Page last updated: 2024-12-06

fosinopril

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Description

Fosinopril: A phosphinic acid-containing angiotensin-converting enzyme inhibitor that is effective in the treatment of hypertension. It is a prodrug that is converted to its active metabolite fosinoprilat. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

fosinopril : A phosphinate ester-containing N-acyl derivative of (4S)-cyclohexyl-L-proline. It is used for the treatment of hypertension and heart failure. A pro-drug, it is hydrolysed in vivo to the corresponding phosphininc acid, fosinoprilat, which is the active metabolite. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID45357796
SCHEMBL ID197718
MeSH IDM0026315
PubMed CID9601226
CHEMBL ID3039598
SCHEMBL ID5928355
MeSH IDM0026315

Synonyms (32)

Synonym
fosenopril
l-proline, 4-cyclohexyl-1-(((2-methyl-1-(1-oxopropoxy)propoxy)(4-phenylbutyl)phosphinyl)acetyl)-, (1(s*(r*)),2alpha,4beta)-
l-proline, 4-cyclohexyl-1-(((2-methyl-1-(1-oxopropoxy)propoxy)(4-phenylbutyl)phosphinyl)acetyl)-, (2alpha,4beta)-
fosinopril [inn:ban]
98048-97-6
fosinopril
unii-r43d2573wo
r43d2573wo ,
AKOS015963652
SCHEMBL197718
DTXSID1023079 ,
(s)-4-cyclohexyl-1-(2-((2-methyl-1-propionyloxy-propoxy)-(4-phenyl-butyl)-phosphinoyl)-acetyl)-pyrrolidine-2-carboxylic acid
dtxcid003079
fosinoprilum
(2s,4s)-4-cyclohexyl-1-(2-((2-methyl-1-propionyloxy-propoxy)-(4-phenyl-butyl)-phosphinoyl)-acetyl)-pyrrolidine-2-carboxylic acid
BIDD:GT0229
fozitec
DB00492
fosinopril [mi]
fosinopril [orange book]
c09aa09
fosinopril [vandf]
(4s)-4-cyclohexyl-1-[2-[(r)-[(1s)-2-methyl-1-(1-oxopropoxy)propoxy](4-phenylbutyl)phosphinyl]acetyl]-l-proline
fosinopril [inn]
fosinopril [who-dd]
CHEMBL3039598
gtpl6456
SCHEMBL5928355
Q62007820
(s)-fosinopril
HY-B0690
CS-0009588

Research Excerpts

Toxicity

Fosinopril is a safe and effective inhibitor of ACE with a long duration of action on serum ACE activity. The very low incidence of clinical and laboratory adverse events, even among the oldest patients, confirms the safety of use.

ExcerptReferenceRelevance
" These data show that fosinopril is a safe and effective inhibitor of ACE with a long duration of action on serum ACE activity."( Pharmacokinetics, safety, and pharmacologic effects of fosinopril sodium, an angiotensin-converting enzyme inhibitor in healthy subjects.
Duchin, KL; Frantz, M; Manning, J; Tu, JI; Waclawski, AP; Willard, DA, 1991
)
0.28
"Pregnant women are advised against using angiotensin-converting enzyme (ACE) inhibitors due to reports of adverse effects on human fetuses."( Fosinopril treatment of pregnant rats: developmental toxicity, fetal angiotensin-converting enzyme inhibition, and fetal angiotensin II receptor regulation.
Forsyth, CS; Frank, AA; Grove, KL; Mayo, RJ; Speth, RC, 1995
)
0.29
" Based on the results obtained in these trials, both dose combinations of Fos/HCTZ taken once daily were safe and effective in the management of patients with mild-to-moderate hypertension."( Efficacy and safety of fosinopril/hydrochlorothiazide combinations on ambulatory blood pressure profiles in hypertension. Fosinopril/Hydrochlorothiazide Investigators.
Battikha, JP; Guthrie, R; Plesher, MM; Reggi, DR; Saini, RK, 1996
)
0.29
" The very low incidence of clinical and laboratory adverse events, even among the oldest patients, confirms the safety of use of fosinopril, predictive of good long-term compliance with treatment."( [Study of the efficacy and safety of fosinopril in general practice in 19,435 hypertensive patients (FLIGHT Study)].
Berdah, J; Guest, M; Salvador, M, 1998
)
0.3
" Fosinopril was well tolerated; serious adverse events occurred infrequently and were generally not attributed to fosinopril."( Is the extrapolated adult dose of fosinopril safe and effective in treating hypertensive children?
Berezny, K; Califf, RM; Cottrill, CM; Deitchman, D; Hazan, L; Hogg, R; Jenkins, RD; Kanani, P; Kilaru, R; Kozlova, L; Li, JS; Mattoo, TK; Portman, R; Weisman, I; Zharkova, L, 2004
)
0.32
"LOCM was less toxic to rat kidney than HOCM."( [Nephrotoxicity of high- and low-osmolar contrast media: Protective role of fosinopril or telmisartan in a rat model].
Duan, SB; Jiang, WL; Li, J; Li, YJ; Liu, FY; Liu, YH; Peng, YM; Wang, YH; Xu, XQ; Zou, Q, 2007
)
0.34
"5 million adverse drug reaction (ADR) reports for 8620 drugs/biologics that are listed for 1191 Coding Symbols for Thesaurus of Adverse Reaction (COSTAR) terms of adverse effects."( Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
Benz, RD; Contrera, JF; Kruhlak, NL; Matthews, EJ; Weaver, JL, 2004
)
0.32

Pharmacokinetics

Fosinopril and HCTZ in a combination tablet display pharmacokinetic profiles similar to those achieved when either drug is administered alone or when coadministered in separate tablets. No statistically significant differences were detected between healthy and hepatically impaired subjects.

ExcerptReferenceRelevance
" Serum aldosterone levels, ACE activity, and sitting blood pressure were determined, as were pharmacokinetic parameters of fosinoprilat, the active diacid of fosinopril."( Pharmacokinetics, safety, and pharmacologic effects of fosinopril sodium, an angiotensin-converting enzyme inhibitor in healthy subjects.
Duchin, KL; Frantz, M; Manning, J; Tu, JI; Waclawski, AP; Willard, DA, 1991
)
0.28
" Pharmacokinetic parameters including area under the serum concentration-time curve (AUC), peak serum concentration (Cmax) and time to peak concentration (tmax), as well as renal function, blood pressure, and plasma renin activity (PRA) and aldosterone levels, were determined on the first and last days of the study."( Comparison of the steady-state pharmacokinetics of fosinopril, lisinopril and enalapril in patients with chronic renal insufficiency.
Cutler, RE; Ford, NF; Parmer, RJ; Sica, DA, 1991
)
0.28
"4 h, Cmax of 182 ng."( Fosinopril pharmacokinetics and pharmacodynamics in chronic ambulatory peritoneal dialysis patients.
Davis, J; Duchin, KL; Fakhry, I; Gehr, TW; Grasela, DM; Sica, DA, 1991
)
0.28
" No statistically significant differences were detected in fosinoprilat pharmacokinetic values between healthy and hepatically impaired subjects."( Single-dose and steady-state pharmacokinetics of fosinopril and fosinoprilat in patients with hepatic impairment.
Ford, NF; Hammett, JL; Lasseter, KC; Manning, J; Raymond, R; Van Harken, DR, 1995
)
0.29
" Pharmacokinetic variables of the patients were similar to those in patients with moderate to severe renal dysfunction."( The pharmacokinetics and pharmacodynamics of fosinopril in haemodialysis patients.
Duchin, KL; Gehr, TW; Grasela, DM; Sica, DA, 1993
)
0.29
"hr/mL and Cmax was 143."( Invasive pharmacodynamics of fosinopril in patients with congestive heart failure.
Ford, NF; Fulmor, IE; Hui, KK; Natarajan, C; Smith, RA, 1995
)
0.29
" The oral half-life of fosinoprilat was significantly longer than the intravenous half-life for both the patients with CHF and normal subjects, without statistically significant differences between the study groups."( Fosinopril: pharmacokinetics and pharmacodynamics in congestive heart failure.
Delaney, C; Garland, WT; Kostis, JB; Liao, WC; Norton, J, 1995
)
0.29
" Furthermore, the available evidence suggests that the pharmacokinetic variables of fosinoprilat in patients receiving haemodialysis were similar to those in patients with moderate to severe renal dysfunction."( Fosinopril. Clinical pharmacokinetics and clinical potential.
Himeno, H; Hiroto, S; Minamisawa, K; Naruse, M; Shionoiri, H; Takasaki, I; Ueda, S, 1997
)
0.3
" Pharmacokinetic parameters were calculated by fitting the plasma or serum concentrations to a three-compartment model."( Pharmacokinetics of fosinoprilat in Chinese and whites after intravenous administration.
Chu, KM; Ding, PY; Hu, OY; Huang, CS; Hwang, GM, 1997
)
0.3
"To evaluate the pharmacokinetic interaction and bioequivalence of a combination formulation of the angiotensin-converting enzyme inhibitor fosinopril and the diuretic hydrochlorothiazide (HCTZ)."( Fosinopril and hydrochlorothiazide combination versus individual components: lack of a pharmacokinetic interaction.
Brennan, J; Chang, SY; Delaney, CL; Liao, W; Morgenthien, EA; Much, DR; Stouffer, BC; Uderman, HD; VanHarken, D; Weaver, J, 1999
)
0.3
"Fosinopril and HCTZ in a combination tablet display pharmacokinetic profiles similar to those achieved when either drug is administered alone or when coadministered in separate tablets."( Fosinopril and hydrochlorothiazide combination versus individual components: lack of a pharmacokinetic interaction.
Brennan, J; Chang, SY; Delaney, CL; Liao, W; Morgenthien, EA; Much, DR; Stouffer, BC; Uderman, HD; VanHarken, D; Weaver, J, 1999
)
0.3
" Non-compartmental pharmacokinetic parameters of fosinoprilat and HCTZ were determined from blood and urine samples obtained over 48 h starting on Day 1 (single dose) and Day 5 (steady state): maximum serum concentration (Cmax ), time to maximum serum concentration (tmax ), area under the serum concentration-time curve during the dosing interval (AUC), cumulative urinary excretion (CUE) and the accumulation index (AI; ratio of AUC-day 5/AUC-day 1)."( Fosinopril/hydrochlorothiazide: single dose and steady-state pharmacokinetics and pharmacodynamics.
Lins, R; Mangold, B; O'Grady, P; Yee, KF, 1999
)
0.3
"Fosinoprilat pharmacokinetic parameters on day 1 in renally impaired vs normal patients: Cmax=387+/-0."( Fosinopril/hydrochlorothiazide: single dose and steady-state pharmacokinetics and pharmacodynamics.
Lins, R; Mangold, B; O'Grady, P; Yee, KF, 1999
)
0.3
"In renally impaired subjects fosinopril and HCTZ can be coadministered without undue increases in fosinoprilat concentrations or any clinically significant pharmacodynamic effects."( Fosinopril/hydrochlorothiazide: single dose and steady-state pharmacokinetics and pharmacodynamics.
Lins, R; Mangold, B; O'Grady, P; Yee, KF, 1999
)
0.3
" Samples of blood were collected for determination of pharmacokinetic parameters."( Comparison of the pharmacokinetics of fosinoprilat with enalaprilat and lisinopril in patients with congestive heart failure and chronic renal insufficiency.
Caspi, A; Greenbaum, R; Liao, WC; Mangold, B; Nouriel, H; O'Grady, P; Paz, R; Sclarovsky, S; Yee, KF; Zucchelli, P, 2000
)
0.31
" Standard pharmacokinetics, including AUC, Cmax Tmax, T 1/2, Vss, bioavailability, total clearance, and renal and nonrenal clearance, were determined as well as pharmacodynamic effects on angiotensin-converting enzyme (ACE) activity."( Fosinopril: pharmacokinetics and pharmacodynamics in Chinese subjects.
Chang, A; Chu, KM; Delaney, CL; Ding, PY; Hu, OY; Huang, GM; Jemal, M; Jeng, JJ; Liao, WC; MacAskill, M; Smith, R; Yang, BC, 1999
)
0.3

Compound-Compound Interactions

ExcerptReferenceRelevance
"To investigate the effects of fosinopril sodium pre-treatment combined with ischemic postconditioning on rat serum and myocardial oxidative stress and proinflammatory cytokines post ischemia/reperfusion."( [Protective effect of fosinopril sodium pretreatment combined with ischemic postconditioning on rat heart underwent myocardial ischemia/reperfusion injury].
Chen, KJ; Liu, JG; Shi, DZ; Wang, CL; Zhang, DW; Zhang, L, 2010
)
0.36

Bioavailability

Fosinopril is one of the most hydrophobic substances among the angiotensin-converting enzyme inhibitors, exhibiting low water solubility and poor bioavailability following oral administration. The RIA has been used routinely in support of the bioavailability and pharmacokinetic studies of fosinipril in humans.

ExcerptReferenceRelevance
" After oral 14C-fosinopril (10 mg), plasma kinetics and bioavailability of fosinoprilat were similar for the three groups of renally impaired patients."( Pharmacokinetics of fosinopril in patients with various degrees of renal function.
Chan, D; Duchin, KL; Hui, KK; Kramer, PK; Kripalani, KJ; Yanagawa, N, 1991
)
0.28
" The RIA has been used routinely in support of the bioavailability and pharmacokinetic studies of fosinopril in humans."( A radioimmunoassay for SQ 27,519, the active phosphinic acid-carboxylic diacid of the prodrug fosinopril in human serum.
Brennan, J; Eckelman, WC; Stouffer, B; Tu, JI, 1990
)
0.28
" The prodrug enalapril is well absorbed from rat jejunum, whereas the parent drug, enalaprilat, is poorly absorbed."( Passive and carrier-mediated intestinal absorption components of two angiotensin converting enzyme (ACE) inhibitor prodrugs in rats: enalapril and fosinopril.
Amidon, GL; Friedman, DI, 1989
)
0.28
" 5 For the solution and capsule doses, respectively, the oral absorption of fosinopril sodium averaged 32% and 36% and the oral bioavailability of SQ 27, 519 averaged 25% and 29%."( Disposition of fosinopril sodium in healthy subjects.
Duchin, KL; Everett, DW; Frantz, M; Morrison, RA; Singhvi, SM; Willard, DA, 1988
)
0.27
" Drug disposition studies in rats, dogs, and monkeys have demonstrated that the method can be readily adapted to any ACE inhibitor and is suitable for determining drug bioavailability and pharmacokinetics."( Radioenzymatic assay of angiotensin-converting enzyme inhibitors in plasma and urine.
Alpaugh, WC; Stauber, KL; Swanson, BN; Weinstein, SH, 1985
)
0.27
" Following oral administration of 14C-fosinopril, mean Cmax, time to maximum plasma concentration (tmax), and fosinoprilat bioavailability values were 197 ng."( The pharmacokinetics and pharmacodynamics of fosinopril in haemodialysis patients.
Duchin, KL; Gehr, TW; Grasela, DM; Sica, DA, 1993
)
0.29
" Absolute bioavailability was approximately 29%."( Fosinopril: pharmacokinetics and pharmacodynamics in congestive heart failure.
Delaney, C; Garland, WT; Kostis, JB; Liao, WC; Norton, J, 1995
)
0.29
" Finally, the possibility that an impaired prostacyclin synthesis or bioavailability is involved in the pathogenesis of the diabetic nephropathy in this model underlies our results."( Effects of cicaprost and fosinopril on the progression of rat diabetic nephropathy.
García-Robles, R; Rábano, A; Ruilope, LM; Villa, E, 1997
)
0.3
" Bioavailability was 22."( Fosinopril: pharmacokinetics and pharmacodynamics in Chinese subjects.
Chang, A; Chu, KM; Delaney, CL; Ding, PY; Hu, OY; Huang, GM; Jemal, M; Jeng, JJ; Liao, WC; MacAskill, M; Smith, R; Yang, BC, 1999
)
0.3
" Renal affection in CCF is primarily caused by activation of the system rennin-angiotensin, inflammation, disturbed bioavailability of nitric oxide, hyperactivation of the sympathetic nervous system."( [Fosinopril in the treatment of cardiorenal syndrome in chronic cardiac failure].
Tereshchenko, SN; Zhirov, IV, 2009
)
0.35
"Fosinopril is one of the most hydrophobic substances among the angiotensin-converting enzyme inhibitors, exhibiting low water solubility and poor bioavailability following oral administration."( Fosinopril-cyclodextrin inclusion complexes: phase solubility and physicochemical analysis.
Bojiţă, M; Drăgan, L; Sbârcea, L; Szabadai, Z; Trandafirescu, C; Udrescu, L, 2011
)
0.37

Dosage Studied

Blacks demonstrated a significant dose response to fosinopril. In vivo studies were conducted, in which FVB wild-type and FVB/Mrp2(-/-) mice were dosed with fosInopril and the known MRP2 substrate methotrexate.

ExcerptRelevanceReference
" Angiotensin-converting enzyme (ACE) inhibitor therapy routinely requires dosage adjustment in the instance of renal insufficiency, as all currently marketed ACE inhibitors are renally eliminated."( Kinetics of angiotensin-converting enzyme inhibitors in renal failure.
Sica, DA, 1992
)
0.28
" This dual elimination allows for the administration of fosinopril using the same starting dosage to any patient, regardless of renal function."( Fosinopril: a new generation of angiotensin-converting enzyme inhibitors.
Weber, MA, 1992
)
0.28
" Dosage reductions may not be necessary in the majority of dialysis patients."( Fosinopril pharmacokinetics and pharmacodynamics in chronic ambulatory peritoneal dialysis patients.
Davis, J; Duchin, KL; Fakhry, I; Gehr, TW; Grasela, DM; Sica, DA, 1991
)
0.28
" In ex vivo dose-response and time-course studies, the inhibitory effects of the seven drugs on tissue ACEs and their relative distributions to SHR tissues were compared following oral administration."( Comparisons in vitro, ex vivo, and in vivo of the actions of seven structurally diverse inhibitors of angiotensin converting enzyme (ACE).
Cushman, DW; DeForrest, JM; Fung, WC; Grover, GJ; Harvey, CM; Mitch, SL; Scalese, RJ; Wang, FL, 1989
)
0.28
" Fosinopril was administered at a dosage of 10 mg once daily for 14 days."( Single-dose and steady-state pharmacokinetics of fosinopril and fosinoprilat in patients with hepatic impairment.
Ford, NF; Hammett, JL; Lasseter, KC; Manning, J; Raymond, R; Van Harken, DR, 1995
)
0.29
" Preliminary studies indicated that only fosinopril (50 mg/kg) temporarily decreased mean arterial pressure, while after chronic dosing fosinopril and captopril (50 mg/kg) were ineffective."( Inhibitors of angiotensin converting enzyme decrease early atherosclerosis in hyperlipidemic hamsters. Fosinopril reduces plasma cholesterol and captopril inhibits macrophage-foam cell accumulation independently of blood pressure and plasma lipids.
Aberg, G; Grove, RI; Kowala, MC, 1994
)
0.29
" After this period, patients with DBP > 95mmHg had the dosage, once daily, increased to 20mg, while the others were maintained with the same dosage for six more weeks."( [Treatment of mild and moderate hypertension with fosinopril. Comparison of adverse effects with other antihypertensive agents].
Franco, RJ; Martín, LC; Velasco-Cornejo, IF, 1994
)
0.29
" Pilot studies confirmed that this dosage produced significant inhibition of LV tissue ACE in vivo."( Angiotensin-converting enzyme inhibition prolongs survival and modifies the transition to heart failure in rats with pressure overload hypertrophy due to ascending aortic stenosis.
Benedict, CR; Douglas, PS; George, D; Kagaya, Y; Litwin, SE; Lorell, BH; Schoen, FJ; Schunkert, H; Weinberg, EO, 1994
)
0.29
" Dosage modifications or supplemental dosing following dialysis are unnecessary."( The pharmacokinetics and pharmacodynamics of fosinopril in haemodialysis patients.
Duchin, KL; Gehr, TW; Grasela, DM; Sica, DA, 1993
)
0.29
" Neither peak nor trough blood pressure changes showed a clear dose-response relationship."( Fosinopril monotherapy: relationship between blood pressure reduction and time of administration.
Alpin, PG; Ford, NF; Fulmor, IE; Herron, JM; Nichola, PS, 1993
)
0.29
" This means that an adjustment in either the dosage and/or the administration interval is needed in patients with moderate to severe renal dysfunction, in order to reduce drug accumulation and the possibility of an excessive decrease in blood pressure or other adverse effects."( Fosinopril. Clinical pharmacokinetics and clinical potential.
Himeno, H; Hiroto, S; Minamisawa, K; Naruse, M; Shionoiri, H; Takasaki, I; Ueda, S, 1997
)
0.3
" Chinese may require a lower fosinoprilat dosage to obtain plasma concentrations similar to whites after intravenous administration."( Pharmacokinetics of fosinoprilat in Chinese and whites after intravenous administration.
Chu, KM; Ding, PY; Hu, OY; Huang, CS; Hwang, GM, 1997
)
0.3
"A drug-excipient compatibility screening model was developed by which potential stability problems due to interactions of drug substances with excipients in solid dosage forms can be predicted."( Selection of solid dosage form composition through drug-excipient compatibility testing.
Fakes, MG; Ghoshal, RN; Morris, KR; Ranadive, SA; Serajuddin, AT; Thakur, AB; Varia, SA, 1999
)
0.3
" Non-compartmental pharmacokinetic parameters of fosinoprilat and HCTZ were determined from blood and urine samples obtained over 48 h starting on Day 1 (single dose) and Day 5 (steady state): maximum serum concentration (Cmax ), time to maximum serum concentration (tmax ), area under the serum concentration-time curve during the dosing interval (AUC), cumulative urinary excretion (CUE) and the accumulation index (AI; ratio of AUC-day 5/AUC-day 1)."( Fosinopril/hydrochlorothiazide: single dose and steady-state pharmacokinetics and pharmacodynamics.
Lins, R; Mangold, B; O'Grady, P; Yee, KF, 1999
)
0.3
"To compare the serum pharmacokinetics of fosinoprilat with enalaprilat and lisinopril after 1 and 10 days of dosing with fosinopril, enalapril and lisinopril."( Comparison of the pharmacokinetics of fosinoprilat with enalaprilat and lisinopril in patients with congestive heart failure and chronic renal insufficiency.
Caspi, A; Greenbaum, R; Liao, WC; Mangold, B; Nouriel, H; O'Grady, P; Paz, R; Sclarovsky, S; Yee, KF; Zucchelli, P, 2000
)
0.31
" A low dosage of fosinopril (5 mg/kg/d) that was still adequate to reduce their plasma ACE activity and LDL propensity to lipid peroxidation was insufficient to lower their blood pressure."( The angiotensin-converting enzyme inhibitor, fosinopril, and the angiotensin II receptor antagonist, losartan, inhibit LDL oxidation and attenuate atherosclerosis independent of lowering blood pressure in apolipoprotein E deficient mice.
Attias, J; Breslow, JL; Brodsky, S; Coleman, R; Hayek, T; Keidar, S; Smith, J, 1999
)
0.3
" Lineweaver-Burk, Dixon, and dose-response analyses revealed that GlySar uptake was competitively inhibited by fosinopril in both Caco-2 (K(i), 35."( Mechanism of intestinal absorption and renal reabsorption of an orally active ace inhibitor: uptake and transport of fosinopril in cell cultures.
Hopfer, U; Shen, H; Shu, C; Smith, DE, 2001
)
0.31
"6% after oral dosing and 42."( Fosinopril: pharmacokinetics and pharmacodynamics in Chinese subjects.
Chang, A; Chu, KM; Delaney, CL; Ding, PY; Hu, OY; Huang, GM; Jemal, M; Jeng, JJ; Liao, WC; MacAskill, M; Smith, R; Yang, BC, 1999
)
0.3
" The drug's effect as well as adverse effects should be actively sought, and dosage alterations made in order to enhance the drug's effect."( Introduction to monitoring. What is what you prescribed actually doing?
George, A; Shakib, S, 2003
)
0.32
"We evaluated the efficacy, safety, and dose-response relationship of fosinopril in children aged 6 to 16 years with hypertension or high-normal blood pressure with an associated medical condition requiring treatment."( Is the extrapolated adult dose of fosinopril safe and effective in treating hypertensive children?
Berezny, K; Califf, RM; Cottrill, CM; Deitchman, D; Hazan, L; Hogg, R; Jenkins, RD; Kanani, P; Kilaru, R; Kozlova, L; Li, JS; Mattoo, TK; Portman, R; Weisman, I; Zharkova, L, 2004
)
0.32
" Blacks, however, demonstrated a significant dose response to fosinopril; those who received the low dosage had a 5 mm Hg decrease in SBP, and those who received the high dosage had a mean 13 mm Hg decrease in SBP."( Racial differences are seen in blood pressure response to fosinopril in hypertensive children.
Benjamin, DK; Berezny, KY; Califf, RM; Deitchman, D; Hazan, L; Hogg, R; Kay, JD; Kilaru, R; Li, JS; Menon, S; Portman, R, 2006
)
0.33
" These methods hold their accuracy and precision well when applied to the determination of ramipril, enalapril maleate and fosinopril in their dosage forms."( Spectrophotometric and atomic absorption determination of ramipril, enalapril maleate and fosinopril through ternary complex formation with molybdenum (V)-thiocyanate (Mo(V)-SCN).
Abd-Alaty, NM; Baraka, MM; El-Sadek, M; Moussa, EM, 2008
)
0.35
" The 35 patients were randomly assigned into 2 groups: A routine dosage fosinopril group received 10 mg once daily and a middle dosage group received 10 mg twice a day for 10 weeks."( [Plasma tissue factor and serum angiotensin II and the therapeutic effect of different dosages of fosinopril on chronic heart failure].
Ma, Q; Ning, Y; Sun, M; Wu, S; Yang, L; Yang, T, 2009
)
0.35
" The middle dosage group changed more than the routine dosage group (P<0."( [Plasma tissue factor and serum angiotensin II and the therapeutic effect of different dosages of fosinopril on chronic heart failure].
Ma, Q; Ning, Y; Sun, M; Wu, S; Yang, L; Yang, T, 2009
)
0.35
" Fosinopril can greatly improve cardiac function and antagonize prethrobotic state,and the therapeutic effect improves with the dosage increase."( [Plasma tissue factor and serum angiotensin II and the therapeutic effect of different dosages of fosinopril on chronic heart failure].
Ma, Q; Ning, Y; Sun, M; Wu, S; Yang, L; Yang, T, 2009
)
0.35
"Models of acute myocardial infarction (AMI) were produced by ligation of left anterior descending coronary artery, 24 hours after operation the rats were randomly divided into control and experiment groups, then respectively administrated with NS, fosinopril and low, middle and high dosage of PNS for four consecutive weeks."( [Effects of Panax notoginseng saponins on ACE2 and TNF-alpha in rats with post-myocardial infarction-ventricular remodeling].
Deng, ZJ; Fu, YH; Guo, JW; Li, LM; Liu, RX; Pan, JQ; Qiu, GQ; Yang, M, 2010
)
0.36
" In vivo studies were conducted, in which FVB wild-type and FVB/Mrp2(-/-) mice were dosed with fosinopril and the known MRP2 substrate methotrexate, and tissues collected after 1 h."( Mrp2 is involved in the efflux and disposition of fosinopril.
Bain, LJ; Green, BR, 2013
)
0.39
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Protein Targets (1)

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Angiotensin-converting enzyme Homo sapiens (human)IC50 (µMol)0.00100.00010.533610.0000AID39767
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (56)

Processvia Protein(s)Taxonomy
response to hypoxiaAngiotensin-converting enzyme Homo sapiens (human)
kidney developmentAngiotensin-converting enzyme Homo sapiens (human)
blood vessel remodelingAngiotensin-converting enzyme Homo sapiens (human)
angiotensin maturationAngiotensin-converting enzyme Homo sapiens (human)
regulation of renal output by angiotensinAngiotensin-converting enzyme Homo sapiens (human)
neutrophil mediated immunityAngiotensin-converting enzyme Homo sapiens (human)
antigen processing and presentation of peptide antigen via MHC class IAngiotensin-converting enzyme Homo sapiens (human)
regulation of systemic arterial blood pressure by renin-angiotensinAngiotensin-converting enzyme Homo sapiens (human)
proteolysisAngiotensin-converting enzyme Homo sapiens (human)
spermatogenesisAngiotensin-converting enzyme Homo sapiens (human)
female pregnancyAngiotensin-converting enzyme Homo sapiens (human)
regulation of blood pressureAngiotensin-converting enzyme Homo sapiens (human)
male gonad developmentAngiotensin-converting enzyme Homo sapiens (human)
response to xenobiotic stimulusAngiotensin-converting enzyme Homo sapiens (human)
embryo development ending in birth or egg hatchingAngiotensin-converting enzyme Homo sapiens (human)
post-transcriptional regulation of gene expressionAngiotensin-converting enzyme Homo sapiens (human)
negative regulation of gene expressionAngiotensin-converting enzyme Homo sapiens (human)
substance P catabolic processAngiotensin-converting enzyme Homo sapiens (human)
bradykinin catabolic processAngiotensin-converting enzyme Homo sapiens (human)
regulation of smooth muscle cell migrationAngiotensin-converting enzyme Homo sapiens (human)
regulation of vasoconstrictionAngiotensin-converting enzyme Homo sapiens (human)
animal organ regenerationAngiotensin-converting enzyme Homo sapiens (human)
response to nutrient levelsAngiotensin-converting enzyme Homo sapiens (human)
response to lipopolysaccharideAngiotensin-converting enzyme Homo sapiens (human)
mononuclear cell proliferationAngiotensin-converting enzyme Homo sapiens (human)
response to laminar fluid shear stressAngiotensin-converting enzyme Homo sapiens (human)
angiotensin-activated signaling pathwayAngiotensin-converting enzyme Homo sapiens (human)
vasoconstrictionAngiotensin-converting enzyme Homo sapiens (human)
hormone metabolic processAngiotensin-converting enzyme Homo sapiens (human)
hormone catabolic processAngiotensin-converting enzyme Homo sapiens (human)
eating behaviorAngiotensin-converting enzyme Homo sapiens (human)
positive regulation of apoptotic processAngiotensin-converting enzyme Homo sapiens (human)
peptide catabolic processAngiotensin-converting enzyme Homo sapiens (human)
positive regulation of vasoconstrictionAngiotensin-converting enzyme Homo sapiens (human)
negative regulation of glucose importAngiotensin-converting enzyme Homo sapiens (human)
regulation of synaptic plasticityAngiotensin-converting enzyme Homo sapiens (human)
lung alveolus developmentAngiotensin-converting enzyme Homo sapiens (human)
amyloid-beta metabolic processAngiotensin-converting enzyme Homo sapiens (human)
arachidonic acid secretionAngiotensin-converting enzyme Homo sapiens (human)
positive regulation of neurogenesisAngiotensin-converting enzyme Homo sapiens (human)
heart contractionAngiotensin-converting enzyme Homo sapiens (human)
regulation of angiotensin metabolic processAngiotensin-converting enzyme Homo sapiens (human)
hematopoietic stem cell differentiationAngiotensin-converting enzyme Homo sapiens (human)
angiogenesis involved in coronary vascular morphogenesisAngiotensin-converting enzyme Homo sapiens (human)
cellular response to glucose stimulusAngiotensin-converting enzyme Homo sapiens (human)
response to dexamethasoneAngiotensin-converting enzyme Homo sapiens (human)
cell proliferation in bone marrowAngiotensin-converting enzyme Homo sapiens (human)
regulation of heart rate by cardiac conductionAngiotensin-converting enzyme Homo sapiens (human)
negative regulation of calcium ion importAngiotensin-converting enzyme Homo sapiens (human)
response to thyroid hormoneAngiotensin-converting enzyme Homo sapiens (human)
blood vessel diameter maintenanceAngiotensin-converting enzyme Homo sapiens (human)
regulation of hematopoietic stem cell proliferationAngiotensin-converting enzyme Homo sapiens (human)
negative regulation of gap junction assemblyAngiotensin-converting enzyme Homo sapiens (human)
cellular response to aldosteroneAngiotensin-converting enzyme Homo sapiens (human)
positive regulation of peptidyl-cysteine S-nitrosylationAngiotensin-converting enzyme Homo sapiens (human)
positive regulation of systemic arterial blood pressureAngiotensin-converting enzyme Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (16)

Processvia Protein(s)Taxonomy
endopeptidase activityAngiotensin-converting enzyme Homo sapiens (human)
carboxypeptidase activityAngiotensin-converting enzyme Homo sapiens (human)
metalloendopeptidase activityAngiotensin-converting enzyme Homo sapiens (human)
calmodulin bindingAngiotensin-converting enzyme Homo sapiens (human)
peptidase activityAngiotensin-converting enzyme Homo sapiens (human)
metallopeptidase activityAngiotensin-converting enzyme Homo sapiens (human)
exopeptidase activityAngiotensin-converting enzyme Homo sapiens (human)
tripeptidyl-peptidase activityAngiotensin-converting enzyme Homo sapiens (human)
peptidyl-dipeptidase activityAngiotensin-converting enzyme Homo sapiens (human)
zinc ion bindingAngiotensin-converting enzyme Homo sapiens (human)
chloride ion bindingAngiotensin-converting enzyme Homo sapiens (human)
mitogen-activated protein kinase kinase bindingAngiotensin-converting enzyme Homo sapiens (human)
bradykinin receptor bindingAngiotensin-converting enzyme Homo sapiens (human)
mitogen-activated protein kinase bindingAngiotensin-converting enzyme Homo sapiens (human)
metallodipeptidase activityAngiotensin-converting enzyme Homo sapiens (human)
heterocyclic compound bindingAngiotensin-converting enzyme Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (10)

Processvia Protein(s)Taxonomy
extracellular spaceAngiotensin-converting enzyme Homo sapiens (human)
extracellular regionAngiotensin-converting enzyme Homo sapiens (human)
extracellular spaceAngiotensin-converting enzyme Homo sapiens (human)
lysosomeAngiotensin-converting enzyme Homo sapiens (human)
endosomeAngiotensin-converting enzyme Homo sapiens (human)
plasma membraneAngiotensin-converting enzyme Homo sapiens (human)
external side of plasma membraneAngiotensin-converting enzyme Homo sapiens (human)
basal plasma membraneAngiotensin-converting enzyme Homo sapiens (human)
brush border membraneAngiotensin-converting enzyme Homo sapiens (human)
extracellular exosomeAngiotensin-converting enzyme Homo sapiens (human)
sperm midpieceAngiotensin-converting enzyme Homo sapiens (human)
plasma membraneAngiotensin-converting enzyme Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (55)

Assay IDTitleYearJournalArticle
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID588220Literature-mined public compounds from Kruhlak et al phospholipidosis modelling dataset2008Toxicology mechanisms and methods, , Volume: 18, Issue:2-3
Development of a phospholipidosis database and predictive quantitative structure-activity relationship (QSAR) models.
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588219FDA HLAED, gamma-glutamyl transferase (GGT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID186841Decreased Mean arterial pressure (MAP) in rat after single oral dose of 30 umol/kg1997Journal of medicinal chemistry, May-23, Volume: 40, Issue:11
Dual metalloprotease inhibitors: mercaptoacetyl-based fused heterocyclic dipeptide mimetics as inhibitors of angiotensin-converting enzyme and neutral endopeptidase.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID588218FDA HLAED, lactate dehydrogenase (LDH) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID588217FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588214FDA HLAED, liver enzyme composite activity2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID588215FDA HLAED, alkaline phosphatase increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID689959Tmax in healthy human at 10 mg dosed as single daily dose2011Journal of medicinal chemistry, Sep-08, Volume: 54, Issue:17
Remarkable potential of the α-aminophosphonate/phosphinate structural motif in medicinal chemistry.
AID689962Cmax in healthy human at 10 mg dosed as single daily dose2011Journal of medicinal chemistry, Sep-08, Volume: 54, Issue:17
Remarkable potential of the α-aminophosphonate/phosphinate structural motif in medicinal chemistry.
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID689960Reduction in diastolic blood pressure in hypertensive patient receiving 10 to 40 mg/day, po dosed as single or multiple dose2011Journal of medicinal chemistry, Sep-08, Volume: 54, Issue:17
Remarkable potential of the α-aminophosphonate/phosphinate structural motif in medicinal chemistry.
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588216FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID689958AUC in healthy human at 10 mg dosed as single daily dose2011Journal of medicinal chemistry, Sep-08, Volume: 54, Issue:17
Remarkable potential of the α-aminophosphonate/phosphinate structural motif in medicinal chemistry.
AID689983Reduction in systolic blood pressure in hypertensive patient receiving 10 to 40 mg/day, po dosed as single or multiple dose2011Journal of medicinal chemistry, Sep-08, Volume: 54, Issue:17
Remarkable potential of the α-aminophosphonate/phosphinate structural motif in medicinal chemistry.
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID689963Drug absorption in healthy human at 10 mg dosed as single daily dose2011Journal of medicinal chemistry, Sep-08, Volume: 54, Issue:17
Remarkable potential of the α-aminophosphonate/phosphinate structural motif in medicinal chemistry.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID39767Inhibitory activity against angiotensin I converting enzyme (ACE)2000Journal of medicinal chemistry, Feb-10, Volume: 43, Issue:3
Protease inhibitors: current status and future prospects.
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID689961Reduction in arterial blood pressure in hypertensive patient receiving 10 to 40 mg/day, po dosed as single or multiple dose2011Journal of medicinal chemistry, Sep-08, Volume: 54, Issue:17
Remarkable potential of the α-aminophosphonate/phosphinate structural motif in medicinal chemistry.
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588990Inhibitors of transporters of clinical importance in the absorption and disposition of drugs, PEPT22010Nature reviews. Drug discovery, Mar, Volume: 9, Issue:3
Membrane transporters in drug development.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (421)

TimeframeStudies, This Drug (%)All Drugs %
pre-199011 (2.61)18.7374
1990's183 (43.47)18.2507
2000's159 (37.77)29.6817
2010's57 (13.54)24.3611
2020's11 (2.61)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials154 (35.57%)5.53%
Trials0 (0.00%)5.53%
Reviews28 (6.47%)6.00%
Reviews3 (30.00%)6.00%
Case Studies32 (7.39%)4.05%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Observational0 (0.00%)0.25%
Other219 (50.58%)84.16%
Other7 (70.00%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (15)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Prevention of Renal and Vascular Endstage Disease Intervention Trial [NCT03073018]Phase 3864 participants (Actual)Interventional1998-04-30Completed
The Effect of Metformin on the Correlation Between Hyperinsulinemia and Hypertension [NCT01342614]140 participants (Actual)Interventional2006-05-31Completed
Association Between Angiotensin Converting Enzyme Inhibitor or Angiotensin Receptor Blocker Use and COVID-19 Severity and Mortality Among US Veterans [NCT04467931]22,213 participants (Actual)Observational2020-01-19Completed
ACE-inhibition and Mechanisms of Skeletal Muscle Weakness in Chronic Obstructive Pulmonary Disease [NCT01014338]Phase 480 participants (Actual)Interventional2009-10-31Completed
A Bioequivalence Study of Test and Reference Fosinopril Sodium/ Hydrochlorothiazide 20/ 12.5 mg Tablets Under Non-Fasting Conditions [NCT00778713]33 participants (Actual)Interventional2003-03-31Completed
Comparison of Efficacy and Safety Between Benidipine and Hydrochlorothiazide in Fosinopril Treated Chronic Kidney Disease Patients With Hypertension: a Randomized Controlled Trial [NCT02646397]Phase 4508 participants (Anticipated)Interventional2016-02-29Not yet recruiting
[NCT00051389]Phase 20 participants Interventional2002-02-28Completed
NT-proBNP Selected PreventiOn of Cardiac eveNts in a populaTion of dIabetic Patients Without A History of Cardiac Disease: a Prospective Randomized Trial [NCT02817360]Phase 42,400 participants (Anticipated)Interventional2016-02-29Recruiting
The Objective of This Study is to Compare the Relative Bioavailability of Fosinopril Sodium 40 mg Tablets (Ranbaxy Laboratories Limited, Lot No. 1238312) With That of Monopril® (Bristol-Myers Squibb, Lot No. 1D47960), in Healthy Adult Subjects Under Fasti [NCT00776334]40 participants (Actual)Interventional2002-10-31Completed
A Bioequivalence Study of Test and Reference Fosinopril Sodium/ Hydrochlorothiazide 20/12.5 mg Tablets Under Fasting Conditions [NCT00777972]34 participants (Actual)Interventional2003-03-31Completed
The Objective of This Study is to Compare the Relative Bioavailability of Fosinopril Sodium 40 mg Tablets (Ranbaxy Laboratories Limited, Lot No. 1238312) With That of Monopril® in Healthy Adult Subjects Under Non-Fasting Conditions [NCT00776672]24 participants (Actual)Interventional2002-10-31Completed
Multi-Center,Double-Blind,Randomized,Controlled Clinical Trial of Fosinopril and/or Losartan in Patients With Chronic Kidney Disease Stage 3 [NCT00565396]400 participants (Anticipated)Interventional2004-09-30Active, not recruiting
Eplerenone, ACE Inhibition and Albuminuria [NCT00315016]Phase 230 participants (Actual)Interventional2007-01-31Completed
Chronic Angiotensin Converting Enzyme Inhibitors in Intermediate Risk Surgery: A Randomized, Single-Blinded Study [NCT01669434]Phase 4291 participants (Actual)Interventional2015-06-01Completed
The CORONAvirus Disease 2019 Angiotensin Converting Enzyme Inhibitor/Angiotensin Receptor Blocker InvestigatiON (CORONACION) Randomized Clinical Trial [NCT04330300]Phase 42,414 participants (Anticipated)Interventional2020-04-30Suspended(stopped due to Challenges with funding and very low incidence of COVID-19 at Irish study site)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT01669434 (6) [back to overview]Acute Renal Failure
NCT01669434 (6) [back to overview]Low Blood Pressure Subgroup
NCT01669434 (6) [back to overview]Number of Participants With Interoperative Hypotension
NCT01669434 (6) [back to overview]Older Age Subgroup
NCT01669434 (6) [back to overview]Postoperative Hypertension
NCT01669434 (6) [back to overview]Postoperative Hypotension

Acute Renal Failure

Creatinine increase of more than 0.3 mg/dl or more than 50% from preoperative level (NCT01669434)
Timeframe: Arrival in post-anesthesia care unit (PACU) to hospital discharge, an expected average of 4 days.

InterventionParticipants (Count of Participants)
ACEI Omission6
ACEI Continuation10

[back to top]

Low Blood Pressure Subgroup

Only patients with systolic blood pressure less than 110 at preoperative evaluation will be included in this analysis. The outcome is the same as the primary outcome: Intraoperative Systolic Blood Pressure under 80 mmHg. (NCT01669434)
Timeframe: During anesthesia, an expected average of 3 hours.

InterventionParticipants (Count of Participants)
ACEI Omission4
ACEI Continuation2

[back to top]

Number of Participants With Interoperative Hypotension

Number of Participants with Interoperative Hypotension (systolic blood pressure under 80 mmHg) (NCT01669434)
Timeframe: During anesthesia, an expected average of 3 hours.

InterventionParticipants (Count of Participants)
ACEI Omission76
ACEI Continuation95

[back to top]

Older Age Subgroup

Only patients above the age of 64 will be included in this analysis. The outcome is the same as the primary outcome: Intraoperative Systolic Blood Pressure under 80 mmHg (NCT01669434)
Timeframe: During anesthesia, an expected average of 3 hours.

InterventionParticipants (Count of Participants)
ACEI Omission48
ACEI Continuation49

[back to top]

Postoperative Hypertension

Any systolic blood pressure greater than 180 mmHg. (NCT01669434)
Timeframe: Arrival in PACU to hospital discharge, an expected average of 4 days.

InterventionParticipants (Count of Participants)
ACEI Omission33
ACEI Continuation17

[back to top]

Postoperative Hypotension

Any systolic blood pressure less than 90 mmHg (NCT01669434)
Timeframe: Arrival in PACU to hospital discharge, an expected average of 4 days.

InterventionParticipants (Count of Participants)
ACEI Omission15
ACEI Continuation31

[back to top]