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1  arrest in response to exposure to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) alone; however, 70-80%
2 e 5-day cycle (1omega) of low-dose 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and a second group rec
3 esponse to the chemotherapy agents 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and cis-diamminedichlo
4 ating-agent-induced methylation by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) at the O(6) position o
5 al administration of radiation and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) chemotherapy in three
6  to inhibit MGMT and to potentiate 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) in a MGMT-positive hum
7 Low concentrations of diamide plus 1,3-bis(2 chloroethyl)-1-nitrosourea (BCNU) increased intracellula
8 tentiate the antitumor efficacy of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) is being tested in cli
9     The bifunctional DNA alkylator 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) is cytotoxic primarily
10 ion of eNOS, by exposure to either 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) or glutathione reducta
11 tion of 30 mg/kg 6-BG and 10 mg/kg 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) or with 40 mg/kg BCNU
12 onal cycles of chemotherapy using 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) resulted in similar in
13 ter resistance to cell killing by 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) than overexpression of
14 ured with buthionine sulfoximine and 1,3-bis(chloroethyl)-1-nitrosourea (BCNU) to inhibit glutathione
15 th adenoviral MnSOD (AdMnSOD) plus 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) would lead to an incre
16 stance to the cytotoxic effects of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a CNU commonly used f
17  study, we examined the effects of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a commonly used CNU,
18 rly hematopoietic progenitors from 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a stem cell toxin, an
19 agenic effects of temozolomide and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), and no further sensit
20 -disulfide oxidoreductase enzymes (1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), arsenite, and phenyla
21        The chemotherapeutic agents 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), carboplatin, and camp
22 ucts and compromise its integrity (1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), cisplatin, H(2)O(2) a
23                In combination with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), the prodrugs were not
24  and to the chloroethylating agent 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), with and without AGT
25 ro, 2,4-dinitrobenzene (CDNB); or 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU).
26 in of safety than the nitrosourea, 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).
27 re > 10-fold resistant to the CENU 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).
28 ncluding melphalan, cisplatin, and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).
29 sferase (AGT) and are sensitive to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).
30 ctive in enhancing cell killing by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).
31 mbucil, melphalan, and carmustine [1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU)] weakly induced lucife
32 -benzylguanine (O6-BG, 20 microM) or 1,3-bis(chloroethyl)-1-nitrosourea (BCNU, 100 microM), resulted
33 roencapsulation of antitumor agent 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU, Carmustine) into biode
34  transduction and O6-benzylguanine/1,3-bis(2-chloroethyl)-1-nitrosourea (BG/BCNU) treatment has been
35 n animals treated with carmustine (1,3-bis(2-chloroethyl)-1-nitrosourea 20 mg/kg/week, i.v. x 2; diff
36  effects of chemotherapy [25 mg/kg 1,3-bis(2-chloroethyl)-1-nitrosourea administered with a single i.
37 iving IL-2-transduced cells or 10% 1,3-bis(2-chloroethyl)-1-nitrosourea alone.
38  also protected HeLa cells against 1,3-bis(2-chloroethyl)-1-nitrosourea and methyl methanesulfonate c
39 e toxic and clastogenic effects of 1,3-bis(2-chloroethyl)-1-nitrosourea and mitomycin C (MMC), as mea
40 rapeutic alkylating agents, namely 1,3-bis(2-chloroethyl)-1-nitrosourea and mitomycin C, indicating t
41  cells and polymers containing 10% 1,3-bis(2-chloroethyl)-1-nitrosourea had significantly improved su
42 reatine:Pi and ATP:Pi ratios after 1,3-bis(2-chloroethyl)-1-nitrosourea treatment indicate improved b
43 oximine) or glutathione reductase (1,3-bis(2-chloroethyl)-1-nitrosourea) in the presence or absence o
44 ozolomide, N-methyl-N-nitrosourea, 1,3-bis(2-chloroethyl)-1-nitrosourea, 9-aminocamptothecin, topotec
45 ne in DNA with the antitumor agent 1,3-bis(2-chloroethyl)-1-nitrosourea, a chemotherapeutic used to c
46 of BLMVECs with the GR inhibitor, 1,3 bis-(2 chloroethyl)-1-nitrosourea, abolished the inhibitory eff
47  had been treated with carmustine (1,3-bis(2-chloroethyl)-1-nitrosourea, or BCNU).
48 0 degrees C and after addition of 1,3-bis-(2-chloroethyl)-1-nitrosourea, there was effective S-thiola
49 -mediated tumor cell resistance to 1,3-bis(2-chloroethyl)-1-nitrosourea, we performed a novel dose es
50 ze human tumor cells to killing by 1,3-bis(2-chloroethyl)-1-nitrosourea, with O6-benzyl-3'-O-(gamma-f
51 lling by the combination of BG and 1,3-bis(2-chloroethyl)-1-nitrosourea.
52 tance to the combination of BG and 1,3-bis(2-chloroethyl)-1-nitrosourea.
53 kyl N-nitrosourea-type drugs, e.g. 1,3-bis(2-chloroethyl)-1-nitrosourea.
54 ne or in combination with 13 mg/m2 1,3-bis(2-chloroethyl)-1-nitrosourea.
55  with 0.5, 1, or 2 x LD10 doses of 1,3-bis(2-chloroethyl)-1-nitrosourea.
56 therapeutic drugs temozolomide and 1,3-bis(2-chloroethyl)-1-nitrosourea.
57 lating agents, such as carmustine [1,3-bis(2-chloroethyl)-1-nitrosourea; BCNU], lomustine [1-(2-chlor
58 ere treated with the alkylator agent 1,3-bis-chloroethyl-1-nitrosourea.
59 of glutathione reductase (GR) with 1,3-bis[2-chloroethyl]-1-nitrosourea or transfection of macrophage
60 cells as compared with 19 exhibited by 4-[(2-chloroethyl)(2-mesyloxyethyl)amino]benzoyl-l-glutamic ac
61 ity differential than the published N-[4-[(2-chloroethyl)(2-mesyloxyethyl)amino]benzoyl]-l-glutamic a
62  of this class, 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)- 2(-)[[2-chloroethyl)-amino]carbonyl]hydraz
63  of this class, 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)-2-(methylamino)carbonylhydrazine (101M).
64  another agent, 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)-2-[(4-nitrobenzyloxy)carbonyl]hy drazine (P
65 ty to sensitize 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)-2-[(methylamino)carbonyl]hydrazine (laromus
66 f these agents, 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)-2-[[1-(4-nitrophenyl)ethoxy]carb onyl]hydra
67 cumulation of a liposome formulation of 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU), an effec
68 motherapy regimen between procarbazine, 1-(2-Chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU), and vinc
69 r response to the chemotherapeutic drug 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea in vitro.
70 ethyl)-1-nitrosourea; BCNU], lomustine [1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea; CCNU], and stre
71 and presence of sublethal nitrosourea ([1-(2-chloroethyl)-3-cyclohexyl-l-nitrosourea]; CCNU) concentr
72 -(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea (ACNU), an alkylating antitum
73  without affecting [3H](+)-7-OH-DPAT (D3); N-chloroethyl-7-OH-DPATs blocked both radioligands in Acc
74 bis(2-chloroethyl)nitrosourea (BCNU)-induced chloroethyl adducts are fully converted into interstrand
75 ted esters provides CNTs functionalized with chloroethyl, allyl, and propargyl groups, which can furt
76 race impurities from the synthesis of tris(2-chloroethyl)amine (HN3) that point to the reagent and th
77 trophiles such as N-acylimidazoles and bis(2-chloroethyl)amines, covalent screening enabled the surpr
78 g PGP (N-p- inverted question markN,N-bis (2-chloroethyl)amino inverted question markphenoxycarbonyl-
79  higher than that of sarcolysin [(L-3-[bis(2-chloroethyl)amino]-L-phenylalanine] against all leukemia
80   ID50 and ID90 values for L-prolyl-L-m-[bis(chloroethyl)amino]-phenylalanyl-L-norvaline ethyl ester
81 a-glutamyl-alpha-amino-beta-[[[2-[[bis[bis(2-chloroethyl)amino]ph osp horyl]oxy]ethyl]sulfonyl]propio
82                       [3,5-Difluoro-4-[bis(2-chloroethyl)amino]phenyl]carbamoyl-l-glutamic acid gave
83  coupling of two key intermediates: 4-[bis(2-chloroethyl)-amino]-L-phenylalanine ethyl ester trifluor
84 s(methylsulfonyl)-1-(2-chloroethyl)- 2(-)[[2-chloroethyl)-amino]carbonyl]hydrazine, was further evalu
85             Electrophilic modules, whether N-chloroethyl aniline or diazirine, have reactive profiles
86 th induced proximity; however, probes with N-chloroethyl aniline were more reactive and more specific
87 ompounds consist of 4-(3-aminopropyl)-N,N-(2-chloroethyl)-aniline linked to 2-(4'-hydroxyphenyl)-3-me
88 We converted PVC and styrene in up to 89% (1-chloroethyl)benzene in less than 1 h of white light irra
89 tothermally recycled styrene achieved 84% (1-chloroethyl)benzene under white LED light in 1 h, and co
90 S plastics via photothermal conversion to (1-chloroethyl)benzene, a commodity chemical with excellent
91 is (chloromethyl)-propane-1,3-diyltetrakis(2-chloroethyl) bisphosphate (V6)).
92 -bis(chloromethyl)propane-1,3-diyltetrakis(2-chloroethyl) bisphosphate, known as V6, is a flame retar
93  this N-substituent could be cleaved using 1-chloroethyl chloroformate.
94 -32 by S-(2-chloroethyl)glutathione and S-(2-chloroethyl)cysteine, in peptides 1-24 and 45-58, was si
95                                            N-chloroethyl derivatives of 7-hydroxy-1,2,3,4-tetrahydron
96 Dichloroborane adducts of monoglyme and beta-chloroethyl ether also showed high reactivity, even at r
97             Dioxane, ethyl acetate, and beta-chloroethyl ether form relatively stable boron trichlori
98                           Monoglyme and beta-chloroethyl ether give stable dichloroborane adducts req
99 ether, dioxane, anisole, ethyl acetate, beta-chloroethyl ether, and monoglyme, were examined as prosp
100 xyphenylsulfone (D-8) (<=230 ng/g ww), bis(2-chloroethyl)ether-4,4'-dihydroxydiphenyl sulfone monomer
101 d sulfur mustard and its chemical simulant 2-chloroethyl ethyl sulfide (CEES) with half-lives less th
102                    Mass spectra for xenon, 2-chloroethyl ethyl sulfide (CEES), and octane were acquir
103 r the oxidation of a mustard gas analogue, 2-chloroethyl ethyl sulfide (CEES), in the presence of an
104  photooxidation of a mustard-gas simulant, 2-chloroethyl ethyl sulfide (CEES), is studied using a por
105 ch we probed by the selective oxidation of 2-chloroethyl ethyl sulfide (CEES).
106  for binding the sulfur mustard surrogate, 2-chloroethyl ethyl sulfide (CEES).
107  parent fabric for a mustard gas simulant, 2-chloroethyl ethyl sulfide (CEES).
108  oxidation of the sulfur mustard simulant, 2-chloroethyl ethyl sulfide (CEES).
109 lytically active for the photooxidation of 2-chloroethyl ethyl sulfide (CEES, a chemical warfare simu
110                          The hydrolysis of 2-chloroethyl ethyl sulfide has been examined in an effort
111 d the adsorption behaviors of n-hexane and 2-chloroethyl ethyl sulfide to explore the structure-prope
112 dditional products in the disappearance of 2-chloroethyl ethyl sulfide with k3 in particular causing
113 nethiol) and one S-type vesicant simulant (2-chloroethyl ethyl sulfide) were found in each case (samp
114 xidation (O(2) oxidation of the thioether, 2-chloroethyl ethyl sulfide, CEES) led to the discovery th
115             Detection of the CWA simulants 2-chloroethyl ethyl sulfide, triethyl phosphate, and dimet
116 CEES to the comparatively nontoxic product 2-chloroethyl ethyl sulfoxide (CEESO) without formation of
117 ES was transformed selectively to nontoxic 2-chloroethyl ethyl sulfoxide and vinyl ethyl sulfoxide us
118           A compound (Alchemix) with the bis-chloroethyl functionality confined to one side chain alk
119  by thioredoxins alkylated at Cys-32 by S-(2-chloroethyl)glutathione and S-(2-chloroethyl)cysteine, i
120  mutations seen in other organisms with S-(2-chloroethyl)glutathione or ethylene dibromide.
121                    The synthetic analog S-(2-chloroethyl)glutathione was used to produce DNA damage;
122 -based assays accompanied replacement of the chloroethyl group with unhalogenated substituents.
123                         In contrast, O(6)-(2-chloroethyl)guanine lesions produced by agents such as l
124 (aminocarbonyl)-1,2-bis(methylsulfonyl)-1-(2-chloroethyl)hydr azi nes were synthesized and primarily
125 ylating species 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)hydrazine (90CE) after bioreductive activati
126 yloxycarbonyl)-1, 2-bis(methylsulfonyl)-1-(2-chloroethyl)hydrazines (4, 6, and 7) were synthesized an
127 ed by agents such as lomustine and the N3-(2-chloroethyl)imidazotetrazine mitozolomide rapidly evolve
128                                        The 2-chloroethyl moiety on selected dithiazoles was also modi
129 ell-line panel at the NCI, indicate that the chloroethyl moiety plays a major role in the enhanced ac
130 wley rats were administered 50 mg/kg i.p. N-(chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) or were
131  NE in the spinal cord dorsal horn with N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (D
132 inistered the noradrenergic neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (D
133 males with the noradrenergic neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (D
134  by cortical NA denervation with DSP-4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride] a
135 rats and in rats pretreated with DSP-4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine], a neurotoxin t
136 tau transgenic mice with the neurotoxin N-(2-chloroethyl)-N-ethyl-bromobenzylamine (DSP-4) starting a
137  both O6-benzylguanine (O6BG) and N,N'-bis(2-chloroethyl)-N-nitroso-urea (BCNU) stably increased the
138 en a single dose of 35 mg/m(2) of N,N'-bis(2-chloroethyl)-N-nitrosourea (BCNU), which was otherwise i
139  and are sensitive to killing by N,N'-bis (2-chloroethyl)-N-nitrosourea (BCNU).
140  synthesis, complicates the use of N,N-bis(2-chloroethyl)-N-nitrosourea as a GR inhibitor.
141 (DBT-FG) sensitized the tumors to N,N'-bis(2-chloroethyl)-N-nitrosourea chemotherapy, as measured by
142  reports of various GR inhibitors, N,N-bis(2-chloroethyl)-N-nitrosourea, an anticancer drug with IC(5
143 olar range, it is more potent than N,N-bis(2-chloroethyl)-N-nitrosourea, which is currently the most
144  such alkylating chemotherapeutic drugs as 2-chloroethyl-N-nitrosourea (CNU) derivatives is countered
145 nes and alkylating antitumor drugs such as 2-chloroethyl-N-nitrosourea (CNU).
146 MT caused increased cellular resistance to 2-chloroethyl-N-nitrosourea suggests a therapeutic signifi
147 on induced by alkylating agents, including 2-chloroethyl-N-nitrosourea-based antitumor drugs.
148 in (SAP) +/- intraperitoneal injection of N-[chloroethyl]-N-ethyl-2-bromobenzylamine (DSP-4) (noradre
149 -nitrobenzyl ester (9) and carbamic acid, (2-chloroethyl)nitroso-2,3,4, 6-tetra-O-acetyl-1-alpha,beta
150              One compound, carbamic acid, (2-chloroethyl)nitroso-4-acetoxybenzyl ester (3), was selec
151 rementioned compound, both carbamic acid, (2-chloroethyl)nitroso-4-nitrobenzyl ester (9) and carbamic
152                                 Seven new (2-chloroethyl)nitrosocarbamates have been synthesized as p
153 er treatment, a time interval in which bis(2-chloroethyl)nitrosourea (BCNU)-induced chloroethyl adduc
154 ic effects of the antitumor agents 1,3-bis(2-chloroethyl)-nitrosourea (BCNU) and temozolomide were st
155 ismatched-BALB/c model followed by N,N-bis(2-chloroethyl)-nitrosourea (BCNU) treatment to enhance don
156 rstrand cross-linking reaction of N,N'-bis(2-chloroethyl)-nitrosourea (BCNU) were investigated using
157 link induction and cytotoxicity of 1,3-bis(2-chloroethyl)-nitrosourea (BCNU).
158 he 5-member exocyclic ring and are formed by chloroethyl nitrosoureas, which are used in cancer thera
159 ide] into the homobenzylic C-Cl bond of 4-(2-chloroethyl)phenol 1.
160 nt (e.g., t(1/2) (HD) approximately 18 s, (2-chloroethyl phenyl sulfide, C(6)H(5)SCH(2)CH(2)Cl) appro
161                           Reactions of alpha-chloroethyl phenyl sulfone (14) and ethyl 2-chloropropio
162                                    Fmoc-4-(1-chloroethyl)-phenylalanine (5) was synthesized in four s
163                                 While tris-2-chloroethyl phosphate, tris(1-chloro-2-propyl)phosphate
164 loro-isopropyl) phosphate (TDCIPP) and bis(2-chloroethyl) phosphate (BCEP)-tris(2-chloroethyl) phosph
165 ations of nine urinary OPE biomarkers: bis(2-chloroethyl) phosphate (BCEtp), bis(1-chloro-2-propyl) p
166  ng/g) had higher concentrations than tris(2-chloroethyl) phosphate (GM: 1608 ng/g) and triphenyl pho
167                                       Tris(2-chloroethyl) phosphate (TCEP) and hexachlorocyclohexane
168                         Furthermore, tris (2-chloroethyl) phosphate (TCEP), a known carcinogen, was f
169                    These OPEs include tris(2-chloroethyl) phosphate (TCEP), tris(2-chloroisopropyl) p
170 ris(2-butoxyethyl) phosphate (TBOEP), tris(2-chloroethyl) phosphate (TCEP), tris(2-chloroisopropyl) p
171 e analyzed for three halogenated OPs (tris(2-chloroethyl) phosphate (TCEP), tris(2-chloroisopropyl) p
172 One mattress contained high levels of tris(2-chloroethyl) phosphate (TCEP), which has been prohibited
173 or exposure pathway for SigmaTCPP and tris(2-chloroethyl) phosphate (TCEP), while participants had hi
174 loroisopropyl) phosphate (TCIPP), and tris(2-chloroethyl) phosphate (TCEP).
175 c risk, with a main contribution from tris(2-chloroethyl) phosphate (TCEP).
176 d bis(2-chloroethyl) phosphate (BCEP)-tris(2-chloroethyl) phosphate (TCEP).
177 phosphate, diethyl cyanophosphonate, tris (2-chloroethyl) phosphate and dichlorvos).
178 hloro-2-propyl)phosphate (TDCIPP) and tris(2-chloroethyl)phosphate (TCEP).
179 propyl)phosphate (TCPP or TCIPP), and tris(2-chloroethyl)phosphate (TCEP).
180 hosphate (TDCIPP; max: 3150 ng/L) and tris(2-chloroethyl)phosphate (TCEP; max: 8450 ng/L).
181 phosphate or TCIPP (303 ng m(-3)) and tris(2-chloroethyl)phosphate or TCEP (139 ng m(-3)), which are
182 to 150 pg/m3, and tributyl phosphate, tris(2-chloroethyl)phosphate, tris(1-chloro-2-propyl)phosphate,
183                                        Bis-2-chloroethyl-phosphate was not associated with alteration
184              In this work, five OPAs [tris(2-chloroethyl) phosphite, triphenyl phosphite, tris(2,4-di
185 pha-amino-beta(2-ethyl-N,N,N', N'-tetrakis(2-chloroethyl)phosphorodiamidate)-sulfonyl-propionyl-( R)-
186 )methanes with DABCO failed to give {4-[N-(2-chloroethyl)piperazin-1-yl]-5H-1,2,3-dithiazol-5-ylidene
187 ct with DABCO in hot PhCl to give N-{4-[N-(2-chloroethyl)piperazin-1-yl]-5H-1,2,3-dithiazol-5-ylidene
188 n-retrocycloaddition strategies from 4-[N-(2-chloroethyl)piperazin-1-yl]-5H-1,2,3-dithiazole-5-thione
189 gallamine (M2), and 4-4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride (4-DAMP mustard; M
190 ) receptor inhibitor, 4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride (4-DAMP; 10(-5) M)
191 3 receptor antagonist 4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride had no effect.
192                                       Six (2-chloroethyl)porphyrins were synthesized from a common di
193 gave 5-substituted 3-(chloromethyl)- or 3-(2-chloroethyl)pyrazoles.
194 D, bis(2-chlororethyl) sulfide) and a range (chloroethyl) sulfide simulants of variable lipophilicity
195 exposure to the DNA-damaging compound bis-(2-chloroethyl) sulfide.
196  toxic chemical warfare agent mustard (bis(2-chloroethyl)sulfide) in the environment and during its d
197 face or within the droplet core, a range of (chloroethyl) sulfides, including HD, spanning some 7 ord
198 he A1/A2 purinergic receptor blocker 7-(beta-chloroethyl) theophylline (CET; given at 5 x 10-6 M and
199  receptor affinity-enhancing effects of 7-(2-chloroethyl) vs 7-methyl were comparable to the known en
200 ance affinity over hydrogen, except for 7-(2-chloroethyl), which enhanced the affinity of theophyllin

 
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