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3 +/-) PECs with the SRC kinase inhibitor 3-(4-chlorophenyl)-1-(1,1-dimethylethyl)-1H-pyrazolo[3,4-d]py
4 ceptors with either sulpiride (SULP) or 4-(4-chlorophenyl)-1-(1H-indol-3-ylmethyl)piperidin-4-ol (L-7
5 or (CB1R) antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-cichlorophenyl)-4-methyl-1H-p yrazo
6 ing cooperativity with [(3)H]SR141716A [5-(4-chlorophenyl)-1-(2,4-dichloro-phenyl)-4-methyl-N-(piperi
7 elective antagonist [3H]N-(piperidinyl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H- pyrazo
8 ion using 3H-labeled N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-p yrazo
9 The biarylpyrazole, N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-p yrazo
10 the CB1R antagonists N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-p yrazo
11 tagonist [SR141716A, N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-p yrazo
12 the CB1R antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-p yrazo
14 ng the CB(1) antagonist N-(piperidinyl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyra zo
15 of the biaryl pyrazole N-(piperidinyl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyra zo
16 the inverse agonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazol
17 st/inverse agonist, N-(piperidiny-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazol
18 l treatment with SR141716 [N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazole
19 y the selective CB1 receptor antagonist 5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-N-(piperid
20 e CB1 receptor antagonist [N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3
21 noid antagonist SR141716A (N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3
22 ptor antagonist SR141716A [N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3
23 ist/antagonist rimonabant [N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3-
24 drug candidates, pyridine derivatives (S)-(4-chlorophenyl)-1-(4-(4-(trifluoromethyl)phenyl)-piperazin
26 nic environmental contaminants such as bis[4-chlorophenyl]-1,1,1-trichloroethane (p,p'-DDT) or its me
29 s were treated with/without CCG-203971 (N-[4-chlorophenyl]-1-[3-(2-furanyl)benzoyl]-3-piperidine carb
30 o insecticides including dieldrin, 1,1-bis(p-chlorophenyl)-2,2,2-trichloroethane (DDT), and pyrethroi
31 entrations of PCBs as well as DDE (1,1-bis(p-chlorophenyl)-2,2-dichloroethene), the degradation produ
32 we identified the novel IDO1 inhibitor N-(4-chlorophenyl)-2-((5-phenylthiazolo[2,3-c][1,2,4]triazol-
34 trogenic isomer, o,p -DDE [1,1-dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl) ethylene], and a mixtur
35 s demonstrated that the prodrug (2R,4S)-4-(3-chlorophenyl)-2-[(3,5-dimethyl-4-(4'-hydroxy-3'-isopropy
36 described here resemble CP-465,022 ((S)-3-(2-chlorophenyl)-2-[2-(6-diethylaminomethyl-pyridin-2-yl)-v
38 agonist CL 316243 [disodium (RR)-5-[2-[[2-(3-chlorophenyl)-2-hydroxyethyl]-amino]propyl]-1,3-benzodio
39 uding BRL 37,344 ((+/-)-(R*,R*)-[4-[2-[[2-(3-chlorophenyl)-2-hydroxyethyl]amino]propyl]phenoxy] aceti
40 commodated a CH2OH moiety (75; 2,2'-bis[1-(4-chlorophenyl)-2-hydroxyethylidene]carbonimidic dihydrazi
42 inhibitors [tatCN21 and KN-93 (N-[2-[[[3-(4-chlorophenyl)-2-propenyl]methylamino]methyl]phenyl]-N-(2
43 , human islets, and Min6 cells with (S)-2-(4-chlorophenyl)-3,3-dimethyl-N-(5-phenylthiazol-2-yl)butan
44 uents resulted in the identification of 3-(4-chlorophenyl)-3-((1-(hydroxymethyl)cyclopropyl)methoxy)-
46 of the most potent compounds, 2-benzyl-3-(4-chlorophenyl)-3-(3-hydroxypropoxy)-2,3-dihydroisoindol-1
47 (76; IC(50) = 15.9 +/- 0.8 microM) and 3-(4-chlorophenyl)-3-(4-hydroxy-3,5-dimethoxybenzyloxy)-2-pro
48 4 receptor agonists, exemplified by (E)-1-(4-chlorophenyl)-3-(4-pyridin-2-ylpiperazin-1-yl)propan-1-o
49 novel small molecule drug SU11274 [(3Z)-N-(3-chlorophenyl)-3-([3,5-dimethyl-4-[(4-methylpiperazin-1-y
50 -4,5-dihydro-1 H-pyrazole and 1-benzoyl-5-(4-chlorophenyl)-3-(thiophen-2-yl)-4,5-dihydro-1H-pyrazole.
51 ious calcium channel assay results for 5-(4- chlorophenyl)-3-[(E)-2-cyclohexylethenyl]-1-(2,4-dichlor
52 e data we developed a new compound, (Z)-2-(4-chlorophenyl)-3-[4-(4-methylpiperazine-1-yl)phenyl]acryl
53 AKT inhibitor AZD5363 [4-amino-N-[(1S)-1-(4-chlorophenyl)-3-hydroxypropyl]-1-(7H-pyrrolo[2,3-d]pyrim
54 ed during the hydrolysis of enantiopure 1-(4-chlorophenyl)-3-phenylallyl and 3-(4-chlorophenyl)-1-phe
55 he laser-flash photolytically generated 1-(4-chlorophenyl)-3-phenylallyl cation with water provided a
56 led that three functional groups (i.e. 3-(4'-chlorophenyl), 4-benzyl, and 7-methoxyl) of this coumari
57 mixed functional activity, a series of 5'-(4-chlorophenyl)-4,5alpha-epoxypyridomorphinans possessing
59 luated the radiotracer (11)C-AS2471907 (3-(2-chlorophenyl)-4-(methyl-(11) C)-5-[2-[2,4,6-trifluorophe
61 (piperidin-1-yl)-1-(2,4-dichlorophenyl)-5-(4-chlorophenyl)-4-methyl-1H- pyrazole-3-carboxamide], a CB
62 (piperidin-1-yl)-1-(2,4-dichlorophenyl)-5-(4-chlorophenyl)-4-methyl-1H-pyrazole -3-carboxamide [AM251
63 razolo[3,4-d]pyrimidinone inhibitor 2-((1-(3-chlorophenyl)-4-oxo-4,5-dihydro-1H-pyrazolo [3,4-d]-pyri
64 The most potent MAO-B inhibitors were N-(3'-chlorophenyl)-4-oxo-4H-chromene-3-carboxamide (20) (IC50
65 24 that reduced Mcl-1 levels and 4-(4-{[2-(4-chlorophenyl)-5,5-dimethyl-1-cyclohexen-1-yl]methyl}-1-p
66 ate (SPB03255) (IC(50), 6.3 microM) and 4-(3-chlorophenyl)-5-(2,4-dichlorobenzylthio)-4H-1,2,4-triazo
67 creased brain cholinergic activity, and 3-(2-chlorophenyl)-5-(5-methyl-1-(piperidin-4-yl)-1H-pyrrazol
68 zole based core and led to 4-{5-[(E)-2-{4-(2-chlorophenyl)-5-[5-(methylsulfonyl)pyridin-2-yl]-4H-1,2,
69 d a series of novel substituted N-(4-amino-2-chlorophenyl)-5-chloro-2-hydroxybenzamide analogues as p
70 antibiotic in the series proved to be [5-(4-chlorophenyl)-5-hydroxy-3-(trifluoromethyl)-4,5-dihydro-
71 he commercial vendor was reassigned as [3-(4-chlorophenyl)-5-hydroxy-5-(trifluoromethyl)-4,5-dihydro-
72 estigated the structural determinants for (3-chlorophenyl)(6,7-dimethoxy-1-((4-methoxyphenoxy)methyl)
73 he substituted tetrahydroisoquinoline CIQ (3-chlorophenyl)(6,7-dimethoxy-1-((4-methoxyphenoxy)methyl)
74 ) and the GluN2C/D-selective potentiator [(3-chlorophenyl)(6,7-dimethoxy-1-((4-methoxyphenoxy)methyl)
75 with the enantiomers of PDE9 inhibitor 1-(2-chlorophenyl)-6-(3,3,3-trifluoro-2-methylpropyl)-1H-pyra
76 ding the brain-penetrant compound 14G: [5-(4-chlorophenyl)-6-(cyclopropylmethoxy)-N-[(1R,2R)-2-hydrox
77 y structural features of pyrimethamine (5-(4-chlorophenyl)-6-ethylpyrimidine-2,4-diamine) that contri
79 aper describes the discovery of N-[(4R)-6-(4-chlorophenyl)-7-(2,4-dichlorophenyl)-2,2-dimethyl-3,4-di
80 selective SFKs inhibitor, PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo [3, 4-d] pyramidine),
81 oride) and Src kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo [3, 4-d] pyrimidine.
82 Src kinase inhibition by either 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo [3,4-d] pyrimidine (P
84 kinase (PTK) inhibitors such as 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d] pyrimidine (PP
85 eatment with a c-Src inhibitor (4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d]pyrimidine) abr
86 d Src-tyrosine kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo [3,4,d]pyrimidine (PP2
87 The chemical Src inhibitor PP2 {4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo [3,4-d]pyrimidine} and
88 cific tyrosine kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo(3,4-d)pyrimidine (PP2)
89 yrosine kinase activity by PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo(3,4-d)pyrimidine) trea
90 scharges was also suppressed by 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-D]pyrimidine (10 m
91 Src kinase activity with 10 mum 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2)
92 he Src kinase family inhibitor, 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2)
93 ed by the Src-kinase inhibitor, 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2)
94 hed by the Src family inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2)
95 ted by the src kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2)
96 resence of Src kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2)
97 the ATP-competitive inhibitors 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine or Sr
98 y the Src kinase inhibitor PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) and
100 ion with the Src inhibitor PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) or o
101 ely inhibited by treatment with 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine, a sp
102 kinase-specific inhibitor PP2 [4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine].
103 ent study, we have found that 4-benzyl-3-(4'-chlorophenyl)-7-methoxycoumarin is a potent competitive
104 c were reversed by treatment of 4-amino-5-(4-chlorophenyl)-7-t-butyl(pyrazolo)[3,4-d]pyrimidine (PP2)
105 he usefulness of 2beta-carbomethoxy-3beta-(4-chlorophenyl)-8-(2-(18)F-fluoroethyl)nortropan e ((18)F-
106 AT ligand [(18)F]2beta-carbomethoxy-3beta-(4-chlorophenyl)-8-(2-fluoroethyl)-nortropane ([(18)F]FECNT
110 Compound 9 (N-{1-[8-(2-chlorophenyl)-9-(4-chlorophenyl)-9H-purin-6-yl]piperidin-4-yl}pentana mide)
113 Here we report a lead structure ethyl 2-((4-chlorophenyl)amino)-thiazole-4-carboxylate, termed O4I2,
114 of five anilino enaminones E139, ethyl 4-(4'-chlorophenyl)amino-6-methyl-2-oxocyclohex-3-en-1-oate (E
115 oxocyclohex-3-en-1-oate (E122), methyl 4-(4'-chlorophenyl)amino-6-methyl-2-oxocyclohex-3-en-1-oate (E
118 ligand, LCu(III)-O(2)CAr(1) (3, Ar(1) = meta-chlorophenyl), and we compare its reactivity to that of
119 c assay for detection and quantitation of (p-chlorophenyl)aniline (CPA) in biological samples was dev
121 y the same cascade of events to produce 1-(o-chlorophenyl)benzo[ghi]fluoranthene, which then suffers
122 ycin by the presence of a hydrophobic N-4-(4-chlorophenyl)benzyl (also referred to as 4'-chlorobiphen
124 0.01-1.20 mg/kg) or the 5-HT(3) agonist l-(m-chlorophenyl)-biguanide hydrochloride (mCPBG; 5.0-15.0 m
125 lic additive tetradodecylammonium tetrakis(4-chlorophenyl)borate (ETH-500) and a cation-sensitive mem
127 e of the ionic additive potassium tetrakis(4-chlorophenyl)borate substantially reduced the selectivit
128 er small ligand molecules such as tetrakis(4-chlorophenyl)borate, metergoline, lidocaine, and bromhex
130 lanine affinity-modifying group with N-(4-(p-chlorophenyl)butanoyl)-Gly and N-(4-(p-methoxyphenyl)but
131 3055 and (68)Ga-HTK03086 bearing the N-(4-(p-chlorophenyl)butanoyl)-Gly and N-(4-(p-methoxyphenyl)but
133 is the nitrogen mustard analog of [4-[[N-(3-chlorophenyl)carbamoyl]oxy]-2-butynyl]trimethylammonium
134 man M(3) receptor with the exception of 4-(m-chlorophenyl-carbamoyloxy)-2-butynyltrimethylammonium (M
135 e SPAK inhibitor, 5-chloro-N-(5-chloro-4-((4-chlorophenyl)(cyano)methyl)-2-methylphenyl)-2-hydroxyben
136 ea glyburide, and the cyanoguanidine N-[1-(3-chlorophenyl)cyclobutyl]-N'-cyano-N"-3-pyridinyl-guanidi
137 an SKCa blocker) but was unaltered by 1-[(2-chlorophenyl) diphenylmethyl]-1H-pyrazole (1 microM TRAM
138 tivity of K(Ca)3.1 to clotrimazole and 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34).
139 visualizing the mechanism of TRAM-34 (1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole), senicapoc (2,
140 romobenzene (HBB), 1,1,1-trichloro-2,2-bis(4-chlorophenyl) ethane (DDT), and tris(2,3-dibromopropyl)
143 ) and its metabolites 1,1-dichloro-2,2-bis(4-chlorophenyl)ethane (DDD) and 1,1-dichloro-2,2-bis(4-chl
144 hether exposure to 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) and its isomers and metabolite
147 The insecticide 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) is still used for disease cont
148 egnancy losses and 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) were limited because they did
149 e of the pesticide 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT), are hormonally active agents.
154 etabolites, 4,4'-DDD [1,1-dichloro-2,2-bis(p-chlorophenyl)ethane] and 4,4'-DDE [1,1-dichloro-2,2-bis(
155 extract 4,4'-DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane] and its metabolites, 4,4'-DDD [1,1-
158 ed biphenyl (PCB)-153; 1-dichloro-2,2-bis (p-chlorophenyl) ethylene (p,p'-DDE), and hexachlorobenzene
159 p -DDE [1,1-dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl) ethylene], and a mixture of both isomers.
160 tiandrogen, p,p -DDE [1,1-dichloro-2,2-bis(p-chlorophenyl) ethylene], the most prevalent and persiste
163 enyl)ethane (DDD) and 1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene (DDE), are often detected in soils
164 her applications, and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE), the main metabolite of the
165 anochlorines such as 1,1,-dichloro-2,2-bis(p-chlorophenyl)ethylene (p,p -DDE), polychlorinated biphen
169 d biphenyls) and DDE [1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene] reduces 6-month infant BCG vaccin
170 ethane] and 4,4'-DDE [1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene], from an historically contaminate
172 onimidic dihydrazide), and 69 (2,2'-bis[1-(4-chlorophenyl)ethylidene]carbonimidic dihydrazide hydroch
174 Introduction of an ortho-tolyl or ortho-chlorophenyl group at the purine C-8 position restored t
177 y inhibited by NH4(+) and carbonyl cyanide m-chlorophenyl hydrazine and was insensitive to the ATP-bi
178 cAMP exchange protein inhibitor alpha-[2-(3-chlorophenyl)hydrazinylidene]-5-(1,1-dimethylethyl)-b-ox
179 Here, we report that both carbonyl cyanide m-chlorophenyl hydrazone (CCCP) treatment and adenosine mo
181 in (a Ca2+ ionophore) and carbonyl cyanide m-chlorophenyl hydrazone (CCCP; a mitochondrial uncoupler)
182 nated by the protonophore carbonyl cyanide m-chlorophenyl hydrazone and is approximately 10-fold high
183 mitochondrial ionophore, carbonyl cyanide m-chlorophenyl hydrazone and other respiratory inhibitors,
184 ondrial depolarization by carbonyl cyanide m-chlorophenyl hydrazone did not induce Parkin translocati
186 Although the uncoupler carbonyl cyanide m-chlorophenyl hydrazone inhibited AGT(P11LG170R) import i
187 iants but does not affect carbonyl cyanide m-chlorophenyl hydrazone or apoptosis-induced cleavage.
188 ential with the uncoupler carbonyl cyanide m-chlorophenyl hydrazone or the release of acidic Ca(2+) s
190 r treatment with NH4Cl or carbonyl cyanide m-chlorophenyl hydrazone, indicating that SWEET17 function
191 h TNF or uncoupling agent carbonyl cyanide m-chlorophenyl hydrazone, suggesting an essential role for
192 n-mediated mitophagy upon carbonyl cyanide m-chlorophenyl hydrazone-induced mitochondrial depolarizat
195 dria with antimycin A1 or carbonyl cyanide m-chlorophenyl-hydrazone, the stimulation-induced increase
196 irect (phenobarbital) and direct CITCO [6-(4-chlorophenyl)imidazo[2,1-b]1,3thiazole-5-carbaldehyde O-
197 picin and the CAR agonist/ligand CITCO [6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde
199 tivators of human CAR than is prototype 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde
200 results of this study demonstrate that 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde-
201 eactivated by the direct CAR activator, 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde-
203 trachlorodibenzo-p-dioxin (TCDD)], CAR [6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde-
204 ed in the presence of the CAR activator 6-(4-chlorophenyl)imidazo[2,1-b]thiazole-5-carbaldehyde O-(3,
205 ter in response to the human CAR ligand 6-(4-chlorophenyl)imidazo[2,1-b]thiazole-5-carbaldehyde O-(3,
206 two phenyl rings, 1-PBI is larger than 1-(4-chlorophenyl)imidazole (1-CPI) and 4-(4-chlorophenyl)imi
207 rystal structure of P450 2B4 bound with 1-(4-chlorophenyl)imidazole (1-CPI) has been determined to de
208 nd testosterone and with the inhibitors 4-(4-chlorophenyl)imidazole (4-CPI) and bifonazole (BIF).
209 1-(4-chlorophenyl)imidazole (1-CPI) and 4-(4-chlorophenyl)imidazole (4-CPI) but smaller than bifonazo
210 P450 2B6 in complex with the inhibitor 4-(4-chlorophenyl)imidazole (4-CPI) has been determined using
211 gand-free P450 2B4 and the complex with 4-(4-chlorophenyl)imidazole (4-CPI) or 1-biphenyl-4-methyl-1H
212 Binding of 4-phenylpyridine (4-PP) or 4-(4-chlorophenyl)imidazole (4-CPI) showed 1:1 stoichiometry
213 gnatures in binding the small inhibitor 4-(4-chlorophenyl)imidazole (4-CPI) versus the large bifonazo
214 g-metabolizing P450 2B6 in complex with 4-(4-chlorophenyl)imidazole (4-CPI) yielded the first atomic
218 me P450 2B4 with the specific inhibitor 4-(4-chlorophenyl)imidazole (CPI) in the active site was dete
220 ures with the small molecule inhibitors 4-(4-chlorophenyl)imidazole and 1-(4-chlorophenyl)imidazole.
225 hroughput screening campaign identified 5-(2-chlorophenyl)indazole compound 4 as an antagonist of the
226 and used to study the biotransformation of p-chlorophenyl isocyanate (CPIC) to CPA in rats administer
227 1195 [(R,S)-N-methyl-N-(1-methylpropyl)-1-(2-chlorophenyl)isoquinoline-3-carboxamide)] or DPA-714 in
229 isingly, 3beta-(4-methylphenyl)-2beta-[3-(4'-chlorophenyl)isoxazol-5-yl]tropane (3p) and 3beta-(4-met
230 lated that C-DIM12 [1,1-bis(3'-indolyl)-1-(p-chlorophenyl) methane] would suppress inflammatory signa
231 s, technical mixture impurities such as tris(chlorophenyl)methane (TCPM), the presumed TCPM metabolit
232 lybrominated diphenyl ethers (PBDEs), tris(4-chlorophenyl)methanol (TCPMOH), and chlordane-related co
233 ne (TCPM), the presumed TCPM metabolite tris(chlorophenyl)methanol (TCPMOH), and structurally related
235 x o-2,3-dihydro-1H-indole-5-sulfonic acid (3-chlorophenyl)methylamide, termed [11C]SU11274 ([11C]14)
237 in the cavity by placing the OMe-indole and chlorophenyl moieties into the V-shaped pockets, respect
238 razoline platform of which (-)-12a ((-)-3-(4-chlorophenyl)-N'-[(4-cyanophenyl)sulfonyl]-4-phenyl- 4,5
240 s oleanolic acid and 3-(2-chlorophenyl)-N-(4-chlorophenyl)-N, 5-dimethylisoxazole-4-carboxamide stimu
242 lamide (AMG0610), capsazepine, and (2E)-3-(4-chlorophenyl)-N-(3-methoxyphenyl)acrylamide (SB-366791)
244 e selective agonists oleanolic acid and 3-(2-chlorophenyl)-N-(4-chlorophenyl)-N, 5-dimethylisoxazole-
245 ts peripherally restricted analog 14H: [5-(4-chlorophenyl)-N-[(1R,2R)-2-hydroxycyclohexyl]-6-(2-metho
246 X inhibitors nordihydroguaiaretic acid, N-(4-chlorophenyl)-N-hydroxy-N'-(3-chlorophenyl)urea, BWA137C
247 f (3)H-PK11195 (PBR probe, (3)H-labeled 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinoline
249 s were similar to that for 17 (PK11195, 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)isoquinoline-3-
250 1)C-PK11195 ((11)C-labeled N-butan-2-yl-1-(2-chlorophenyl)-N-methylisoquinoline-3-carboxamide), which
251 that (11)C-ER176 ((11)C-(R)-N-sec-butyl-4-(2-chlorophenyl)-N-methylquinazoline-2-carboxamide), a new
252 show that the specific Na(v)1.8 blocker 5-(4-chlorophenyl-N-(3,5-dimethoxyphenyl)furan-2-carboxamide
253 er for activated microglia, [(11)C](R)-(1-[2-chlorophenyl]-N-methyl-N-[1-methylpropyl]-3-isoquinoline
254 monitored in vivo by (11)C-(R)-PK11195 (1-[2-chlorophenyl]-N-methyl-N-[1-methylpropyl]-3-isoquinoline
256 hlorophenyl [(+/-)-4n], naphthyl (4r), and 3-chlorophenyl or 3-propyl analogues 4s and 4t, respective
257 modified substituents at the 10-position (4'-chlorophenyl or phenylethyl groups), and a chlorine atom
258 red over meta and ortho regioisomers, with p-chlorophenyl (p-ClPh) being one of the most predominant
259 ernization of the nitrogen atom of 2-amino-4-chlorophenyl phenyl sulfide analogues of chlorpromazine
261 yl p-nitrophenyl phosphate (I) and diethyl p-chlorophenyl phosphate (II) demonstrated that the ioniza
262 olysis for the sluggish substrate, diethyl p-chlorophenyl phosphate, and a decrease in the kinetic co
263 d identify a highly active derivative ((4-(3-chlorophenyl)piperazin-1-yl)(2-ethoxyphenyl)methanone),
264 molecule repressor of LRH-1, SR1848 (6-[4-(3-chlorophenyl)piperazin-1-yl]-3-cyclohexyl-1H-pyrimidine-
265 the D4 receptor antagonist L745870 (3-[[4-(4-chlorophenyl)piperazin-1-yl]methyl]-1H-pyrrolo[2,3-b]pyr
266 thio)-2-morpholinopropiophenone (MMMP), 1-(3-chlorophenyl) piperazine (mCPP), and 5-(2-Aminopropyl) I
267 bstrates: fenfluramine, d-fenfluramine, 1-(m-chlorophenyl)piperazine (mCPP) and 1-(m-trifluoromethylp
268 s work with the 5-HT2C receptor agonist 1-(m-chlorophenyl)-piperazine hydrochloride (mCPP), which enh
270 l(THF)2]+[Co(CO)4]- (1; ClTPP = meso-tetra(4-chlorophenyl)porphyrinato; THF = tetrahydrofuran), which
271 electron deficient aromatic groups at the 4-chlorophenyl position for activity at the CB1 receptor,
272 cked by either AIP or KN93 (N-[2-[[[(E)-3-(4-chlorophenyl)prop-2-enyl]-methylamino]methyl]phenyl]-N-(
273 s( p-chlorophenyl)-propene) and DDPS (bis( p-chlorophenyl)-propane) after chemical treatments evidenc
274 p-chlorophenyl)-bromoethylene), DDPU (bis( p-chlorophenyl)-propene) and DDPS (bis( p-chlorophenyl)-pr
275 thoxyphenyl)propenone (1b), and 3-azido-1-(4-chlorophenyl)propenone (1c) exhibit dramatic mechanical
276 propyl]-6-methylphenyl]-4-[(2R )-methyl-3-(4-chlorophenyl)propionyl]piperazine (10d), was identified
277 CaSR-specific allosteric modulators N-(3-[2-chlorophenyl]propyl)-(R)-alpha-methyl-3-methoxybenzylami
278 hydro-N-phenylpyridinium (a), N-(3-dehydro-5-chlorophenyl)pyridinium (b), and N-(3-dehydrophenyl)pyri
279 w series of compounds in which the 2-amino-5-chlorophenyl ring of phenstatin analogue 7 was replaced
281 in the bent domain interface, whereas two p-chlorophenyl rings extend into two wings of the interfac
282 4-, 235-, 236-, 245-, 2345-, 2346-, and 2356-chlorophenyl rings, as indicated by the underscores.
283 the derivatization of the methoxyphenyl and chlorophenyl rings, in addition to the diazepine ternary
284 Compounds with a ligand containing the 4-chlorophenyl substituent (6a and 6b) exhibited the stron
285 yridomorphinan (6, SRI-22138) possessing a 4-chlorophenyl substituent at the 5'-position on the pyrid
289 ated the mechanism of CCG-4986 [methyl-N-[(4-chlorophenyl)sulfonyl]-4-nitro-benzenesulfinimidoate], a
290 Of 3028 compounds screened, 1, methyl N-[(4-chlorophenyl)sulfonyl]-4-nitrobenzenesulfinimidoate (CCG
291 Using the Src inhibitor PP2 [4-amino-5-(4-chlorophenyl)-(t-butyl)pyrazolo[3,4-d]pyrimidine], we de
292 tants for the hydrolysis of II and diethyl p-chlorophenyl thiophosphate (IV) were determined for the
293 in naive animals: pretreatment with 3beta-(p-chlorophenyl)tropan-2beta-carboxylic acid p-isothiocyana
294 s whether the phenyltropane analog, 3beta-(4-Chlorophenyl) tropane-2beta-[3-(4'-methylphenyl) isoxazo
295 h the DAT ligand 2beta-carbophenoxy-3beta-(4-chlorophenyl)tropane (9, RTI-113) failed to displace [18
298 ective analogues such as GBR 12 909 and 3-(4-chlorophenyl)tropane-2-carboxylic acid phenyl ester (RTI
299 e irreversible cocaine analog [125I]3beta-(p-chlorophenyl)tropane-2beta-carboxylic acid, 4'-azido-3'-
300 vatable irreversible cocaine analog 3beta-(p-chlorophenyl)tropane-2beta-carboxylic acid, 4'-azido-3'-
301 tic acid, N-(4-chlorophenyl)-N-hydroxy-N'-(3-chlorophenyl)urea, BWA137C, and eicosatetraynoic acid re