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1 isotope effect of 10.1 was measured in human liver microsomes.
2 he derivatives significantly in pooled human liver microsomes.
3 ism were identified by incubation with human liver microsomes.
4 lectively potent under hypoxia and stable to liver microsomes.
5 tin as pironetin's major metabolite in human liver microsomes.
6 s to a complete absence of UGT1A proteins in liver microsomes.
7 tisol was detected in dog, human, and monkey liver microsomes.
8 og liver microsomes than in human and monkey liver microsomes.
9 alkylation activity of human, mouse, and rat liver microsomes.
10 ster hydrolase activity from solubilized rat liver microsomes.
11 ronidation activity of mouse, rat, and human liver microsomes.
12 etabolism in human intestinal microsomes and liver microsomes.
13 ylation takes place in both rodent and human liver microsomes.
14 The product was also formed in human liver microsomes.
15 bited cytochrome P450 3A4 enzyme (CYP3A4) in liver microsomes.
16 ncentrations but had no effect on cardiac or liver microsomes.
17 d proteins that bind apolipoprotein B in rat liver microsomes.
18 degradation similar to that observed in rat liver microsomes.
19 rapidly and selectively degraded in isolated liver microsomes.
20 S analysis of metabolites generated from rat liver microsomes.
21 etabolites was demonstrated in rat and human liver microsomes.
22 ctivity exhibited by CYP4F2 and rat or human liver microsomes.
23 substrates for cytochrome P450 2D6 in human liver microsomes.
24 ed by erythromycin N-demethylase activity in liver microsomes.
25 h activities similar to those found in human liver microsomes.
26 tabolically activated in the presence of rat liver microsomes.
27 tics was analyzed in both patients and human liver microsomes.
28 impairment of nifedipine oxidation by human liver microsomes.
29 ed conversion of TAX to 6-HT by 41% in human liver microsomes.
30 idine 5'-diphosphoglucuronic acid and rabbit liver microsomes.
31 led to an increase in total SCD activity in liver microsomes.
32 ize UDP-GlcA in cartilage microsomes and rat liver microsomes.
33 ficantly improved metabolic stability to rat liver microsomes.
34 e (DCCY) from cyclophosphamide (CY) in human liver microsomes.
35 roximately 30%) the 4-hydroxylation in human liver microsomes.
36 roperoxide-induced lipid peroxidation in rat liver microsomes.
37 of erythromycin with cytochromes P450 in rat liver microsomes.
38 the major cytochrome P-450 enzymes in human liver microsomes.
39 MO3 were comparable to Km values from rabbit liver microsomes.
40 ophenol and N,N-dimethylnitrosamine by fetal liver microsomes.
41 hich were 12-27% of those exhibited by adult liver microsomes.
42 glycero-3-phosphocholine (1-acyl-GPC) by rat liver microsomes.
43 is detectable in 90- but not 21-day-old rat liver microsomes.
44 se I metabolism assays performed using human liver microsomes.
45 tion favoring (-)-1a was also found in human liver microsomes.
46 elative to the corresponding wild-type mouse liver microsomes.
47 le inhibition of cytochrome P450s from human liver microsomes.
48 of vemurafenib in in vitro assays with human liver microsomes.
49 moderate stability (t1/2 = 44 min) in mouse liver microsomes.
50 to 40-fold increases in half-lives in mouse liver microsomes.
51 g good in vitro metabolic stability in human liver microsomes.
52 d higher metabolic stability than 5 in human liver microsomes.
53 ta(6)-PZQ)Cr(CO)3 (1 and 2), by use of human liver microsomes.
54 te that this compound is stable in serum and liver microsomes.
55 lyzed (S)-mephenytoin hydroxylation in human liver microsomes.
56 man IMPDH type 2 and good stability in mouse liver microsomes.
57 ediated biotransformation assay based on rat liver microsomes.
58 metabolic stability in the presence of human liver microsomes.
65 cy, metabolic stabilities in mouse and human liver microsomes, along with acceptable cytotoxicity pro
70 and quinidine, two prototypic substrates, in liver microsomes and a reconstituted enzyme system with
71 ility in the presence of tumor cells and rat liver microsomes and achieves rapid ingress into cell nu
76 phase I metabolic stability studies in mouse liver microsomes and compared to cocaine in locomotor ac
79 e assessment of metabolic stability in human liver microsomes and cytochrome P450 inhibition potentia
80 genic metabolites was not observed in medaka liver microsomes and cytochrome P450 was not induced wit
81 microenvironments were incubated with human liver microsomes and cytosol (HLM/HLC) simulating Phase
83 This compound was metabolically stable in liver microsomes and displayed anti-tumor activity in xe
84 etabolically stable in rat plasma and in rat liver microsomes and efficacious in rats when given oral
85 ver lipids, activity of HMG-CoA reductase in liver microsomes and EPA+DHA incorporation in liver, hea
86 of methadone into its main metabolite by rat liver microsomes and for demonstrating the potential of
87 d TBMEHP for deiodinase inhibition using rat liver microsomes and for peroxisome proliferator-activat
88 human liver microsomes, metabolism by human liver microsomes and hepatocytes, and in vivo dispositio
90 Glucuronidation of these retinoids by human liver microsomes and human recombinant UDP-glucuronosylt
91 e were able to profile active enzymes in rat liver microsomes and identify pyrethroid-metabolizing en
92 ism studies were investigated in rat and dog liver microsomes and in the filamentous fungus Cunningha
93 ro metabolic stability of 6a and 6m in mouse liver microsomes and in vivo pharmacokinetic profiles in
97 Incubation of dihydrotestosterone with human liver microsomes and NADPH yielded the 18- and 19-hydrox
99 frontrunner compounds with good stability in liver microsomes and no hERG channel inhibition liabilit
101 xygen species induction, and stability under liver microsomes and P450-cytochrome species were invest
103 stability when incubated with rat and human liver microsomes and showed no significant cytochrome P4
104 ere prepared by incubation with female human liver microsomes and subjected to binding experiments wi
105 alogs with low predicted metabolism in human liver microsomes and which showed prolonged exposure in
106 ough in vitro (kinase assay), ex vivo (human liver microsomes) and in vivo (mouse) model systems.
107 l microsomal in vitro assay (Wistar-Han rats liver microsomes), and with concomitant formation of PFC
108 0 nM), moderate metabolic stability in human liver microsomes, and a hERG/DAT affinity ratio = 28.
109 ADC following its incubation in hepatocytes, liver microsomes, and buffers, as illustrated by the ide
110 alian models (human liver microsomes, murine liver microsomes, and commercial porcine liver esterase)
111 nM), shows high metabolic stability in human liver microsomes, and displays excellent selectivity in
112 vitro metabolic stability, slow clearance in liver microsomes, and excellent blood-brain barrier perm
113 a-hydroxylases (C7alphaH) from human and rat liver microsomes, and from transformed Escherichia coli
114 uman serum, low rates of metabolism in human liver microsomes, and high oral bioavailability in anima
115 ounds are stable in simulated gastric fluid, liver microsomes, and human blood and are largely free f
116 ell culture, enhanced metabolic stability in liver microsomes, and improved tolerability in mice.
117 degradation in both human and rat plasma and liver microsomes, and is rapidly absorbed following an i
118 metabolic stability when incubated with rat liver microsomes, and rate of uptake and subcellular loc
119 of HCY to the same extent observed in human liver microsomes, and the addition of orphenadrine to in
120 droceramide into ceramide in vitro using rat liver microsomes, and the formation of tritiated water a
121 above reactions were carried out using human liver microsomes, and the metabolites were detected by E
123 f tamoxifen (tam) formed by animal and human liver microsomes are mono-N-demethylated tam, 4-hydroxy-
124 was introduced by using stability toward rat liver microsomes as a predictor of bioavailability.
125 ) showed improved metabolic stability in rat liver microsomes as compared to the previously reported
126 re favorably with those obtained using human liver microsomes as well as those of reconstituted in vi
127 g of representative analogues in an in vitro liver microsome assay indicated that the alkyl substitue
129 e describe the purification of TPST from rat liver microsomes based on its affinity for the N-termina
131 lent metabolic stability in mouse plasma and liver microsomes but showed only limited oral bioavailab
133 d into two glutathione regioisomers by human liver microsomes, but only the 5-(glutathion-S-yl)-alpha
134 protease was purified some 700-fold from rat liver microsomes by a combination of differential deterg
135 Inhibition of DNA adduct formation in human liver microsomes by alpha-lipoic acid, an inhibitor of N
143 this, when 8 was incubated in vitro with rat liver microsomes coupled to catalase and yeast A1DH, the
144 ults affirm the hypothesis that, as in human liver microsomes, CYP 1A2 in human lung cells appears to
145 the enzyme is comparable to that observed in liver microsomes, CYP3A4 behaves similarly to that obser
146 petitive intermolecular experiments with rat liver microsomes {(D)V = 12.5; (D)(V/K) = 10.9} but was
150 n Km (DK = DKm/HKm), but not on kcat, in rat liver microsomes (e.g. N-nitrosodimethylamine, ethanol,
155 e P450 isoform(s) involved in RA metabolism, liver microsomes from AHR-null and wild-type mice were s
157 Pg-/- mice was markedly diminished, whereas liver microsomes from control mice showed rapid SCD degr
158 rone formation (a minor metabolite formed in liver microsomes from control mice) was increased by app
160 on TST hydroxylation was measured ex vivo in liver microsomes from individually genotyped animals.
161 with pooled human liver microsomes (HLMs) or liver microsomes from male guinea pig, hamster, monkey,
162 bition by these Mabs was also observed using liver microsomes from male mice treated with phenobarbit
163 iphenyl-3'-ol (OH-PCB 102), respectively, by liver microsomes from male rats pretreated with differen
164 as elevated 11.4-fold over control values in liver microsomes from male rats treated with phenobarbit
166 omes from wild-type littermate control mice, liver microsomes from Pg-/- mice had significantly highe
169 ecies (ROS) formation were examined by using liver microsomes from scup and rat and expressed human C
170 ured as midazolam 1'- and 4-hydroxylation in liver microsomes from these knockout mice revealed a ran
174 ted a long half-life in both human and mouse liver microsomes, good permeability, modest protein bind
175 o address early issues such as a short mouse liver microsome half-life and a modest mouse pharmacokin
178 ly higher (P < 0.05) number of subjects with liver microsomes having high NNAL-N-Gluc formation activ
179 ly (P < 0.05) higher number of subjects with liver microsomes having low NNAL-O-Gluc formation activi
180 4, resulting in increased stability in human liver microsome (HLM) preparations relative to 2 (T1/2(H
182 -tetrabromodiphenyl ether (BDE-47) by human liver microsomes (HLM) and recombinant human CYPs, and t
184 , 4-ethylphenol, and 3-methylindole in human liver microsomes (HLM) were analyzed by HPLC coupled wit
185 *2) on SAHA glucuronidation phenotype, human liver microsomes (HLM) were analyzed for glucuronidation
190 tabolite (AM) from 2-oxoclopidogrel by human liver microsomes (HLMs) is greatly affected by the thiol
191 representative chiral PCB, with pooled human liver microsomes (HLMs) or liver microsomes from male gu
192 For kinetic studies, CYP2B6 and pooled human liver microsomes (HLMs) were incubated with BDE-47 (0-60
194 set of metabolic enzymes from human and rat liver microsomes, human and rat liver cytosol, and mouse
196 s, including (i) NADPH- and O2-fortified rat liver microsomes, (ii) cytochrome P450 (P450) 2B1 Suppor
197 penclomedine was also investigated using rat liver microsomes in an attempt to identify the ultimate
198 od involves incubation of cold compound with liver microsomes in the presence of [14C]potassium cyani
199 es of the metabolism of clopidogrel to human liver microsomes in the presence of four reductants, nam
204 detected norbuprenorphine formation in human liver microsomes incubated with 5-82 nM buprenorphine, w
205 ha- and beta-adduction was observed in mouse liver microsomes incubated with styrene at various conce
207 o design biologically active interfaces with liver microsomes is suggested to have immense significan
208 ETE by hematin (a nonenzymatic reaction), by liver microsomes isolated from control and phenobarbital
209 ity experiments were conducted in vitro with liver microsomes isolated from experimental CKD and cont
210 While 11 had good metabolic stability in rat liver microsomes, it showed modest solubility and blood-
211 FMOs, from Schizosaccharomyces pombe and hog liver microsomes) leads to the hypothesis that PvdA cata
212 es exhibit poor metabolic stability in mouse liver microsomes, likely due to the central tetrahydroqu
213 observed using cryopreserved hepatocytes or liver microsomes (LMs) supplemented for cytochrome P450
214 etabolism in human intestinal microsomes and liver microsomes make phosphoramidate 16 a prospective c
215 ma proteins, metabolic stability using human liver microsomes, metabolism by human liver microsomes a
216 olic half-lives of greater than 1 h in mouse liver microsomes (MLMs), and were active antinociceptive
217 d in three different mammalian models (human liver microsomes, murine liver microsomes, and commercia
218 ndent metabolism of estradiol and estrone by liver microsomes of BHA-treated animals as determined by
219 r the demonstration of the catalysis, by rat liver microsomes, of the conversion of 7-dehydrocholeste
220 ruthenium poly(vinylpyridine), DNA, and rat liver microsomes or bicistronically expressed human cyt
221 s of radioactive 17beta-estradiol with human liver microsomes or recombinant human cytochrome P450 is
222 s, we demonstrated that incubations of human liver microsomes or various human cytochrome P450 isofor
227 major components of technical chlordane, by liver microsomes prepared from male rats treated with co
228 Selectivity for CYP2B was demonstrated using liver microsomes prepared from rats and mice treated wit
229 vitro generation of QAC metabolites by human liver microsomes produced a series of oxidized metabolit
230 ydrogenases (IC50 = approximately 1 microM), liver microsomes provide 93% of the total retinal synthe
232 shown good metabolic stability in plasma and liver microsomes (rat and human), and 32 did not inhibit
233 ,3-b]indole (HONH-AalphaC) formed with human liver microsomes, recombinant human UGT isoforms, and hu
235 itonavir with reconstituted CYP3A4 and human liver microsomes resulted in a covalent binding stoichio
236 eed, incubating LMP400 and LMP776 with human liver microsomes resulted in two major metabolites of ea
237 fluorescent substrates were applied to human liver microsomes, results suggested that there was at le
238 lysis with recombinant CYP4F2 and with human liver microsomes revealed a substrate K(m) of 8 to 10 mi
239 N-(3,3-diphenyl-propyl)-nicotinamide in rat liver microsomes revealed extensive oxidative metabolism
241 time point substrate depletion assay in rat liver microsomes (RLM) is employed at the National Cente
242 with rat esophageal microsomes (REM) or rat liver microsomes (RLM) to give [3H]pentaldehyde (depenty
243 rosomal protein were determined for a pooled liver microsome sample, suggesting that this enzyme is a
245 One phase I metabolite was formed by human liver microsomes, seven phase I and II metabolites were
247 onist potency (cAMPi EC(50) = 162 nM), human liver microsome stability (T(1/2) = 62 min), and pharmac
248 tionally, OSU-ERbeta-12 displayed high human liver microsome stability and negligible CYP, hERG, and
249 hits were tested for caco-2 permeability and liver microsome stability to give two potential leads: J
250 nd promising values characterizing the mouse liver microsome stability, aqueous solubility, and mouse
251 exhibited low cytotoxicity and satisfactory liver microsomes stability and plasma protein binding.
252 sn-1 acyltransferase activity in murine liver microsomes stereospecifically and preferentially u
255 nary squirrel monkey imaging and human serum/liver microsome studies were performed to gain informati
256 roxyeicosatetraenoic acid (15S-HPETE) in rat liver microsomes suggested such a specific reaction.
257 etin has a short half-life (<7 min) in human liver microsomes, suggesting that its limited in vivo ef
258 ere rapidly metabolized in rodents and human liver microsomes, suggesting the possibility of rapid in
259 at recombinant CYP4F2 (Supersomes) and human liver microsomes supplemented with NADPH converted VK1 t
260 , and metabolic stability in human and mouse liver microsomes, supporting its potential for in vivo u
261 er, the favorable metabolic stability in rat liver microsomes supports future studies in in vivo mode
263 displays a good metabolic stability in human liver microsomes (t1/2 approximately 3 h and CLint = 3.5
264 h more membrane permeable and more stable to liver microsomes than a similar non-statine-containing d
265 h a five times higher conversion rate in dog liver microsomes than in human and monkey liver microsom
266 ously identified proteolytic activity in rat liver microsomes that cleaves an intact tripeptide, VIS,
268 tocol, the substrate is incubated with human liver microsomes, the reaction is quenched, and the subs
269 is denitrified to nitrite and acetone by rat liver microsomes; the denitrification rate is increased
270 C after incubation of racemic BPD with human liver microsomes; these were identified as monoglucuroni
272 hylpiperidine (2,2,6,6-TMPi) moiety in human liver microsomes to a ring-contracted 2,2-dimethylpyrrol
273 carried out to evaluate the ability of human liver microsomes to catalyze this reaction, compare the
274 re identified, and the extracts treated with liver microsomes to mimic physiological metabolism, with
275 RA 4-hydroxylase activity of wild-type mouse liver microsomes to the levels of AHR-null mouse liver.
276 ronidation activity of mouse, rat, and human liver microsomes toward the carcinogenic arylamine 4-ami
277 ing enzyme was partially purified from mouse liver microsomes using a fluorescent reporter similar in
278 We examined this process in purified rat liver microsomes using a rapid filtration technique and
281 , and its formation rate in a panel of human liver microsomes was strongly correlated with CYP3A4 con
283 etergent-solubilized, desaturase-induced rat liver microsomes we have characterized a protease that d
289 rphenadrine inhibition was observed in human liver microsomes (which has been taken to indicate CYP2B
291 PAP) and (13)C6-APAP were incubated with rat liver microsomes, which are known to bioactivate APAP to
293 2-ClHA is omega-oxidized in the presence of liver microsomes with initial omega-hydroxylation of 2-C
294 , the activity has been solubilized from rat liver microsomes with n-octyl-beta-D-glucoside and recon
295 one is quickly metabolized in vitro by mouse liver microsomes with NADPH (cytochrome P450) forming 7-
298 oline (PC) vesicles by solubilization of rat liver microsomes with the two substrates lysoPC and acyl
299 good metabolic stability in mouse and human liver microsomes, with half-lives of 29 and >60 min, res
300 nt source of 25OHD(3) hydroxylation by human liver microsomes, with the formation of 4beta,25-dihydro