~! 10~~	+
-	~~! 20~~	+
-	~~! 5~~	+
-	~~! 20~~	+
-	~~! 10~~	+
-	~~! 4~~	+
-	~~! 2~~	+
-	\|-	+
-	~~! Metabolism~~	+
-	~~! Hepatic (CYP2D6)~~	+
-	~~! None~~	+
-	~~! Hepatic~~	+
-	~~! Hepatic (CYP3A4)~~	+
-	~~! Hepatic~~	+
-	~~! Hepatic~~	+
-	~~! Hepatic (CYP2D6 & CYP2C9)~~	+
-	\|}	+

	==References==		==References==

David Canner at 11:23, 9 December 2010

David Canner — Thu, 09 Dec 2010 11:23:30 GMT

←Older revision		Revision as of 11:23, 9 December 2010
Line 7:		Line 7:
	* 1996 Peak Sales: $2.5 Billion		* 1996 Peak Sales: $2.5 Billion
	* Importance: One of the best selling [[Angiotensin-Converting Enzyme]] Inhibitors of all time. Was developed by Merck as a replacement for [[Captopril]] with a better side effect profile.		* Importance: One of the best selling [[Angiotensin-Converting Enzyme]] Inhibitors of all time. Was developed by Merck as a replacement for [[Captopril]] with a better side effect profile.
-	* ~~The following is a list of Pharmacokinetic Parameters.~~ See: [[Pharmaceutical Drugs]] for more information	+	* See [[Pharmaceutical Drugs]] for more information about other drugs and diseases.

	===Mechanism of Action===		===Mechanism of Action===
Line 15:		Line 15:
	{\| class="wikitable" border="1" width="50%" style="text-align:center"		{\| class="wikitable" border="1" width="50%" style="text-align:center"
	\|-		\|-
-	! colspan="8" align="center"\| ACE-Inhibitor [[~~Pharmaceutical_Drugs#Pharmacokinetics_Translated\|~~Pharmacokinetics]] Comparison at Equivalent Dosages <ref>PMID: 7867683</ref><ref>DOI: 10.1111/j.1365-2710.2005.00646.x</ref><ref>PMID: 16075412</ref><ref>PMID:7527101</ref>	+	! colspan="8" align="center"\| ACE-Inhibitor [[Pharmacokinetics]] Comparison at Equivalent Dosages <ref>PMID: 7867683</ref><ref>DOI: 10.1111/j.1365-2710.2005.00646.x</ref><ref>PMID: 16075412</ref><ref>PMID:7527101</ref>
	\|-		\|-
	! Parameter		! Parameter
Line 26:		Line 26:
	! [[Trandolapril]]		! [[Trandolapril]]
	\|-		\|-
-	! [[~~Pharmaceutical_Drugs~~#Tmax\|T<sub>max</sub>]] (hr)	+	! [[Pharmacokinetics#Tmax\|T<sub>max</sub>]] (hr)
	! .98		! .98
	! 6.5		! 6.5
Line 35:		Line 35:
	! .72		! .72
	\|-		\|-
-	! [[~~Pharmaceutical_Drugs~~#Cmax\|C<sub>max</sub>]] (ng/ml)	+	! [[Pharmacokinetics#Cmax\|C<sub>max</sub>]] (ng/ml)
	! 1210		! 1210
	! 79		! 79
Line 44:		Line 44:
	! 1.68		! 1.68
	\|-		\|-
-	! [[~~Pharmaceutical_Drugs~~#Bioavailability_.28F.29\|Bioavailability]] (%)	+	! [[Pharmacokinetics#Bioavailability_.28F.29\|Bioavailability]] (%)
	! 72		! 72
	! 25		! 25
Line 53:		Line 53:
	! 10		! 10
	\|-		\|-
-	! [[~~Pharmaceutical_Drugs~~#Protein_Binding\|Protein Binding]] (%)	+	! [[Pharmacokinetics#Protein_Binding\|Protein Binding]] (%)
	! 97		! 97
	! 0		! 0
Line 62:		Line 62:
	! 80		! 80
	\|-		\|-
-	! [[~~Pharmaceutical_Drugs~~#Half_Life_.28T1.2F2.29\|T<sub>1/2</sub>]] (hr)	+	! [[Pharmacokinetics#Half_Life_.28T1.2F2.29\|T<sub>1/2</sub>]] (hr)
	! .56		! .56
	! 10.1		! 10.1
Line 71:		Line 71:
	! .68		! .68
	\|-		\|-
-	! [[~~Pharmaceutical_Drugs~~#Area_Under_the_Curve_.28AUC.29\|AUC]] (ng/ml/hr)	+	! [[Pharmacokinetics#Area_Under_the_Curve_.28AUC.29\|AUC]] (ng/ml/hr)
	! 1673		! 1673
	! 1016		! 1016
Line 80:		Line 80:
	! 1.86		! 1.86
	\|-		\|-
-	! [[~~Pharmaceutical_Drugs~~#Inhibitory_Concentration_.28IC50.29\|IC<sub>50</sub>]] (nM)	+	! [[Pharmacokinetics#Inhibitory_Concentration_.28IC50.29\|IC<sub>50</sub>]] (nM)
	! 1.1		! 1.1
	! 5.5		! 5.5

David Canner at 12:29, 1 December 2010

David Canner — Wed, 01 Dec 2010 12:29:29 GMT

←Older revision		Revision as of 12:29, 1 December 2010
Line 6:		Line 6:
	* Date of FDA Approval (Patent Expiration): 1985 (2000)<br />		* Date of FDA Approval (Patent Expiration): 1985 (2000)<br />
	* 1996 Peak Sales: $2.5 Billion		* 1996 Peak Sales: $2.5 Billion
-	* ~~Why You Should Care~~: One of the best selling [[Angiotensin-Converting Enzyme]] Inhibitors of all time. Was developed by Merck as a replacement for [[Captopril]] with a better side effect profile.	+	* Importance: One of the best selling [[Angiotensin-Converting Enzyme]] Inhibitors of all time. Was developed by Merck as a replacement for [[Captopril]] with a better side effect profile.
	* The following is a list of Pharmacokinetic Parameters. See: [[Pharmaceutical Drugs]] for more information		* The following is a list of Pharmacokinetic Parameters. See: [[Pharmaceutical Drugs]] for more information
		+
	===Mechanism of Action===		===Mechanism of Action===
	Angiotensin II has been implicated in cardiac, renal and vascular diseases. <ref>PMID:17083068</ref> Bradykinin, a small peptide that counterbalance the effects of Angiotensin II by acting as a strong vasodilator upon binding AT2, is degraded by the same ACE-1 enzyme. Since ACE-1 is the primary producer of Angiotensin II and degrader of Bradykinins, inhibition of ACE-1 has proven an effective treatment for Hypertension and Congestive Heart Failure. Enalapril is quickly metabolized into Enalaprilat, the more active metabolite of Enalapril predominantly by the Hepatic enzyme CYP3A4. Enalaprilat binds to the active site of <scene name='Enalapril/Ace/1'>Angiotensin-Converting Enzyme</scene>, preventing ACE-1 from binding and converting Angiotensin I into Angiotensin II. <scene name='Enalapril/Enalalprilat/2'>Enalaprilat is bound </scene>to ACE-1 via electrostatic interactions with His 353, Ala 354 (Backbone oxygen), Glue 384, Lys 511, His 513, Tyr 520 and Tyr 523 along with the zinc cation. <ref>PMID:15236580</ref>		Angiotensin II has been implicated in cardiac, renal and vascular diseases. <ref>PMID:17083068</ref> Bradykinin, a small peptide that counterbalance the effects of Angiotensin II by acting as a strong vasodilator upon binding AT2, is degraded by the same ACE-1 enzyme. Since ACE-1 is the primary producer of Angiotensin II and degrader of Bradykinins, inhibition of ACE-1 has proven an effective treatment for Hypertension and Congestive Heart Failure. Enalapril is quickly metabolized into Enalaprilat, the more active metabolite of Enalapril predominantly by the Hepatic enzyme CYP3A4. Enalaprilat binds to the active site of <scene name='Enalapril/Ace/1'>Angiotensin-Converting Enzyme</scene>, preventing ACE-1 from binding and converting Angiotensin I into Angiotensin II. <scene name='Enalapril/Enalalprilat/2'>Enalaprilat is bound </scene>to ACE-1 via electrostatic interactions with His 353, Ala 354 (Backbone oxygen), Glue 384, Lys 511, His 513, Tyr 520 and Tyr 523 along with the zinc cation. <ref>PMID:15236580</ref>

David Canner at 13:30, 29 November 2010

David Canner — Mon, 29 Nov 2010 13:30:57 GMT

←Older revision		Revision as of 13:30, 29 November 2010
Line 14:		Line 14:
	{\| class="wikitable" border="1" width="50%" style="text-align:center"		{\| class="wikitable" border="1" width="50%" style="text-align:center"
	\|-		\|-
-	! colspan="8" align="center"\| ACE-Inhibitor [[Pharmaceutical_Drugs#Pharmacokinetics_Translated\|Pharmacokinetics]] Comparison at Equivalent Dosages <ref>PMID: 7867683</ref><ref>DOI: 10.1111/j.1365-2710.2005.00646.x~~</ref><ref>PMID: 15985045~~</ref><ref>PMID: 16075412</ref><ref>PMID:7527101</ref>	+	! colspan="8" align="center"\| ACE-Inhibitor [[Pharmaceutical_Drugs#Pharmacokinetics_Translated\|Pharmacokinetics]] Comparison at Equivalent Dosages <ref>PMID: 7867683</ref><ref>DOI: 10.1111/j.1365-2710.2005.00646.x</ref><ref>PMID: 16075412</ref><ref>PMID:7527101</ref>
	\|-		\|-
	! Parameter		! Parameter

David Canner at 11:40, 29 November 2010

David Canner — Mon, 29 Nov 2010 11:40:48 GMT

←Older revision		Revision as of 11:40, 29 November 2010
Line 2:		Line 2:
	===Better Known as: Vasotec===		===Better Known as: Vasotec===
	* Marketed By: Merck & Co.<br />		* Marketed By: Merck & Co.<br />
-	* Major Indication: Hypertension & Congestive Heart Failure<br />	+	* Major Indication: [[Hypertension & Congestive Heart Failure]]<br />
	* Drug Class: [[ACE]] Inhibitor		* Drug Class: [[ACE]] Inhibitor
	* Date of FDA Approval (Patent Expiration): 1985 (2000)<br />		* Date of FDA Approval (Patent Expiration): 1985 (2000)<br />

David Canner at 10:52, 29 November 2010

David Canner — Mon, 29 Nov 2010 10:52:29 GMT

←Older revision		Revision as of 10:52, 29 November 2010
Line 9:		Line 9:
	* The following is a list of Pharmacokinetic Parameters. See: [[Pharmaceutical Drugs]] for more information		* The following is a list of Pharmacokinetic Parameters. See: [[Pharmaceutical Drugs]] for more information
	===Mechanism of Action===		===Mechanism of Action===
-	Angiotensin II has been implicated in cardiac, renal and vascular diseases. <ref>PMID:17083068</ref> Bradykinin, a small peptide that counterbalance the effects of Angiotensin II by acting as a strong vasodilator upon binding AT2, is degraded by the same ACE-1 enzyme. Since ACE-1 is the primary producer of Angiotensin II and degrader of Bradykinins, inhibition of ACE-1 has proven an effective treatment for Hypertension and Congestive Heart Failure. Enalapril is quickly metabolized into Enalaprilat, the more active metabolite of Enalapril predominantly by the Hepatic enzyme CYP3A4. Enalaprilat binds to the active site of <scene name='Enalapril/~~Enalalprilat~~/2'>Angiotensin-Converting Enzyme</scene>, preventing ACE-1 from binding and converting Angiotensin I into Angiotensin II. <scene name='Enalapril/~~Ace~~/1'>Enalaprilat is bound </scene>to ACE-1 via electrostatic interactions with His 353, Ala 354 (Backbone oxygen), Glue 384, Lys 511, His 513, Tyr 520 and Tyr 523 along with the zinc cation. <ref>PMID:15236580</ref>	+	Angiotensin II has been implicated in cardiac, renal and vascular diseases. <ref>PMID:17083068</ref> Bradykinin, a small peptide that counterbalance the effects of Angiotensin II by acting as a strong vasodilator upon binding AT2, is degraded by the same ACE-1 enzyme. Since ACE-1 is the primary producer of Angiotensin II and degrader of Bradykinins, inhibition of ACE-1 has proven an effective treatment for Hypertension and Congestive Heart Failure. Enalapril is quickly metabolized into Enalaprilat, the more active metabolite of Enalapril predominantly by the Hepatic enzyme CYP3A4. Enalaprilat binds to the active site of <scene name='Enalapril/Ace/1'>Angiotensin-Converting Enzyme</scene>, preventing ACE-1 from binding and converting Angiotensin I into Angiotensin II. <scene name='Enalapril/Enalalprilat/2'>Enalaprilat is bound </scene>to ACE-1 via electrostatic interactions with His 353, Ala 354 (Backbone oxygen), Glue 384, Lys 511, His 513, Tyr 520 and Tyr 523 along with the zinc cation. <ref>PMID:15236580</ref>

	===Pharmacokinetics===		===Pharmacokinetics===

David Canner at 10:51, 29 November 2010

David Canner — Mon, 29 Nov 2010 10:51:51 GMT

←Older revision		Revision as of 10:51, 29 November 2010
Line 10:		Line 10:
	===Mechanism of Action===		===Mechanism of Action===
	Angiotensin II has been implicated in cardiac, renal and vascular diseases. <ref>PMID:17083068</ref> Bradykinin, a small peptide that counterbalance the effects of Angiotensin II by acting as a strong vasodilator upon binding AT2, is degraded by the same ACE-1 enzyme. Since ACE-1 is the primary producer of Angiotensin II and degrader of Bradykinins, inhibition of ACE-1 has proven an effective treatment for Hypertension and Congestive Heart Failure. Enalapril is quickly metabolized into Enalaprilat, the more active metabolite of Enalapril predominantly by the Hepatic enzyme CYP3A4. Enalaprilat binds to the active site of <scene name='Enalapril/Enalalprilat/2'>Angiotensin-Converting Enzyme</scene>, preventing ACE-1 from binding and converting Angiotensin I into Angiotensin II. <scene name='Enalapril/Ace/1'>Enalaprilat is bound </scene>to ACE-1 via electrostatic interactions with His 353, Ala 354 (Backbone oxygen), Glue 384, Lys 511, His 513, Tyr 520 and Tyr 523 along with the zinc cation. <ref>PMID:15236580</ref>		Angiotensin II has been implicated in cardiac, renal and vascular diseases. <ref>PMID:17083068</ref> Bradykinin, a small peptide that counterbalance the effects of Angiotensin II by acting as a strong vasodilator upon binding AT2, is degraded by the same ACE-1 enzyme. Since ACE-1 is the primary producer of Angiotensin II and degrader of Bradykinins, inhibition of ACE-1 has proven an effective treatment for Hypertension and Congestive Heart Failure. Enalapril is quickly metabolized into Enalaprilat, the more active metabolite of Enalapril predominantly by the Hepatic enzyme CYP3A4. Enalaprilat binds to the active site of <scene name='Enalapril/Enalalprilat/2'>Angiotensin-Converting Enzyme</scene>, preventing ACE-1 from binding and converting Angiotensin I into Angiotensin II. <scene name='Enalapril/Ace/1'>Enalaprilat is bound </scene>to ACE-1 via electrostatic interactions with His 353, Ala 354 (Backbone oxygen), Glue 384, Lys 511, His 513, Tyr 520 and Tyr 523 along with the zinc cation. <ref>PMID:15236580</ref>
-
-

	===Pharmacokinetics===		===Pharmacokinetics===

David Canner at 10:51, 29 November 2010

David Canner — Mon, 29 Nov 2010 10:51:44 GMT

←Older revision		Revision as of 10:51, 29 November 2010
Line 9:		Line 9:
	* The following is a list of Pharmacokinetic Parameters. See: [[Pharmaceutical Drugs]] for more information		* The following is a list of Pharmacokinetic Parameters. See: [[Pharmaceutical Drugs]] for more information
	===Mechanism of Action===		===Mechanism of Action===
-	Angiotensin II has been implicated in cardiac, renal and vascular diseases. <ref>PMID:17083068</ref> Bradykinin, a small peptide that counterbalance the effects of Angiotensin II by acting as a strong vasodilator upon binding AT2, is degraded by the same ACE-1 enzyme. Since ACE-1 is the primary producer of Angiotensin II and degrader of Bradykinins, inhibition of ACE-1 has proven an effective treatment for Hypertension and Congestive Heart Failure.	+	Angiotensin II has been implicated in cardiac, renal and vascular diseases. <ref>PMID:17083068</ref> Bradykinin, a small peptide that counterbalance the effects of Angiotensin II by acting as a strong vasodilator upon binding AT2, is degraded by the same ACE-1 enzyme. Since ACE-1 is the primary producer of Angiotensin II and degrader of Bradykinins, inhibition of ACE-1 has proven an effective treatment for Hypertension and Congestive Heart Failure. Enalapril is quickly metabolized into Enalaprilat, the more active metabolite of Enalapril predominantly by the Hepatic enzyme CYP3A4. Enalaprilat binds to the active site of <scene name='Enalapril/Enalalprilat/2'>Angiotensin-Converting Enzyme</scene>, preventing ACE-1 from binding and converting Angiotensin I into Angiotensin II. <scene name='Enalapril/Ace/1'>Enalaprilat is bound </scene>to ACE-1 via electrostatic interactions with His 353, Ala 354 (Backbone oxygen), Glue 384, Lys 511, His 513, Tyr 520 and Tyr 523 along with the zinc cation. <ref>PMID:15236580</ref>
-	Enalapril is quickly metabolized into Enalaprilat, the more active metabolite of Enalapril.	+

-	Ramiprilat binds to the active site of <scene name='Ramipril/Angio/1'>Angiotensin-Converting Enzyme</scene>, actively inhibiting ACE-1 from binding and converting Angiotensin I into Angiotensin II. ACE-1 <scene name='Ramipril/Ramiprilat_binding/1'> binds Ramiprilat</scene> using residues Glu 395, His 497, Lys 495, Gln 265, Tyr 504, Tyr 496 and Tyr 507, tightly affixing the inhibitor to the active site of ACE-1.
-	<scene name='Angiotensin-Converting_Enzyme/Enalalprilat/2'>Enalaprilat, a third competitive inhibitor</scene>, binds via electrostatic interactions with His 353, Ala 354 (Backbone oxygen), Glue 384, Lys 511, His 513, Tyr 520 and Tyr 523 along with the zinc cation. All three inhibitors are very effective and are FDA approved for treatment of Angiotensin II related hypertension and other cardiovascular and renal disorders. <ref>PMID:15236580</ref>

-	<scene name='Enalapril/Enalalprilat/2'>TextToBeDisplayed</scene>
-	<scene name='Enalapril/Ace/1'>TextToBeDisplayed</scene>
	===Pharmacokinetics===		===Pharmacokinetics===
	{\| class="wikitable" border="1" width="50%" style="text-align:center"		{\| class="wikitable" border="1" width="50%" style="text-align:center"

David Canner at 10:47, 29 November 2010

David Canner — Mon, 29 Nov 2010 10:47:28 GMT

←Older revision		Revision as of 10:47, 29 November 2010
Line 10:		Line 10:
	===Mechanism of Action===		===Mechanism of Action===
	Angiotensin II has been implicated in cardiac, renal and vascular diseases. <ref>PMID:17083068</ref> Bradykinin, a small peptide that counterbalance the effects of Angiotensin II by acting as a strong vasodilator upon binding AT2, is degraded by the same ACE-1 enzyme. Since ACE-1 is the primary producer of Angiotensin II and degrader of Bradykinins, inhibition of ACE-1 has proven an effective treatment for Hypertension and Congestive Heart Failure.		Angiotensin II has been implicated in cardiac, renal and vascular diseases. <ref>PMID:17083068</ref> Bradykinin, a small peptide that counterbalance the effects of Angiotensin II by acting as a strong vasodilator upon binding AT2, is degraded by the same ACE-1 enzyme. Since ACE-1 is the primary producer of Angiotensin II and degrader of Bradykinins, inhibition of ACE-1 has proven an effective treatment for Hypertension and Congestive Heart Failure.
-	~~Ramipril~~ is quickly metabolized into ~~Ramiprilat~~, the ~~most~~ active ~~inhibitor~~ of ~~Ramipril~~. Ramiprilat binds to the active site of <scene name='Ramipril/Angio/1'>Angiotensin-Converting Enzyme</scene>, actively inhibiting ACE-1 from binding and converting Angiotensin I into Angiotensin II. ACE-1 <scene name='Ramipril/Ramiprilat_binding/1'> binds Ramiprilat</scene> using residues Glu 395, His 497, Lys 495, Gln 265, Tyr 504, Tyr 496 and Tyr 507, tightly affixing the inhibitor to the active site of ACE-1.	+	Enalapril is quickly metabolized into Enalaprilat, the more active metabolite of Enalapril.
		+
		+	Ramiprilat binds to the active site of <scene name='Ramipril/Angio/1'>Angiotensin-Converting Enzyme</scene>, actively inhibiting ACE-1 from binding and converting Angiotensin I into Angiotensin II. ACE-1 <scene name='Ramipril/Ramiprilat_binding/1'> binds Ramiprilat</scene> using residues Glu 395, His 497, Lys 495, Gln 265, Tyr 504, Tyr 496 and Tyr 507, tightly affixing the inhibitor to the active site of ACE-1.
		+	<scene name='Angiotensin-Converting_Enzyme/Enalalprilat/2'>Enalaprilat, a third competitive inhibitor</scene>, binds via electrostatic interactions with His 353, Ala 354 (Backbone oxygen), Glue 384, Lys 511, His 513, Tyr 520 and Tyr 523 along with the zinc cation. All three inhibitors are very effective and are FDA approved for treatment of Angiotensin II related hypertension and other cardiovascular and renal disorders. <ref>PMID:15236580</ref>
		+
	<scene name='Enalapril/Enalalprilat/2'>TextToBeDisplayed</scene>		<scene name='Enalapril/Enalalprilat/2'>TextToBeDisplayed</scene>
	<scene name='Enalapril/Ace/1'>TextToBeDisplayed</scene>		<scene name='Enalapril/Ace/1'>TextToBeDisplayed</scene>