PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
10821135-4	2000	Either imidaprilat or cilazaprilat increased CBF, FS, and LER with increases in cardiac bradykinin and NO levels.	cilazaprilat	22-34	kininogen 1	Canis lupus familiaris	88-98
9440700-10	1998	Total cardiac Ang II-forming activity was only partially inhibited by cilazaprilat (4.1+/-0.1 fmol x min(-1) x mg[-1]) and on a larger extent by chymostatin (2.6+/-0.3 fmol x min(-1) x mg[-1]) compared with control values (5.6+/-0.4 fmol x min(-1) x mg[-1]).	cilazaprilat	70-82	angiotensinogen	Rattus norvegicus	14-20
10541285-6	1999	This cilazaprilat-induced vasodilation and natriuresis was abolished by a bradykinin antagonist (N(alpha)-adamantaneacetyl-D-Arg-[Hyp3,Thi5,8,D-Phe7]b radykinin).	cilazaprilat	5-17	kininogen 1	Canis lupus familiaris	74-84
10541285-7	1999	In parallel with these results, cilazaprilat increased renal bradykinin content, more greatly in the medulla than in the cortex (5.7 +/- 0.4 versus 4.6 +/- 0.1 ng/g).	cilazaprilat	32-44	kininogen 1	Canis lupus familiaris	61-71
10541285-8	1999	Similarly, cilazaprilat elicited greater bradykinin-dependent increases of nitrite/nitrate in the medulla.	cilazaprilat	11-23	kininogen 1	Canis lupus familiaris	41-51
9989969-2	1999	The present study was designed to examine whether an ACE inhibitor, cilazaprilat, directly protects cardiac myocytes against hypoxia/reoxygenation (H/R) injury.	cilazaprilat	68-80	angiotensin I converting enzyme	Rattus norvegicus	53-56
9989969-6	1999	The protective effect of cilazaprilat was significantly inhibited by Hoe 140 (a bradykinin B2 receptor antagonist), NG-monomethyl-L-arginine monoacetate (L-NMMA) (an NO synthase inhibitor), and methylene blue (a soluble guanylate cyclase inhibitor) but not by staurosporine (a protein kinase C inhibitor), aminoguanidine (an inhibitor of inducible NO synthase), or indomethacin (a cyclooxygenase inhibitor).	cilazaprilat	25-37	nitric oxide synthase 2	Rattus norvegicus	338-359
9925380-6	1998	During an infusion of either imidaprilat or cilazaprilat, bradykinin and the end-products of NO (nitrate + nitrite) concentrations of coronary venous blood were markedly increased, which were attenuated by either HOE-140 (an inhibitor of bradykinin receptors) or by N(omega)-nitro-L-arginine methyl ester (an inhibitor of NO synthase).	cilazaprilat	44-56	kininogen 1	Canis lupus familiaris	238-248
9925380-7	1998	We also observed increases in cardiac bradykinin and NO levels due to either imidaprilat or cilazaprilat in the low constant coronary blood flow condition.	cilazaprilat	92-104	kininogen 1	Canis lupus familiaris	38-48
9765319-7	1998	A good linear correlation was observed for the inhibitory effect of angiotensin-converting enzyme inhibitors (benazeprilat, cilazaprilat, delaprilat and enalaprilat) between isolated hepatocytes and oatp1-expressing cells.	cilazaprilat	124-136	solute carrier organic anion transporter family, member 1a1	Rattus norvegicus	199-204
9622144-4	1998	The ACE inhibitor cilazaprilat was administered into the coronary artery 10 minutes before coronary occlusion, and infusion was continued until 1 hour after reperfusion.	cilazaprilat	18-30	angiotensin I converting enzyme	Canis lupus familiaris	4-7
9622144-5	1998	The bradykinin and NO concentrations in coronary venous blood 10 minutes after the onset of reperfusion were significantly higher in dogs treated with cilazaprilat (3 microg x kg(-1) x min(-1)) than in control animals.	cilazaprilat	151-163	kininogen 1	Canis lupus familiaris	4-14
10604521-6	1999	Cilazaprilat (CIL, 10 microM) was used for inhibition of ACE.	cilazaprilat	0-12	LOW QUALITY PROTEIN: angiotensin-converting enzyme	Cavia porcellus	57-60
10604521-6	1999	Cilazaprilat (CIL, 10 microM) was used for inhibition of ACE.	cilazaprilat	14-17	LOW QUALITY PROTEIN: angiotensin-converting enzyme	Cavia porcellus	57-60
7556269-8	1995	When organoids were cultured in the combined presence of Ang II and the ACE inhibitor cilazaprilat, labelling indices of intact organoids were also significantly increased above control, but to a lower level than those obtained in the presence of Ang II alone.	cilazaprilat	86-98	angiotensin I converting enzyme	Rattus norvegicus	72-75
9405170-13	1997	P-selectin expression rose from 100% (control) to 146% after 1 mm H2O2 without CILA, but only to 114% in the presence of CILA.	cilazaprilat	79-83	selectin P	Homo sapiens	0-10
9405170-13	1997	P-selectin expression rose from 100% (control) to 146% after 1 mm H2O2 without CILA, but only to 114% in the presence of CILA.	cilazaprilat	121-125	selectin P	Homo sapiens	0-10
9405170-18	1997	Irrespectively, CILA reduced the upregulation of P-selectin at the higher H2O2 concentration, indicating that this process is regulated independently of the cellular redox status.	cilazaprilat	16-20	selectin P	Homo sapiens	49-59
7641379-7	1995	During an infusion of cilazaprilat, the bradykinin concentration of coronary venous blood was markedly increased.	cilazaprilat	22-34	kininogen 1	Canis lupus familiaris	40-50
7641379-8	1995	The increased coronary blood flow due to cilazaprilat was attenuated by HOE-140 (an inhibitor of bradykinin receptors; coronary blood flow: 35 +/- 2 mL/100 g per minute), and by N omega-nitro-L-arginine methyl ester (an inhibitor of nitric oxide synthase; coronary blood flow: 34 +/- 2 mL/100 g per minute).	cilazaprilat	41-53	kininogen 1	Canis lupus familiaris	97-107
7641379-9	1995	Intracoronary administration of bradykinin mimicked the beneficial effects of cilazaprilat.	cilazaprilat	78-90	kininogen 1	Canis lupus familiaris	32-42
9534860-9	1997	The ACE-inhibitor cilazaprilat (Cila, 2 microM) and the NO-synthase inhibitor nitro-L-arginine (NOLAG, 10 microM) were used to modulate nitric oxide formation of the heart.	cilazaprilat	18-30	LOW QUALITY PROTEIN: angiotensin-converting enzyme	Cavia porcellus	4-7
8739812-15	1996	The inhibition of ACE in relationship to time and the plasma concentrations of cilazaprilat were similar in the two groups, although the changes in PRA and aldosterone suggest an ethnic difference in the responses of the renin-angiotensin-aldosterone system.	cilazaprilat	79-91	angiotensin I converting enzyme	Homo sapiens	18-21
7556269-8	1995	When organoids were cultured in the combined presence of Ang II and the ACE inhibitor cilazaprilat, labelling indices of intact organoids were also significantly increased above control, but to a lower level than those obtained in the presence of Ang II alone.	cilazaprilat	86-98	angiotensinogen	Rattus norvegicus	247-253
1327596-8	1992	The potency of the active diacids in inhibiting plasma ACE activity was perindoprilat greater than cilazaprilat greater than enalaprilat.	cilazaprilat	99-111	angiotensin I converting enzyme	Homo sapiens	55-58
1279292-6	1992	The degree of ACE inhibition correlated with the plasma concentration-time profile of cilazaprilat and the maximum decrease in blood pressure (BP).	cilazaprilat	86-98	angiotensin I converting enzyme	Homo sapiens	14-17
1279292-7	1992	The EC50 for ACE inhibition by cilazaprilat was 7.7 ng/ml after acute treatment and was not significantly altered during chronic administration or by concomitant administration of CPTZ.	cilazaprilat	31-43	angiotensin I converting enzyme	Homo sapiens	13-16
1312513-4	1992	The most potent converting enzyme inhibitors toward aminopeptidase P were the carboxylalkyl compounds, cilazaprilat, enalaprilat, and ramiprilat (I50 values of 3-12 microM).	cilazaprilat	103-115	X-prolyl aminopeptidase 2	Sus scrofa	52-68
8445218-2	1993	The angiotensin-converting enzyme (ACE)-inhibitor, cilazapril, is converted to its active metabolite, cilazaprilat, by ester hydrolysis in the liver.	cilazaprilat	102-114	angiotensin I converting enzyme	Homo sapiens	35-38
1318793-3	1992	In rings of coronary artery with endothelium, relaxations to bradykinin were potentiated by the ACE inhibitors cilazaprilat and perindoprilat.	cilazaprilat	111-123	kininogen 1	Canis lupus familiaris	61-71
1318793-3	1992	In rings of coronary artery with endothelium, relaxations to bradykinin were potentiated by the ACE inhibitors cilazaprilat and perindoprilat.	cilazaprilat	111-123	angiotensin I converting enzyme	Canis lupus familiaris	96-99
1325885-2	1992	ACE from rat lung and testis was characterized by radioligand binding studies using [125I]-Ro 31-8472, the radioiodinated hydroxy derivative of the potent ACE inhibitor cilazaprilat.	cilazaprilat	169-181	angiotensin I converting enzyme	Rattus norvegicus	0-3
1325885-2	1992	ACE from rat lung and testis was characterized by radioligand binding studies using [125I]-Ro 31-8472, the radioiodinated hydroxy derivative of the potent ACE inhibitor cilazaprilat.	cilazaprilat	169-181	angiotensin I converting enzyme	Rattus norvegicus	155-158
1325885-6	1992	There was marked variation in ACE inhibitor binding affinity at the two binding sites of lung ACE across the panel of ACE inhibitors studied (equilibrium dissociation constant; Kd; pmol/L) for site one vs site two: cilazaprilat 40 +/- 3 vs 430 +/- 92*; lisinopril 25 +/- 1 vs 848 +/- 107**; and quinaprilat 4 +/- 1 vs 1869 +/- 720; *P less than 0.05; **P less than 0.005, t-test, n = 3).	cilazaprilat	215-227	angiotensin I converting enzyme	Rattus norvegicus	30-33
1325885-6	1992	There was marked variation in ACE inhibitor binding affinity at the two binding sites of lung ACE across the panel of ACE inhibitors studied (equilibrium dissociation constant; Kd; pmol/L) for site one vs site two: cilazaprilat 40 +/- 3 vs 430 +/- 92*; lisinopril 25 +/- 1 vs 848 +/- 107**; and quinaprilat 4 +/- 1 vs 1869 +/- 720; *P less than 0.05; **P less than 0.005, t-test, n = 3).	cilazaprilat	215-227	angiotensin I converting enzyme	Rattus norvegicus	94-97
1325885-6	1992	There was marked variation in ACE inhibitor binding affinity at the two binding sites of lung ACE across the panel of ACE inhibitors studied (equilibrium dissociation constant; Kd; pmol/L) for site one vs site two: cilazaprilat 40 +/- 3 vs 430 +/- 92*; lisinopril 25 +/- 1 vs 848 +/- 107**; and quinaprilat 4 +/- 1 vs 1869 +/- 720; *P less than 0.05; **P less than 0.005, t-test, n = 3).	cilazaprilat	215-227	angiotensin I converting enzyme	Rattus norvegicus	94-97
1712269-6	1991	The potency of cilazaprit, defined as the concentration of cilazaprilat causing 50% inhibition of ACE, was approximately 1 microgram/L plasma.	cilazaprilat	59-71	angiotensin I converting enzyme	Homo sapiens	98-101
1916998-2	1991	In coronary arteries incubated with indomethacin, cilazaprilat potentiated endothelium-dependent relaxations to bradykinin.	cilazaprilat	50-62	kininogen 1	Canis lupus familiaris	112-122
1916998-3	1991	In superfusion-perfusion bioassay studies with femoral arteries, cilazaprilat augmented the release of nonprostanoid endothelium-derived relaxing factors caused by bradykinin.	cilazaprilat	65-77	kininogen 1	Canis lupus familiaris	164-174
1712269-5	1991	A close positive correlation was found between the cilazaprilat plasma concentration and degree of ACE inhibition.	cilazaprilat	51-63	angiotensin I converting enzyme	Homo sapiens	99-102
1712272-7	1991	Our study strongly indicates that enalaprilat has pro-inflammatory properties, whereas the new long-acting ACE inhibitor cilazaprilat does not.	cilazaprilat	121-133	LOW QUALITY PROTEIN: angiotensin-converting enzyme	Cavia porcellus	107-110
2532460-1	1989	In clinical pharmacology studies cilazapril, after its bioactivation to cilazaprilat, was characterized as a potent, reversible angiotensin-converting enzyme (ACE) inhibitor with a terminal half-life of 30 to 50 hours consistent with saturable binding to ACE.	cilazaprilat	72-84	angiotensin I converting enzyme	Homo sapiens	159-162
2532460-6	1989	A close and steep correlation between cilazaprilat plasma concentration and ACE inhibition was found.	cilazaprilat	38-50	angiotensin I converting enzyme	Homo sapiens	76-79
2532460-7	1989	The potency of cilazaprilat, defined as the concentration of cilazaprilat causing 50 percent ACE inhibition, was approximately 1 ng/ml plasma.	cilazaprilat	15-27	angiotensin I converting enzyme	Homo sapiens	93-96
2532460-7	1989	The potency of cilazaprilat, defined as the concentration of cilazaprilat causing 50 percent ACE inhibition, was approximately 1 ng/ml plasma.	cilazaprilat	61-73	angiotensin I converting enzyme	Homo sapiens	93-96
2527528-3	1989	Cilazaprilat has an IC50 of 1.9 nM as an inhibitor of rabbit lung ACE in vitro making it one of the most potent ACE inhibitors currently available.	cilazaprilat	0-12	angiotensin-converting enzyme	Oryctolagus cuniculus	66-69
2476598-6	1989	At doses greater than 78 ng/min, cilazaprilat and enalaprilat completely inhibited angiotensin I-induced venoconstriction.	cilazaprilat	33-45	angiotensinogen	Homo sapiens	83-96
2476598-10	1989	We conclude that cilazaprilat and enalaprilat are inhibitors of ACE associated with the vein wall, but there is no evidence for either drug of direct, ACE-independent, prostaglandin-mediated vasodilation.	cilazaprilat	17-29	angiotensin I converting enzyme	Homo sapiens	64-67
2527535-2	1989	Cilazaprilat is an inhibitor of angiotensin converting enzyme (ACE) and is the active metabolite of cilazapril.	cilazaprilat	0-12	angiotensin I converting enzyme	Homo sapiens	32-61
2527528-3	1989	Cilazaprilat has an IC50 of 1.9 nM as an inhibitor of rabbit lung ACE in vitro making it one of the most potent ACE inhibitors currently available.	cilazaprilat	0-12	angiotensin-converting enzyme	Oryctolagus cuniculus	112-115
2527535-2	1989	Cilazaprilat is an inhibitor of angiotensin converting enzyme (ACE) and is the active metabolite of cilazapril.	cilazaprilat	0-12	angiotensin I converting enzyme	Homo sapiens	63-66
2527531-8	1989	After 10 min infusion of cilazaprilat, the mean plasma concentration was 194 ng ml-1, and ACE inhibition was almost 100%.	cilazaprilat	25-37	angiotensin I converting enzyme	Homo sapiens	90-93
2527535-16	1989	The plasma concentrations of cilazaprilat required for 90% ACE inhibition were similar at 4.7 and 4.8 ng ml-1 in the elderly and young respectively.	cilazaprilat	29-41	angiotensin I converting enzyme	Homo sapiens	59-62
2527537-4	1989	Intravenous infusion of 2 mg cilazaprilat resulted in a significant and short lasting inhibition of ACE as evidenced by a decrease of plasma angiotensin II and an increase in plasma renin activity.	cilazaprilat	29-41	angiotensin I converting enzyme	Homo sapiens	100-103
2527537-4	1989	Intravenous infusion of 2 mg cilazaprilat resulted in a significant and short lasting inhibition of ACE as evidenced by a decrease of plasma angiotensin II and an increase in plasma renin activity.	cilazaprilat	29-41	angiotensinogen	Homo sapiens	141-155
2527537-4	1989	Intravenous infusion of 2 mg cilazaprilat resulted in a significant and short lasting inhibition of ACE as evidenced by a decrease of plasma angiotensin II and an increase in plasma renin activity.	cilazaprilat	29-41	renin	Homo sapiens	182-187
2527539-19	1989	When creatinine clearance was below 15 ml min-1 cilazaprilat concentrations were increased, half-lives were prolonged and ACE inhibition remained above 90% for at least 24 h. A reduced dosage is indicated for these patients.	cilazaprilat	48-60	CD59 molecule (CD59 blood group)	Homo sapiens	42-47
2548553-9	1989	The pharmacokinetics of cilazaprilat and the pharmacodynamics of plasma ACE inhibition were well described by a one compartment model with saturable binding to ACE.	cilazaprilat	24-36	angiotensin I converting enzyme	Homo sapiens	160-163
2548553-11	1989	The coefficients of the model which related to plasma ACE and its interaction with cilazaprilat were in good agreement with model independent observations.	cilazaprilat	83-95	angiotensin I converting enzyme	Homo sapiens	54-57
3036166-3	1987	Binding of 125I MK351A to rat serum ACE was reduced in a concentration dependent manner in vitro by the ACE inhibitors MK521 (lisinopril), S9780, and Ro 31-3113-000 (Cilazapril diacid).	cilazaprilat	166-183	angiotensin I converting enzyme	Homo sapiens	36-39
3036166-3	1987	Binding of 125I MK351A to rat serum ACE was reduced in a concentration dependent manner in vitro by the ACE inhibitors MK521 (lisinopril), S9780, and Ro 31-3113-000 (Cilazapril diacid).	cilazaprilat	166-183	angiotensin I converting enzyme	Homo sapiens	104-107
14769805-7	2004	In contrast, in the presence of E4177+l-NAME, cilazaprilat still caused 8%+/-3% dilation of juxtamedullary Aff, which was completely eliminated by proadifen, a cytochrome-P450 and K(Ca) channel blocker.	cilazaprilat	46-58	Cytochrome P450 1A1	Canis lupus familiaris	160-175