1. Acovil
2. Altace
3. Carasel
4. Delix
5. Hoe 498
6. Hoe-498
7. Hoe498
8. Ramace
9. Triatec
10. Tritace
11. Vesdil
12. Zabien
1. 87333-19-5
2. Tritace
3. Altace
4. Ramace
5. Triatec
6. Delix
7. Carasel
8. Vesdil
9. Cardace
10. Hoe-498
11. Pramace
12. Ramiprilum [latin]
13. Ramiprilum
14. Unipril
15. Hoe 498
16. Quark
17. Altace (tn)
18. Corpril
19. Ramipres
20. Ecator
21. Hopace
22. Acovil
23. C09aa05
24. Lostapres
25. Hytren
26. (2s,3as,6as)-1-[(2s)-2-[[(2s)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino]propanoyl]-3,3a,4,5,6,6a-hexahydro-2h-cyclopenta[b]pyrrole-2-carboxylic Acid
27. Nsc-758933
28. Chembl1168
29. L35jn3i7sj
30. Chebi:8774
31. (2s,3as,6as)-1-((s)-n-((s)-1-carboxy-3-phenylpropyl)alanyl)octahydrocyclopenta(b)pyrrole-2-carboxylic Acid, 1-ethyl Ester
32. Ramipro
33. Naprix
34. Mfcd00865775
35. Dsstox_cid_3551
36. Dsstox_rid_77077
37. Dsstox_gsid_23551
38. (2s,3as,6as)-1-(((s)-1-ethoxy-1-oxo-4-phenylbutan-2-yl)-l-alanyl)octahydrocyclopenta[b]pyrrole-2-carboxylic Acid
39. (2s,3as,6as)-1-((s)-2-(((s)-1-ethoxy-1-oxo-4-phenylbutan-2-yl)amino)propanoyl)octahydrocyclopenta[b]pyrrole-2-carboxylic Acid
40. (2s,3as,6as)-1-[(2s)-2-[[(2s)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]azaniumyl]propanoyl]-3,3a,4,5,6,6a-hexahydro-2h-cyclopenta[b]pyrrole-2-carboxylate
41. (2s,3as,6as)-1-[(2s)-2-{[(2s)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino}propanoyl]-octahydrocyclopenta[b]pyrrole-2-carboxylic Acid
42. (2s-(1(r*(r*)),2alpha,3abeta,6abeta))-1-(2-((1-(ethoxycarbonyl)-3-phenylpropyl)amino)-1-oxopropyl)octahydrocyclopenta(b)pyrrole-2-carboxylic Acid
43. Hoe498
44. Ramipril (altace)
45. (2s,3as,6as)-1-[(2s)-2-{[(2s)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino}propanoyl]octahydrocyclopenta[b]pyrrole-2-carboxylic Acid (non-preferred Name)
46. Cyclopenta[b]pyrrole-2-carboxylic Acid, 1-[(2s)-2-[[(1s)-1-(ethoxycarbonyl)-3-phenylpropyl]amino]-1-oxopropyl]octahydro-, (2s,3as,6as)-
47. Smr000466386
48. Ramipril (usp/inn)
49. Sr-05000001908
50. Unii-l35jn3i7sj
51. Ramipril [usan:usp:inn:ban]
52. Ncgc00016955-01
53. Cyclopenta(b)pyrrole-2-carboxylic Acid, 1-((2s)-2-(((1s)-1-(ethoxycarbonyl)-3-phenylpropyl)amino)-1-oxopropyl)octahydro-, (2s,3as,6as)-
54. Cas-87333-19-5
55. (2s,3as,6as)-1-((s)-n-((s)-1-ethoxycarbonyl-3-phenylpropyl)alanyl)octahydrocyclopenta(b)pyrrol-2-carbonsaeure
56. Spectrum_001958
57. Ramipril [usan]
58. Ramipril [inn]
59. Ramipril [jan]
60. Ramipril [mi]
61. Ramipril [vandf]
62. Spectrum3_001794
63. Spectrum4_001269
64. Spectrum5_001721
65. Ramipril [mart.]
66. Ramipril [usp-rs]
67. Ramipril [who-dd]
68. Schembl16059
69. Bspbio_003347
70. Kbiogr_001858
71. Kbioss_002512
72. Ramipril, (+)-
73. Cyclopenta(b)pyrrole-2-carboxylic Acid, 1-(2-((1-(ethoxycarbonyl)-3-phenylpropyl)amino)-1-oxopropyl)octahydro-, (2s-(1(r*(r*)),2alpha,3abeta,6abeta))-
74. Mls000759523
75. Mls001216547
76. Mls001423965
77. N-(1s-carboethoxy-3-phenylpropyl)-s-alanyl-cis,endo-2-azabicyclo[3.3.0]octane-3s-carboxylic Acid
78. Bidd:gt0803
79. Spectrum1505214
80. Ramipril [orange Book]
81. Gtpl6339
82. Ramipril [ep Monograph]
83. Ramipril, >=98% (hplc)
84. Dtxsid8023551
85. Ramipril [usp Monograph]
86. Hsdb 8393
87. Kbio2_002504
88. Kbio2_005072
89. Kbio2_007640
90. Kbio3_002849
91. Polycap Component Ramipril
92. Npd2431
93. Hms2051e04
94. Hms2090l11
95. Hms2093m10
96. Hms2231m05
97. Hms3259j07
98. Hms3715m16
99. Pharmakon1600-01505214
100. Cyclopenta(b)pyrrole-2-carboxylic Acid, 1-(2-((1-(ethoxycarbonyl)-3-phenylpropyl)amino)-1-oxopropyl)octahydro-, (2s-(1(r*(r*)),2.alpha.,3a.beta.,6a.beta.))-
101. Hy-b0279
102. Zinc3798757
103. Tox21_110708
104. Bbl033964
105. Bdbm50084681
106. Nsc758933
107. S1793
108. Stk801937
109. Akos005622534
110. Tox21_110708_1
111. Ac-1347
112. Ccg-100833
113. Db00178
114. Ks-1103
115. Nc00083
116. Nc00627
117. Nsc 758933
118. Ncgc00178127-01
119. Ncgc00178127-02
120. (2s,3as,6as)-1((s)-n-((s)-1-carboxy-3-phenylpropyl)alanyl)octahydrocyclopenta(b)pyrrole-2-carboxylic
121. (2s,3as,6as)-1-((s)-2-((s)-1-ethoxy-1-oxo-4-phenylbutan-2-ylamino)propanoyl) Octahydrocyclopenta[b]pyrrole-2-carboxylic Acid
122. (2s,3as,6as)-1-((s)-2-((s)-1-ethoxy-1-oxo-4-phenylbutan-2-ylamino)propanoyl)-octahydrocyclopenta[b]p
123. (2s,3as,6as)-1-[(2s)-2-[[(1s)-1-(ethoxycarbonyl)-3-phenylpropyl]amino]-1-oxopropyl]octahydro-cyclopenta[b]pyrrole-2-carboxylic Acid
124. (2s,3as,6as)-1-[(2s)-2-{[(1s)-1-ethoxycarbonyl-3-phenylpropyl]amino}propanoyl]octahydrocyclopenta[b]pyrrole-2-carboxylic Acid
125. (2s,3as,6as)-1-[(s)-2-((s)-1-ethoxycarbonyl-3-phenyl-propylamino)-propionyl]-octahydro-cyclopenta[b]
126. [2s,3as,6as]-1-[(2s)-2-[[(1s)-1-(ethoxycarbonyl)-3-phenylpropyl]amino]-1-oxopropyl]octahydrocyclopen
127. Br164319
128. Sbi-0206728.p001
129. B2208
130. R0219
131. D00421
132. Ab00698339-07
133. Ab00698339-08
134. Ab00698339_09
135. Ab00698339_10
136. 333r195
137. Q412666
138. Sr-05000001908-1
139. Sr-05000001908-2
140. Ramipril, British Pharmacopoeia (bp) Reference Standard
141. Ramipril, European Pharmacopoeia (ep) Reference Standard
142. Z1946144927
143. Ramipril, United States Pharmacopeia (usp) Reference Standard
144. Ramipril, Pharmaceutical Secondary Standard; Certified Reference Material
145. (2s,3as,6as)-1-[(2s)-2-[[(1s)-1-(ethoxycarbonyl)-3-phenylpropyl]amino]-1-oxopropyl]octahydrocyclopenta[b]pyrrole-2-carboxylic Acid
146. (2s,3as,6as)-1-[(2s)-2-[[(2s)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino]propanoyl]-3,3a,4,5,6,6a-hexahydro-2h-cyclopenta[d]pyrrole-2-carboxylic Acid
147. 1-[2-(1-ethoxycarbonyl-3-phenyl-propylamino)-propionyl]-octahydro-cyclopenta[b]pyrrole-2-carboxylic Acid(ramipril)
148. 1-[2-(1-ethoxycarbonyl-3-phenylpropylamino)propionyl]octahydrocyclopenta[b]- Pyrrole-2-carboxylic Acid
149. 1028843-43-7
| Molecular Weight | 416.5 g/mol |
|---|---|
| Molecular Formula | C23H32N2O5 |
| XLogP3 | 1.4 |
| Hydrogen Bond Donor Count | 2 |
| Hydrogen Bond Acceptor Count | 6 |
| Rotatable Bond Count | 10 |
| Exact Mass | 416.23112213 g/mol |
| Monoisotopic Mass | 416.23112213 g/mol |
| Topological Polar Surface Area | 95.9 Ų |
| Heavy Atom Count | 30 |
| Formal Charge | 0 |
| Complexity | 619 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 5 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
| 1 of 4 | |
|---|---|
| Drug Name | Altace |
| PubMed Health | Ramipril (By mouth) |
| Drug Classes | Antihypertensive, Cardiovascular Agent, Renal Protective Agent |
| Drug Label | Ramipril is a 2-aza-bicyclo [3.3.0]-octane-3-carboxylic acid derivative. It is a white, crystalline substance soluble in polar organic solvents and buffered aqueous solutions. Ramipril melts between 105112C.The CAS Registry Number is 87333-19-... |
| Active Ingredient | Ramipril |
| Dosage Form | Capsule |
| Route | Oral |
| Strength | 2.5mg; 5mg; 1.25mg; 10mg |
| Market Status | Prescription |
| Company | King Pharms |
| 2 of 4 | |
|---|---|
| Drug Name | Ramipril |
| PubMed Health | Ramipril (By mouth) |
| Drug Classes | Antihypertensive, Cardiovascular Agent, Renal Protective Agent |
| Drug Label | Ramipril is a 2-aza-bicyclo [3.3.0]-octane-3-carboxylic acid derivative. It is a white, crystalline substance soluble in polar organic solvents and buffered aqueous solutions. Ramipril melts between 105and 112Ramipril's chemical name is (2S,3aS,6aS)- |
| Active Ingredient | Ramipril |
| Dosage Form | Tablet; Capsule |
| Route | Oral |
| Strength | 2.5mg; 1.25mg; 5mg; 10mg |
| Market Status | Prescription |
| Company | Mylan Pharms; Apotex; Accord Hlthcare; Aurobindo Pharma; Lupin; Sandoz; Invagen Pharms; Roxane; Watson Labs; Teva Pharms; Zydus Pharms Usa; Dr Reddys Labs |
| 3 of 4 | |
|---|---|
| Drug Name | Altace |
| PubMed Health | Ramipril (By mouth) |
| Drug Classes | Antihypertensive, Cardiovascular Agent, Renal Protective Agent |
| Drug Label | Ramipril is a 2-aza-bicyclo [3.3.0]-octane-3-carboxylic acid derivative. It is a white, crystalline substance soluble in polar organic solvents and buffered aqueous solutions. Ramipril melts between 105112C.The CAS Registry Number is 87333-19-... |
| Active Ingredient | Ramipril |
| Dosage Form | Capsule |
| Route | Oral |
| Strength | 2.5mg; 5mg; 1.25mg; 10mg |
| Market Status | Prescription |
| Company | King Pharms |
| 4 of 4 | |
|---|---|
| Drug Name | Ramipril |
| PubMed Health | Ramipril (By mouth) |
| Drug Classes | Antihypertensive, Cardiovascular Agent, Renal Protective Agent |
| Drug Label | Ramipril is a 2-aza-bicyclo [3.3.0]-octane-3-carboxylic acid derivative. It is a white, crystalline substance soluble in polar organic solvents and buffered aqueous solutions. Ramipril melts between 105and 112Ramipril's chemical name is (2S,3aS,6aS)- |
| Active Ingredient | Ramipril |
| Dosage Form | Tablet; Capsule |
| Route | Oral |
| Strength | 2.5mg; 1.25mg; 5mg; 10mg |
| Market Status | Prescription |
| Company | Mylan Pharms; Apotex; Accord Hlthcare; Aurobindo Pharma; Lupin; Sandoz; Invagen Pharms; Roxane; Watson Labs; Teva Pharms; Zydus Pharms Usa; Dr Reddys Labs |
Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents
National Library of Medicine's Medical Subject Headings. Ramipril. Online file (MeSH, 2017). Available from, as of Oct 4, 2017: https://meshb.nlm.nih.gov/search
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Ramipril is included in the database.
NIH/NLM; ClinicalTrials.Gov. Available from, as of August 30, 2017: https://clinicaltrials.gov/
Ramipril capsules are indicated for the treatment of hypertension, to lower blood pressure. Lowering blood pressure reduces the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions. These benefits have been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes including this drug. ... Ramipril capsules may be used alone or in combination with thiazide diuretics. /Included in US product label/
NIH; DailyMed. Current Medication Information for Ramipril Capsule (Updated: June 2017). Available from, as of October 25, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d6d57158-e8f9-4c91-8317-0374e0c87d33
Ramipril capsules are indicated in stable patients who have demonstrated clinical signs of congestive heart failure within the first few days after sustaining acute myocardial infarction. Administration of ramipril capsules to such patients have been shown to decrease the risk of death (principally cardiovascular death) and to decrease the risks of failure-related hospitalization and progression to severe/resistant heart failure. /Included in US product label/
NIH; DailyMed. Current Medication Information for Ramipril Capsule (Updated: June 2017). Available from, as of October 25, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d6d57158-e8f9-4c91-8317-0374e0c87d33
For more Therapeutic Uses (Complete) data for Ramipril (8 total), please visit the HSDB record page.
/BOXED WARNING/ When pregnancy is detected, discontinue ramipril as soon as possible. Drugs that act directly on the renin-angiotensin system can cause injury and death to the developing fetus.
NIH; DailyMed. Current Medication Information for Ramipril Capsule (Updated: June 2017). Available from, as of October 25, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d6d57158-e8f9-4c91-8317-0374e0c87d33
Use of drugs that act on the renin-angiotensin system during the second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death. Resulting oligohydramnios can be associated with fetal lung hypoplasia and skeletal deformations. Potential neonatal adverse effects include skull hypoplasia, anuria, hypotension, renal failure, and death. When pregnancy is detected, discontinue ramipril as soon as possible. These adverse outcomes are usually associated with use of these drugs in the second and third trimester of pregnancy. Most epidemiologic studies examining fetal abnormalities after exposure to antihypertensive use in the first trimester have not distinguished drugs affecting the renin-angiotensin system from other antihypertensive agents. Appropriate management of maternal hypertension during pregnancy is important to optimize outcomes for both mother and fetus.
NIH; DailyMed. Current Medication Information for Ramipril Capsule (Updated: June 2017). Available from, as of October 25, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d6d57158-e8f9-4c91-8317-0374e0c87d33
Angiotensin-converting enzyme (ACE) inhibitors can cause fetal and neonatal morbidity and mortality when used in pregnancy during the second and third trimesters. ACE inhibitors also increase the risk of major congenital malformations when administered during the first trimester of pregnancy. Discontinue as soon as possible when pregnancy is detected, unless continued use is considered lifesaving. Nearly all women can be transferred successfully to alternative therapy for the remainder of their pregnancy. /Angiotensin-converting enzyme (ACE) inhibitors/
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017, p. 2097
Rare angiotensin-converting enzyme (ACE) inhibitor-associated clinical syndrome manifested initially by cholestatic jaundice may occur; may progress to fulminant hepatic necrosis and is potentially fatal. Patients receiving an ACE inhibitor, including ramipril, who develop jaundice or marked elevations in hepatic enzymes should discontinue the drug and receive appropriate monitoring.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017, p. 2097
For more Drug Warnings (Complete) data for Ramipril (18 total), please visit the HSDB record page.
For the management of mild to severe hypertension. May be used to reduce cardiovascular mortality following myocardial infarction in hemodynamically stable individuals who develop clinical signs of congestive heart failure within a few days following myocardial infarction. To reduce the rate of death, myocardial infarction and stroke in individuals at high risk of cardiovascular events. May be used to slow the progression of renal disease in individuals with hypertension, diabetes mellitus and microalubinuria or overt nephropathy.
FDA Label
Ramipril is an ACE inhibitor similar to benazepril, fosinopril and quinapril. It is an inactive prodrug that is converted to ramiprilat in the liver, the main site of activation, and kidneys. Ramiprilat confers blood pressure lowing effects by antagonizing the effect of the RAAS. The RAAS is a homeostatic mechanism for regulating hemodynamics, water and electrolyte balance. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from the granular cells of the juxtaglomerular apparatus in the kidneys. In the blood stream, renin cleaves circulating angiotensinogen to ATI, which is subsequently cleaved to ATII by ACE. ATII increases blood pressure using a number of mechanisms. First, it stimulates the secretion of aldosterone from the adrenal cortex. Aldosterone travels to the distal convoluted tubule (DCT) and collecting tubule of nephrons where it increases sodium and water reabsorption by increasing the number of sodium channels and sodium-potassium ATPases on cell membranes. Second, ATII stimulates the secretion of vasopressin (also known as antidiuretic hormone or ADH) from the posterior pituitary gland. ADH stimulates further water reabsorption from the kidneys via insertion of aquaporin-2 channels on the apical surface of cells of the DCT and collecting tubules. Third, ATII increases blood pressure through direct arterial vasoconstriction. Stimulation of the Type 1 ATII receptor on vascular smooth muscle cells leads to a cascade of events resulting in myocyte contraction and vasoconstriction. In addition to these major effects, ATII induces the thirst response via stimulation of hypothalamic neurons. ACE inhibitors inhibit the rapid conversion of ATI to ATII and antagonize RAAS-induced increases in blood pressure. ACE (also known as kininase II) is also involved in the enzymatic deactivation of bradykinin, a vasodilator. Inhibiting the deactivation of bradykinin increases bradykinin levels and may sustain the effects of ramiprilat by causing increased vasodilation and decreased blood pressure.
Angiotensin-Converting Enzyme Inhibitors
A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility. (See all compounds classified as Angiotensin-Converting Enzyme Inhibitors.)
Antihypertensive Agents
Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS. (See all compounds classified as Antihypertensive Agents.)
C09AA05
S76 | LUXPHARMA | Pharmaceuticals Marketed in Luxembourg | Pharmaceuticals marketed in Luxembourg, as published by d'Gesondheetskeess (CNS, la caisse nationale de sante, www.cns.lu), mapped by name to structures using CompTox by R. Singh et al. (in prep.). List downloaded from https://cns.public.lu/en/legislations/textes-coordonnes/liste-med-comm.html. Dataset DOI:10.5281/zenodo.4587355
C - Cardiovascular system
C09 - Agents acting on the renin-angiotensin system
C09A - Ace inhibitors, plain
C09AA - Ace inhibitors, plain
C09AA05 - Ramipril
Absorption
The extent of absorption is at least 50-60%.. Food decreases the rate of absorption from the GI tract without affecting the extent of absorption. The absolute bioavailabilities of ramipril and ramiprilat were 28% and 44%, respectively, when oral administration was compared to intravenous administration. The serum concentration of ramiprilat was unchanged when capsules were opened and the contents dissolved in water, dissolved in apple juice, or suspended in apple sauce.
Route of Elimination
Following oral administration, about 60% of the dose is eliminated in the urine as unchanged ramipril (<2%) and its metabolites. About 40% of the dose is found in the feces, representing both unabsorbed drug and drugs and metabolites eliminated via biliary excretion. The urinary excretion of ramipril may be reduced in patients with impaired renal function.
Clearance
The renal clearance of ramipril and ramiprilat was reported to be 7.2 and 77.4 mL/min/1.73m2. The mean renal clearance of ramipril and ramiprilat is reported to be 10.7 and 126.8 mL/min in healthy elderly patients with normal renal function, additionally the Cmax of ramiprilat is approximately 20% higher in this population. While the pharmacokinetics of ramipril appear unaffected by reduced renal function, the plasma concentration and half-life of ramiprilat are increased. In patient's with hepatic failure the concentration of ramipril is initially increased while the tmax of ramiprilat is prolonged due to a reduced ability to metabolize the drug. However, steady state concentrations of ramiprilat are the same in hepatic failure as in healthy patients.
/MILK/ Ingestion of a single 10 mg oral dose of ramipril resulted in undetectable amounts of ramipril and its metabolites in breast milk.
NIH; DailyMed. Current Medication Information for Ramipril Capsule (Updated: June 2017). Available from, as of October 25, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d6d57158-e8f9-4c91-8317-0374e0c87d33
Following oral administration of ramipril, peak plasma concentrations (Cmax) of ramipril are reached within 1 hour. The extent of absorption is at least 50% to 60%, and is not significantly influenced by the presence of food in the gastrointestinal tract, although the rate of absorption is reduced.
NIH; DailyMed. Current Medication Information for Ramipril Capsule (Updated: June 2017). Available from, as of October 25, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d6d57158-e8f9-4c91-8317-0374e0c87d33
Plasma concentrations of ramiprilat decline in a triphasic manner (initial rapid decline, apparent elimination phase, terminal elimination phase). The initial rapid decline, which represents distribution of the drug into a large peripheral compartment and subsequent binding to both plasma and tissue ACE, has a half-life of 2 to 4 hours. Because of its potent binding to ACE and slow dissociation from the enzyme, ramiprilat shows two elimination phases. The apparent elimination phase corresponds to the clearance of free ramiprilat and has a half-life of 9 to 18 hours. The terminal elimination phase has a prolonged half-life (>50 hours) and probably represents the binding/dissociation kinetics of the ramiprilat/ACE complex. It does not contribute to the accumulation of the drug. After multiple daily doses of ramipril 5 mg to 10 mg, the half-life of ramiprilat concentrations within the therapeutic range was 13 to 17 hours. /Ramiprilat/
NIH; DailyMed. Current Medication Information for Ramipril Capsule (Updated: June 2017). Available from, as of October 25, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d6d57158-e8f9-4c91-8317-0374e0c87d33
Plasma concentrations of ramipril and ramiprilat increase with increased dose, but are not strictly dose-proportional. The 24-hour AUC for ramiprilat, however, is dose-proportional over the 2.5 mg to 20 mg dose range. The absolute bioavailabilities of ramipril and ramiprilat were 28% and 44%, respectively, when 5 mg of oral ramipril was compared with the same dose of ramipril given intravenously.
NIH; DailyMed. Current Medication Information for Ramipril Capsule (Updated: June 2017). Available from, as of October 25, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d6d57158-e8f9-4c91-8317-0374e0c87d33
For more Absorption, Distribution and Excretion (Complete) data for Ramipril (7 total), please visit the HSDB record page.
Hepatic metabolism accounts for 75% of total ramipril metabolism. 25% of hepatic metabolism produces the active metabolite ramiprilat via liver esterase enzymes. 100% of renal metabolism converts ramipril to ramiprilat. Other metabolites, diketopiperazine ester, the diketopiperazine acid, and the glucuronides of ramipril and ramiprilat, are inactive.
Cleavage of the ester group (primarily in the liver) converts ramipril to its active diacid metabolite, ramiprilat. Peak plasma concentrations of ramiprilat are reached 2 to 4 hours after drug intake. The serum protein binding of ramipril is about 73% and that of ramiprilat about 56%; in vitro, these percentages are independent of concentration over the range of 0.01 ug/mL to 10 mcg/mL.
NIH; DailyMed. Current Medication Information for Ramipril Capsule (Updated: June 2017). Available from, as of October 25, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d6d57158-e8f9-4c91-8317-0374e0c87d33
After oral administration to dogs, ramipril is rapidly converted via de-esterification into ramiprilat. Bioavailability of ramiprilat after a dose of 0.25 mg/kg per day of ramipril is approximately 6.7%.
Plumb D.C. Veterinary Drug Handbook. 8th ed. (pocket). Ames, IA: Wiley-Blackwell, 2015., p. 1263
Ramipril is a prodrug and has little pharmacologic activity until hydrolyzed in the liver to ramiprilat.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017, p. 2098
Ramipril is almost completely metabolized to ramiprilat, which has about 6 times the angiotensin-converting enzyme (ACE) inhibitory activity of ramipril, and to the diketopiperazine ester, the diketopiperazine acid, and the glucuronides of ramipril and ramiprilat, all of which are inactive.
NIH; DailyMed. Current Medication Information for Ramipril Capsule (Updated: June 2017). Available from, as of October 25, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d6d57158-e8f9-4c91-8317-0374e0c87d33
Plasma concentrations of ramiprilat decline in a triphasic manner. Initial rapid decline represents distribution into tissues and has a half life of 2-4 hours. The half life of the apparent elimination phase is 9-18 hours, which is thought to represent clearance of free drug. The half-life of the terminal elimination phase is > 50 hours and thought to represent clearance of drug bound to ACE due to its slow dissociation. The half life of ramiprilat after multiple daily doses (MDDs) is dose-dependent, ranging from 13-17 hours with 5-10 mg MDDs to 27-36 hours for 2.5 mg MDDs.
Plasma concentrations of ramiprilat /metabolite of ramipril/ decline in a triphasic manner (initial rapid decline, apparent elimination phase, terminal elimination phase). The initial rapid decline, which represents distribution of the drug into a large peripheral compartment and subsequent binding to both plasma and tissue ACE, has a half-life of 2 to 4 hours. Because of its potent binding to ACE and slow dissociation from the enzyme, ramiprilat shows two elimination phases. The apparent elimination phase corresponds to the clearance of free ramiprilat and has a half-life of 9 to 18 hours. The terminal elimination phase has a prolonged half-life (>50 hours) and probably represents the binding/dissociation kinetics of the ramiprilat/ACE complex. It does not contribute to the accumulation of the drug. After multiple daily doses of ramipril 5 mg to 10 mg, the half-life of ramiprilat concentrations within the therapeutic range was 13 to 17 hours. /Ramiprilat/
NIH; DailyMed. Current Medication Information for Ramipril Capsule (Updated: June 2017). Available from, as of October 25, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d6d57158-e8f9-4c91-8317-0374e0c87d33
Ramipril inhibits the RAAS system by binding to and inhibiting ACE thereby preventing the conversion of angiotensin I to angiotensin II. As plasma levels of angiotensin II fall, less activation of the G-protein coupled receptors angiotensin receptor I (AT1R) and angiotensin receptor II (AT2R) occurs. AT1R mediates vasoconstriction, inflammation, fibrosis, and oxidative stress through a variety of signaling pathways. These include Gq coupling to the inositol triphosphate pathway, activation of phospholipases C, A2, and D which contribute to eicosanoid production, activation of Ca2+-dependent and MAP kinases, Gi and G12/13, and eventual activation of the Jak/STAT pathway leading to cell growth and production of extracellular matrix components. AT1R activation also leads to increased activity of membrane-bound NADH/NADPH oxidase which contributes to production of reactive oxygen species. Decreased activation of this receptor mediates the renoprotective, antihypertensive, and cardioprotective effects of ramipril by reducing inflammation and vasoconstriction. AT2R acts in opposition to the effects of AT1R by activating phosphotyrosine phosphatases which inhibit MAP kinases, inhibiting Ca2+ channel opening, and stimulating cGMP and nitric oxide production leading to vasodilation. These counteracting effects are shared by the Mas receptor which is activated by Ang(1-7), a subtype of angiotensin produced by plasma esterases from AngI or by ACE2 from AngII produced through a secondary pathway by tonin and cathepsin G. Ang(1-7) also activates AT2R although the bulk of its effect is mediated by MasR. ACE is also responsible for the breakdown of bradykinin. The resulting buildup of bradykinin due to ACE inhibition is thought to mediate the characteristic dry-cough as a side effect of ACE inhibitor medications.
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