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1 nt with enalapril, an angiotensin converting enzyme inhibitor.
2 ind here that pyrazinoic acid is only a weak enzyme inhibitor.
3 h) changes it into a powerful broad-spectrum enzyme inhibitor.
4 C1INH is a relatively weak contact system enzyme inhibitor.
5 s a powerful approach for the development of enzyme inhibitors.
6 use of the biosensor as a screening tool for enzyme inhibitors.
7 te, offering opportunities for new lectin or enzyme inhibitors.
8 to identify and measure the effectiveness of enzyme inhibitors.
9 (AmBF3) to generate monovalent or trivalent enzyme inhibitors.
10 compounds function as reversible competitive enzyme inhibitors.
11 ation in the construction of mechanism-based enzyme inhibitors.
12 uretics, digoxin, and angiotensin converting enzyme inhibitors.
13 and acyclonucleoside analogues as potential enzyme inhibitors.
14 esters have been developed as small-molecule enzyme inhibitors.
15 receptor blockers or angiotensin-converting enzyme inhibitors.
16 e-like diuretics over angiotensin-converting enzyme inhibitors.
17 on, PPAR-alpha antagonists, and neurosteroid-enzyme inhibitors.
18 placement therapy, or angiotensin-converting enzyme inhibitors.
21 g azathioprine and an angiotensin-converting enzyme inhibitor, 171 (12.9%) were taking a sulfonylurea
23 nts were treated with angiotensin-converting enzyme inhibitors, 34% (95% CI: 28%-41%) with beta-block
25 assess the effects of angiotensin-converting enzyme inhibitors (ACE-Is) and angiotensin receptor bloc
26 ensin system, such as angiotensin-converting enzyme inhibitors (ACE-Is) and angiotensin receptor bloc
27 of beta blockers and angiotensin-converting-enzyme inhibitors (ACE-Is) or angiotensin receptor block
28 of the casein-derived angiotensin converting enzyme-inhibitor (ACE-I) peptides VPP, IPP, RYLGY, RYLG,
29 no consensus whether angiotensin-converting enzyme inhibitor (ACEI) and angiotensin receptor blocker
30 hether chronic use of angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker
31 rapy, use and dose of angiotensin-converting enzyme inhibitor (ACEI)/angiotensin II receptor blocker
32 e association between angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (AR
33 e association between angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blocke
35 d discontinued use of angiotensin-converting enzyme inhibitors (ACEi) or angiotensin II receptor bloc
36 dence that the use of angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor bloc
37 Although statins, angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blocker
38 d therapy with either angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blocker
40 n fraction, including angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers
41 lockers, statins, and angiotensin-converting enzyme inhibitors (ACEI)/angiotensin II receptor blocker
42 = 0.01), specifically angiotensin-converting enzyme inhibitors (ACEIs) (beta = -1.66; 95% CI, -2.57 t
43 m excretion caused by angiotensin-converting enzyme inhibitors (ACEis) and angiotensin receptor block
47 ave shown that use of angiotensin-converting enzyme inhibitors (ACEIs) potentially decreased amyotrop
49 een hypothesized that angiotensin-converting enzyme inhibitors (ACEIs)/angiotensin receptor blockers
50 let therapy, statins, angiotensin-converting enzyme inhibitors [ACEIs] or angiotensin receptor blocke
51 medication was taken (angiotensin-converting enzyme inhibitors [ACEIs], angiotensin receptor blockers
52 ry effectiveness than angiotensin-converting enzyme inhibitors: acute myocardial infarction (HR 0.84,
53 al and X-ray crystallographic studies of the enzyme-inhibitor adducts helped us to rationalize the ob
55 e target protein to the ligand perturbs this enzyme-inhibitor affinity due to the generation of steri
57 matching (1:1) of the angiotensin-converting enzyme inhibitor and angiotensin receptor blocker groups
58 , -7.27 to -2.16) for angiotensin-converting enzyme inhibitors and -3.07 mm Hg (95% CI, -4.99 to -1.4
59 he patients receiving angiotensin-converting enzyme inhibitors and 2.87 per 100 person-years for thos
60 ked mice treated with angiotensin-converting enzyme inhibitors and a single bolus of icatibant (HOE-1
61 rug classes: statins, angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers,
62 compare the effect of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers on t
63 al therapy, including angiotensin-converting enzyme inhibitors and angiotensin receptor blockers use,
65 rtainty evidence that angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers are
68 We hypothesized that angiotensin-converting enzyme inhibitors and beta-blockers could prevent trastu
69 n leveraged in the design of mechanism-based enzyme inhibitors and has influenced the metabolic fate
70 mistry are showcased herein with examples of enzyme inhibitors and ligands for G protein-coupled rece
71 outs to predict the impact of both metabolic enzyme inhibitors and metabolic pathways exploited to ov
74 eutic avenues for discovering small-molecule enzyme inhibitors and redefines our current understandin
75 in pregnancy, such as angiotensin-converting enzyme inhibitors and statins, should be discontinued.
76 retics superiority to angiotensin-converting enzyme inhibitors and the inferiority of non-dihydropyri
79 standard therapy with angiotensin-converting enzyme inhibitors and/or angiotensin receptor blockers a
80 (beta-blockers), ACE (angiotensin-converting enzyme) inhibitors and ANG (angiotensin) II blockers, ne
81 lved in signaling have lower affinities than enzyme-inhibitor and antibody-antigen complexes, and the
82 rgic blocking agents, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers in
83 pirin, beta blockers, angiotensin-converting enzyme inhibitors, and statins) in pharmacies gathered f
84 erval, 0.64-0.98] for angiotensin-converting enzyme inhibitors; and relative risk, 0.7 [95% confidenc
85 rug treatment with an angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, calcium
87 azide-like diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, dihydr
88 /g) and taking stable angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, or bot
89 rapid up-titration of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, or sac
90 classes examined were angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, alpha-
91 d background drugs of angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta b
92 medications including angiotensin-converting-enzyme inhibitors, angiotensin-receptor blockers, beta-b
93 of medications (i.e., angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, calciu
94 ospital and discharge angiotensin-converting enzyme inhibitor/angiotensin II receptor blockers, beta-
95 istics (shock, use of angiotensin-converting enzyme inhibitor/angiotensin II receptor blockers, lacta
96 in, beta-blocker, and angiotensin-converting enzyme inhibitor/angiotensin receptor blocker use in pat
97 ide, pkVO2, NYHA, and angiotensin-converting enzyme inhibitor/angiotensin receptor blocker use-is wel
98 a standard dose of an angiotensin converting enzyme inhibitor/angiotensin receptor blocker, and hydro
99 >50% target dose for angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, beta-bloc
100 teristics, treatment (angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, beta-bloc
101 ived at least 1 GDMT (angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, or beta-b
103 tion fraction, use of angiotensin-converting enzyme inhibitors/angiotensin receptor antagonists, use
104 0.1) and reversed for angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (66% ver
105 eta-blockers (BB) and angiotensin converting enzyme inhibitors/angiotensin receptor blockers (ACEI/AR
106 re less likely to use angiotensin-converting enzyme inhibitors/angiotensin receptor blockers and beta
107 s, beta-blockers, and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers decrease
108 ment with statins and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers on outco
109 patients on statins, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and bet
110 nce to beta-blockers, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and sta
111 ion of beta-blockers, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and sta
112 ents were on statins, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, beta-bl
113 scharge with statins, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, beta-bl
114 5%, 76%, and 61% used angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, beta-bl
115 atins, beta-blockers, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, P2Y12 i
117 rmacologic effects of angiotensin-converting enzyme inhibitors are partly mediated by increased brady
120 otein structure determination and to develop enzyme inhibitors as angiogenic regulators to treat meta
121 ed approaches are used routinely to discover enzyme inhibitors as cellular tools and potential therap
123 ramipril for 7 days (angiotensin-converting enzyme inhibitors) before hemorrhagic shock, 4) shocked
125 e genetic proxies for angiotensin-converting enzyme inhibitors, beta-blockers, and calcium channel bl
127 elet agents, statins, angiotensin-converting enzyme inhibitors, blood pressure control, lipid control
128 f COX-2 protein, which was restored by COX-2 enzyme inhibitors but not by proteasomal and lysosomal i
129 he presence of associated protein matrix and enzyme inhibitors, but accelerated by endogenous amyloly
131 demonstrate that the coadministration of key enzyme inhibitors can effectively prolong the survival o
132 results indicate that targeted gut microbial enzyme inhibitors can improve cancer chemotherapeutic ou
133 II receptor blockers, angiotensin-converting enzyme inhibitors) can modify the host response to infla
134 and valsartan and the angiotensin-converting enzyme inhibitor captopril on wound healing in diabetic
136 ety of the inhibitor was absent in the final enzyme-inhibitor complex due to the hydrolysis of the es
138 the release mechanism of avibactam from the enzyme-inhibitor complex has been scarcely studied from
139 n reactivity to achieve potency, noncovalent enzyme-inhibitor complex partitioning between inhibitor
141 e active site of the enzyme, resulting in an enzyme-inhibitor complex that replicates the enzyme's te
142 ibitor complexes exist en route to the final enzyme-inhibitor complex with full inhibitory activity.
143 binding rather than the ground state of the enzyme-inhibitor complex, and demonstrates the important
144 tron diffraction data from the perdeuterated enzyme-inhibitor complex, we were able to determine the
148 strate dehydroepiandrosterone sulfate or the enzyme inhibitor COUMATE, influenced behavior in a novel
149 t categories, namely, angiotensin-converting enzyme inhibitor, cyclooxygenase inhibitor, and dopamine
150 ntly, SKI-1 inhibition by the cell-permeable enzyme inhibitor decanoyl-RRLL-chloromethylketone (dec-R
152 00 mg daily) with the angiotensin-converting enzyme inhibitor enalapril (20 mg daily) in 8399 patient
153 F), compared with the angiotensin-converting enzyme inhibitor enalapril, and improves peripheral insu
154 wering medication and angiotensin-converting enzyme inhibitors, especially if they had cardiovascular
155 rough combinatorial effects of multiple DNFA enzyme inhibitors, exerts potent cytotoxic effects on bo
156 luding cytokines and chemokines, enzymes and enzyme inhibitors, extracellular matrix proteins, and me
159 ors could offer an orthogonal alternative to enzyme inhibitors for perturbation of enzyme activity in
160 use of systemically administered epigenetic enzyme inhibitors for relapse prevention in human drug u
161 promising strategy for creating multivalent enzyme inhibitors for selectively imaging extracellular
162 s, beta-blockers, and angiotensin-converting enzyme inhibitors given to patients after myocardial inf
165 ficantly lower in the angiotensin-converting enzyme inhibitor group than in the other groups (p < 0.0
166 icantly higher in the angiotensin-converting enzyme inhibitor group than in the other groups, particu
167 ving beta-blockers or angiotensin-converting enzyme inhibitors had a higher risk of developing severe
168 date, those receiving angiotensin-converting enzyme inhibitors had a higher risk of sepsis, septic sh
169 he patients receiving angiotensin-converting enzyme inhibitors had a higher risk of septic shock (adj
171 ly before anesthesia (angiotensin-converting enzyme inhibitors + icatibant), and 5) shocked mice trea
172 novel potent and selective NEDD8-activating enzyme inhibitor in a panel of MCL cell lines, primary M
173 ocker, statin, and an angiotensin-converting enzyme inhibitor in patients with left ventricular eject
174 or was superior to an angiotensin-converting enzyme inhibitor in reducing mortality in patients with
175 antly associated with angiotensin-converting-enzyme inhibitors in our metabolome-wide association ana
176 is and mortality than angiotensin-converting enzyme inhibitors in the patients with chronic obstructi
178 ional docking studies provided insights into enzyme-inhibitor interactions and a rationale for the ob
179 y of PRDelta4 is attributable to stabilizing enzyme-inhibitor interactions in the P2 and P2' pockets
180 ing to FXIIIa, in turn, the knowledge of the enzyme-inhibitor interactions might bring about comprehe
184 e was reversed by the angiotensin-converting enzyme inhibitor (lisinopril) and thus was dependent on
185 Hg) and to either an angiotensin-converting-enzyme inhibitor (lisinopril) plus an angiotensin-recept
186 cell lineage commitment and suggest that Car enzyme inhibitors may possess therapeutic potential that
188 te that metals can be therapeutically viable enzyme inhibitors; moreover, enzymes that share homology
189 antagonists (n=6) or angiotensin-converting enzyme inhibitors (n=6) exhibited no significant differe
190 ceived beta-blockers, angiotensin-converting enzyme inhibitors, nitrates, and statins (all p < 0.05).
191 dual inhibitors targeting both IN and other enzymes, inhibitors of enzymes that activate IN, activat
192 ms of covalent irreversible, mechanism-based enzyme inhibitors often focus on optimization of potency
193 e effect of 2-chloroacetamidine (2CA), a PAD enzyme inhibitor, on OVA-immunized and airway-challenged
194 e pathway, such as an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker, sho
195 isease with either an angiotensin-converting enzyme inhibitor or an angiotensin type 1 receptor block
196 iving stable doses of angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker ther
197 given in addition to angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker trea
198 of patients not on an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker were
199 nephropathy receiving angiotensin converting enzyme inhibitor or angiotensin receptor blocker backgro
200 ta-blocker and either angiotensin-converting enzyme inhibitor or angiotensin receptor blocker in elig
201 nsive therapy with an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker in pers
202 atients (84%) used an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker through
203 renal function, lower angiotensin-converting enzyme inhibitor or angiotensin receptor blocker usage d
204 e classification, and angiotensin converting enzyme inhibitor or angiotensin receptor blocker usage w
205 <90 mm Hg diastolic), angiotensin-converting enzyme inhibitor or angiotensin receptor blocker use, an
207 ears, with subsequent angiotensin-converting enzyme inhibitor or beta-blocker treatment for patients
208 e therapy with either angiotensin-converting enzyme inhibitor or beta-blockers experienced fewer inte
210 t of albuminuria (eg, angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers),
211 s with intolerance to angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers.
212 ose only treated with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (18.2
213 ge were not receiving angiotensin-converting enzyme inhibitors or angiotensin receptor blockers at ad
214 disease who received angiotensin-converting enzyme inhibitors or angiotensin receptor blockers for m
215 not support stopping angiotensin-converting enzyme inhibitors or angiotensin receptor blockers in pa
216 nfection, the role of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers requi
217 of HF, initiation of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was i
218 >1 g/d, maintained on angiotensin-converting enzyme inhibitors or angiotensin receptor blockers with
219 atins, beta-blockers, angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, and
221 contraindications for angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, beta
222 ibitors, statins, and angiotensin-converting enzyme inhibitors or angiotensin receptor blockers.
223 ystem with the use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers.
224 beta-blockers and 81% angiotensin-converting enzyme inhibitors or angiotensin receptor blockers.
225 edications other than angiotensin-converting enzyme inhibitors or angiotensin receptor blockers.
226 , and 84% were taking angiotensin-converting enzyme inhibitors or angiotensin receptor blockers.
227 to monotherapy with angiotensin-I converting enzyme inhibitors or angiotensin-II receptor type 1 bloc
228 re monotherapy with angiotensin-I converting enzyme inhibitors or angiotensin-II receptor type 1 bloc
229 blockade therapy with angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers after
230 s who were prescribed angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers after
231 ropriate medications (angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers and s
232 ropriate medications (angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers and s
233 nts were treated with angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers.
234 to determine whether angiotensin-converting enzyme inhibitors or beta-blockers reduce the rate of tr
236 ombination therapy with ubiquitin-activating enzyme inhibitors or by specific inhibition of the BMI/R
237 While this approach has been applied to enzyme inhibitors or receptor antagonists, to date it re
238 ystem, either an ACE (angiotensin-converting enzyme) inhibitor or an ARB (angiotensin receptor blocke
239 ys of initiating ACE (angiotensin-converting enzyme) inhibitor or angiotensin II receptor blocker the
240 CI, 0.69-1.35]), ACE (angiotensin-converting enzyme) inhibitor or angiotensin receptor blocker if lef
241 ation therapy of ACE (angiotensin-converting enzyme) inhibitors or ARBs (angiotensin receptor blocker
242 lure medication (ACE [angiotensin-converting enzyme] inhibitor or angiotensin II receptor blocker) an
244 who tolerate an ACEI (angiotensin-converting enzyme inhibitor) or ARB (angiotensin II receptor blocke
245 ibition by enalapril (angiotensin-converting enzyme inhibitor) or losartan (angiotensin-receptor bloc
246 neprilysin inhibitor, angiotensin-converting enzyme inhibitor, or angiotensin receptor blocker as fou
247 clude a beta-blocker, angiotensin-converting enzyme inhibitor, oral antidiabetic agent, calcium, and
248 vered for statins and angiotensin-converting enzyme inhibitors, patients were stratified as fully adh
249 ion of Skp2 using the neddylation-activating enzyme inhibitor pevonedistat decreased growth of Rb/p53
250 stration of the M13-metalloproteinase family enzyme-inhibitor phosphoramidon, using the senescence-ac
251 mice pretreated with angiotensin-converting enzyme inhibitors potentiated IFN-gamma production by Ag
253 eceptor blockers, and angiotensin-converting enzyme inhibitors; prophylactic surgery for aneurysm; su
254 proach for the extensive characterization of enzyme-inhibitor reaction kinetics within a single exper
257 ium-channel blockers, angiotensin-converting-enzyme inhibitors, serotonin-specific reuptake inhibitor
259 ids was inhibited by the TNFalpha converting enzyme inhibitor TAPI-0 indicating normal processing of
260 proof of concept, we tested the effect of an enzyme inhibitor (targeting matrix metalloproteinase 12)
261 ing of a cytotoxic agent, through a covalent enzyme inhibitor that is detrimental to tumor tissue in
263 of beta-blockers and angiotensin-converting enzyme inhibitors that are symptomatic and unspecific to
264 intained to mitigate effects of biosynthetic enzyme inhibitors that substantially change the proporti
265 ibiotic) and pacritinib (an 18-membered-ring enzyme inhibitor), the Z-isomer of which is less potent
266 necrosis, and use of angiotensin-converting enzyme inhibitor therapy for microalbuminuria in adults
267 nts with COPD in whom angiotensin-converting enzyme inhibitor therapy improves renal and lung functio
268 tril-valsartan versus angiotensin-converting enzyme inhibitor therapy in patients with chronic heart
269 clinical benefit from angiotensin-converting enzyme inhibitor therapy regardless of renal function.
273 sin Inhibitor With an Angiotensin-Converting Enzyme Inhibitor to Determine Impact on Global Mortality
274 ilysin Inhibitor With Angiotensin Converting Enzyme Inhibitor to Determine Impact on Global Mortality
275 inhibitor) with ACEI (angiotensin-converting enzyme inhibitor) to Determine Impact on Global Mortalit
276 Inhibitor] With ACEI [Angiotensin-Converting-Enzyme Inhibitor] to Determine Impact on Global Mortalit
277 Inhibitor] with ACEI [Angiotensin-Converting-Enzyme Inhibitor] to Determine Impact on Global Mortalit
278 Inhibitor] with ACEI [Angiotensin-Converting-Enzyme Inhibitor] to Determine Impact on Global Mortalit
280 uld be of interest in angiotensin-converting enzyme inhibitor-treated patients during both emergency
283 the possibility that angiotensin-converting enzyme inhibitor treatment might limit PEC activation an
284 ospective analysis of angiotensin-converting enzyme inhibitor trials and prospective comparisons with
285 We show that the histone deacetylase (HDAC) enzyme inhibitor trichostatin A blocks the ability of li
286 n II receptor blocker/angiotensin-converting enzyme inhibitor use were associated with reduced early
287 ght, premature birth, angiotensin-converting enzyme inhibitor use, angiotensin receptor blocker use,
288 il/valsartan, over an angiotensin-converting enzyme inhibitor, was consistent regardless of backgroun
290 xtures containing bioactive compounds (i.e., enzyme inhibitors), while the second step uses bioselect
291 sponse and the development of anti-CoV PLpro enzyme inhibitors will be a challenging undertaking.
292 ified as a potent and highly selective PDE2a enzyme inhibitor with favorable rat pharmacokinetic prop
293 lly bioavailable and brain penetrating PDE1B enzyme inhibitor with potent memory-enhancing effects in
294 easible to rapidly and reliably identify Nox enzyme inhibitors with a markedly lower rate of false po
296 ls that have compared angiotensin-converting enzyme inhibitors with drugs that inhibit both the renin
297 ization of the series yielding submicromolar enzyme inhibitors with promising cellular activity.
298 ign of unique allosteric sites for potential enzyme inhibitors with regulatory or therapeutic benefit
299 a, and 10b showed increased potency as PDE4D enzyme inhibitors with respect to 2 and a good selectivi
300 hat the in vivo coadministration of specific enzyme inhibitors would improve peptide bioavailability