ライフサイエンスコーパス: isobutyl

1 ective than those with large groups (propyl, isobutyl).

2 s phenyl, 4-pyridyl, 2-pyridyl, indolyl, and isobutyl.

3 d the sensitivity of CFTR to activation by 3-isobutyl 1-methyl xanthine (IBMX), as expected if these

4 Forskolin or 3-isobutyl-1-methyl xanthine (IBMX), 2 inducers of adenyla

5 sults were obtained with the PDE inhibitor 3-isobutyl-1-methyl-xanthine (IBMX) or with 8-pCPT-cGMP an

6 vinpocetine, SKF-94120, dipyridamole, and 3-isobutyl-1-methyl-xanthine but is inhibited (IC50 = 35 m

7 or with the PKA activators forskolin plus 3-isobutyl-1-methyl-xanthine or dibutyryl cyclic adenosine

8 well by either the nonselective inhibitor 3-isobutyl-1-methyl-xanthine or the new selective PDE5 inh

9 phosphate (cAMP) (forskolin (1-10 microM), 3-isobutyl-1-methylxanthine (0.1-1 mM), rolipram (10 micro

10 e similar IC(50) values for the inhibitors 3-isobutyl-1-methylxanthine (20 microM) and sildenafil (Vi

11 mbination of forskolin (20 micromol/L) and 3-isobutyl-1-methylxanthine (20 micromol/L), also inhibite

12 elective phosphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine (20 mumol/L).

13 ntiated by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (5x10(-5) mol/L).

14 omercuribenzene sulphonate (21 microM) and 3-isobutyl-1-methylxanthine (970 microM, partial inhibitio

15 ls by the combination of dexamethasone and 3-isobutyl-1-methylxanthine (DM) is suppressed by 2,3,7,8

16 nd its crystal structure as a complex with 3-isobutyl-1-methylxanthine (IBMX) at 1.55 A resolution.

17 The nonselective inhibitor 3-isobutyl-1-methylxanthine (IBMX) binds to a similar subp

18 s crystal structures in the unliganded and 3-isobutyl-1-methylxanthine (IBMX) bound forms at 1.9 and

19 The phosphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine (IBMX) did not elevate cGMP on

20 continuously treated with forskolin and/or 3-isobutyl-1-methylxanthine (IBMX) in light-dark (LD) and

21 3-Isobutyl-1-methylxanthine (IBMX) or 8-bromoadenosine 3',

22 dogenous cAMP levels with either forskolin/3-isobutyl-1-methylxanthine (IBMX) or the V2 receptor agon

23 posed to VIP, carbachol, forskolin, and/or 3-isobutyl-1-methylxanthine (IBMX) to determine whether th

24 GMP, vardenafil, sildenafil, tadalafil, or 3-isobutyl-1-methylxanthine (IBMX) were respectively weake

25 In the presence of 3-isobutyl-1-methylxanthine (IBMX), 10 microM SNC was suff

26 3-Isobutyl-1-methylxanthine (IBMX), a non-specific phospho

27 Moreover, 3-isobutyl-1-methylxanthine (IBMX), an inhibitor of cAMP p

28 glucose and 10 mmol/l arginine, 0.1 mmol/l 3-isobutyl-1-methylxanthine (IBMX), and 5 micromol/l carba

29 of RINm5F cells to cAMP-increasing agents, 3-isobutyl-1-methylxanthine (IBMX), and forskolin complete

30 A nonselective PDE inhibitor, 3-isobutyl-1-methylxanthine (IBMX), and the PDE3 selective

31 or without the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), decreased the period (

32 exposed to the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), the circulating curren

33 was increased by the use of forskolin and 3-isobutyl-1-methylxanthine (IBMX), we show that increase

34 In transient transfections, forskolin plus 3-isobutyl-1-methylxanthine (IBMX), which increases intrac

35 the variants, leading to stable, forskolin+3-isobutyl-1-methylxanthine (IBMX)-activated whole-cell cu

36 nged treatment with an adipogenic inducer, 3-isobutyl-1-methylxanthine (IBMX).

37 ntained in the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX).

38 s with 5'-GMP, vardenafil, sildenafil, and 3-isobutyl-1-methylxanthine (IBMX).

39 NAP), and the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX).

40 resence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX, 750 microM) reversibly

41 Incubating cells with PDGF and 3-isobutyl-1-methylxanthine (IBMX, a phosphodiesterase inh

42 competent in succinate-, ketoisocaproate-, 3-isobutyl-1-methylxanthine (IBMX-), KCl-, and tolbutamide

43 r, 10 micromol/L; >3-fold), potentiated by 3-isobutyl-1-methylxanthine (IBMX; phosphodiesterase type

44 gamma (PPARgamma) by dexamethasone (DEX), 3-isobutyl-1-methylxanthine (MIX), and insulin.

45 sphodiesterase (cAMP-PDE) inhibitors, e.g. 3-isobutyl-1-methylxanthine [(IBMX) or caffeine, 10 mg/kg]

46 ASL; (ii). activating CFTR with forskolin/3-isobutyl-1-methylxanthine alkalinized NL ASL but acidifi

47 roinjection of matched doses (300 nmol) of 3-isobutyl-1-methylxanthine and 7-deacetyl-7-O-(N-methylpi

48 These effects were potentiated by 3-isobutyl-1-methylxanthine and attenuated by the adenylyl

49 ncreases in intracellular cAMP prompted by 3-isobutyl-1-methylxanthine and forskolin partially mimick

50 However, 3-isobutyl-1-methylxanthine and forskolin treatment of a m

51 in in complex with non-selective inhibitor 3-isobutyl-1-methylxanthine and kinetic analysis on the mu

52 in (PDE5/6cd) complexed with sildenafil or 3-isobutyl-1-methylxanthine and the Pgamma-inhibitory pept

53 Release was also stimulated by 3-isobutyl-1-methylxanthine and was additive with forskoli

54 DE6 with vardenafil or sildenafil (but not 3-isobutyl-1-methylxanthine and zaprinast) induced a disti

55 induced by 10 microm forskolin, 40 microm 3-isobutyl-1-methylxanthine caused a 50% reduction in myos

56 These structures together with the PDE5A1-isobutyl-1-methylxanthine complex show that the H-loop (

57 in complex with the nonselective inhibitor 3-isobutyl-1-methylxanthine have been determined at medium

58 skolin and the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine in proportion to increases in

59 resence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine in the medium, suggesting extr

60 3-isobutyl-1-methylxanthine increased insulin secretion bu

61 ment with the broad-spectrum PDE inhibitor 3-isobutyl-1-methylxanthine induced T cell CREB phosphoryl

62 The receptor inhibitor 3-isobutyl-1-methylxanthine inhibited the calcium response

63 reatment with forskolin, 8-bromo-cAMP, and 3-isobutyl-1-methylxanthine or by overexpression of the ca

64 3-Isobutyl-1-methylxanthine potentiated ATP-induced calciu

65 f T cells with 8-bromo cAMP, forskolin, or 3-isobutyl-1-methylxanthine prevented the CD47-mediated ap

66 ty, Km for cGMP, and IC50 for zaprinast or 3-isobutyl-1-methylxanthine were found among wild-type and

67 hibitors, it is most potently inhibited by 3-isobutyl-1-methylxanthine with an IC(50) of 2.1 microM.

68 :5'-cyclic monophospate sodium), and IBMX (3-isobutyl-1-methylxanthine) also changed the splicing pat

69 0 nM forskolin, 1 mM 8-bromo-cAMP, or 1 mM 3-isobutyl-1-methylxanthine) had no effect on the amplitud

70 clase activity was measured with the IBMX (3-isobutyl-1-methylxanthine) jump technique.

71 potent phosphodiesterase inhibitor, IBMX (3-isobutyl-1-methylxanthine).

72 nhibit the response of other ORNs to IBMX (3-isobutyl-1-methylxanthine)/forskolin in a PI3K-dependent

73 of 1) phorbol myristic acid, forskolin and 3-isobutyl-1-methylxanthine, 2) BPDZ 154, or 3) 4-phenylbu

74 t by dPGJ2 was enhanced in the presence of 3-isobutyl-1-methylxanthine, a cAMP phosphodiesterase inhi

75 In Leydig cells from wild-type mice, 3-isobutyl-1-methylxanthine, a compound that inhibits all

76 + and blocked by 2',5'-dideoxyadenosine or 3-isobutyl-1-methylxanthine, an inhibitor of phosphodieste

77 f Tudor-SN (MEF-KO) impairs dexamethasone, 3-isobutyl-1-methylxanthine, and insulin (DMI)-induced adi

78 that increase [cAMP] (forskolin, rolipram, 3-isobutyl-1-methylxanthine, and papaverine) or mimic cAMP

79 Rp-cAMPs and was mimicked by 8-bromo-cAMP, 3-isobutyl-1-methylxanthine, and Sp-cAMP.

80 cles with the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, and the adenylate cyclase act

81 P, or with the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, caused a rightward shift in t

82 nts known not to act on the cyclase, or by 3-isobutyl-1-methylxanthine, creatine phosphate, or creati

83 increase in tyrosinase activity by either 3-isobutyl-1-methylxanthine, dibutyryl cAMP, or forskolin.

84 acid methyl ester hydrochloride (T-0156), 3-isobutyl-1-methylxanthine, EDTA, or cGMP, but not by cAM

85 ibition of phosphodiesterase activity with 3-isobutyl-1-methylxanthine, indicating that alpha-adrener

86 Following treatment with these diols or 3-isobutyl-1-methylxanthine, melanin and tyrosinase activi

87 PDE5 constructs had similar affinities for 3-isobutyl-1-methylxanthine, sildenafil, tadalafil, and UK

88 187 or a combination of dibutyryl cAMP and 3-isobutyl-1-methylxanthine, which increase intracellular

89 3-isobutyl-1-methylxanthine, which potentiates the cGMP/cA

90 PDE inhibitors for their ability to mimic 3-isobutyl-1-methylxanthine-induced ATF-1/CREB phosphoryla

91 The forskolin/3-isobutyl-1-methylxanthine-stimulated whole-cell conducta

92 lone before CFTR activation with forskolin/3-isobutyl-1-methylxanthine.

93 of CFTRDeltaF508 channel activity by 2 mm 3-isobutyl-1-methylxanthine.

94 PDE5 inhibitors, sildenafil, or zaprinast 3-isobutyl-1-methylxanthine.

95 resence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine.

96 8, including the nonspecific PDE inhibitor 3-isobutyl-1-methylxanthine.

97 cromol/l forskolin, 1 mmol/l 8-Br-cAMP, or 3-isobutyl-1-methylxanthine.

98 chlorophenylthio-cAMP, dibutyryl-cAMP, and 3-isobutyl-1-methylxanthine.

99 s of protein kinase A such as forskolin or 3-isobutyl-1-methylxanthine.

100 l preconstriction but not glibenclamide or 3-isobutyl-1-methylxanthine.

101 cipal cells after stimulation by forskolin/3-isobutyl-1-methylxanthine.

102 cts from monolayers treated with forskolin/3-isobutyl-1-methylxanthine.

103 ulating pGC by ANP/BNP, or blocking PDE by 3-isobutyl-1-methylxanthine/zaprinast caused significant i

104 pendent protein kinase (PKA), MgATP, cGMP, 3-isobutyl-1-methylxanthine], shown earlier to produce Ser

105 1bR)-9-(3-fluoropropoxy)-2-(hydroxymethyl)-3-isobutyl-10-methoxy-2,3,4,6, 7,11b-hexahydro-1H-pyrido[2

106 an-13-yl)-9-methyl-but-11-enyl benzoate (1), isobutyl-13-(6-(benzoyloxy)-10-methylpentyl)-tetrahydro-

107 ison and decreased towards maturation, and 3-isobutyl-2-methoxyprazine decreased with increasing matu

108 s (TSS) and proline, and lower malic acid, 3-isobutyl-2-methoxypyrazine (IBMP) and arginine.

109 e identified as (Z)-1,5-octadien-3-one and 3-isobutyl-2-methoxypyrazine.

110 ibitor batimastat ([4-(N-hydroxyamino)-2-(R)-isobutyl-3-(S)-(2-thiophenethiomethyl)s uccinyl]-(S)-phe

111 rmined using two representative volatiles: 2-isobutyl-3-methoxypyrazine (IBMP) and linalool.

112 We observe that lithium (S)-N-isobutyl-3-methyl-1-((triisopropylsilyl)oxy)butan-2-amid

113 opylsilyl)oxy)ethyl)propan-2-amine, or (S)-N-isobutyl-3-methyl-1-((triisopropylsilyl)oxy)butan-2-amin

114 The ionic liquid, 1-isobutyl-3-methylimidazolium bis(trifluoromethane-sulfon

115 We have examined the effects of 1-isobutyl-3-methylxanthine (IBMX) and forskolin, agonists

116 Moreover, when administered to mice, 1-isobutyl-3-oxo-3,5,6,7-tetrahydro-2H-cyclopenta[c]pyridi

117 rom hydrogen substitution by isopropyl (3d), isobutyl (3f), cyclopentyl (3g), and pyrano- (2) inhibit

118 ective process for the preparation of 1 from isobutyl (3S)-3-[methyl[(1S)-1-phenylethyl]amino]butanoa

119 ists 3-N-propylxanthine (enprofylline) and 3-isobutyl-8-pyrrolidinoxanthine (IPDX) on AdoR-mediated H

120 ists 3-N-propylxanthine (enprofylline) and 3-isobutyl-8-pyrrolidinoxanthine (IPDX), and the A(1)-sele

121 ced it, and the selective A(2B) antagonist 3-isobutyl-8-pyrrolidinoxanthine prevented it.

122 AT2 inhibitor Ro 4-1284 (2-hydroxy-2-ethyl-3-isobutyl-9,10-dimethoxy-1,2,3,4,6,7-hexahydrobenzo[al ph

123 ne ([(18)F]FP-DTBZ), [(18)F](+)-2-oxiranyl-3-isobutyl-9-(3-fluoropropoxy)-10-methoxy-2,3,4,6,7,11b-he

124 demonstrate the utility of this approach for isobutyl acetate (IBA) production, wherein IBA productio

125 nversion of the alcohol function to acetate, isobutyl acetate (TIDBIBA), or to trimethyl acetate lead

126 ome of the compounds in the spreads, such as isobutyl acetate, butyl butyrate, 3-hexen-1-yl acetate o

127 -borne odorants ((methyl ethyl ketone (MEK), isobutyl alcohol (i-BuAl), benzene (B), toluene (T), p-x

128 Capabilities are demonstrated using isobutyl alcohol droplets.

129 uM of the NHE1-specific inhibitor N-Methyl-N-isobutyl Amiloride (MIA) dramatically disrupted branchin

130 ibition of the Na+/H+ antiporter with methyl isobutyl amiloride (MIA) would decrease postischemic per

131 opropyl) amiloride or 10microM 5-(N-methyl-N-isobutyl) amiloride, both selective inhibitors of Na(+)-

132 since it could be inhibited by 5-(N-methyl-N-isobutyl)amiloride and by anti-NHX1 antibodies.

133 However, the larger 1,3-dialkyl groups (isobutyl and butyl) resulted in a decrease in both A(2B)

134 meric peptoids decorated with N-isopropyl, N-isobutyl, and N-benzyl substituents.

135 active octanoic acid esters (ethyl-, butyl-, isobutyl- and (iso)amyl octanoate) using lipase Palatase

136 tammetry of the ethyl-, n-propyl-, n-butyl-, isobutyl-, and adenosyl-substituted cobalamin was studie

137 carbon and the new stereocenter bearing the isobutyl appendage corresponding to that of the alkaloid

138 Herein we report that isobutyl-beta-C-galactoside (IBCG) is also a promising i

139 The substituents employed were the isobutyl, butyl, and benzyl groups to give peptidomimeti

140 (PLG) was substituted at the 3-position with isobutyl, butyl, and benzyl moieties to give the PLG pep

141 samples (food, cosmetics and water) based on isobutyl chloroformate (IBCF) derivatisation and preconc

142 he nerve agent metabolites ethyl, isopropyl, isobutyl, cyclohexyl, and pinacolyl methylphosphonic aci

143 plant morphogenetic processes, from which N-isobutyl decanamide is one of the most active compounds

144 N-isobutyl decanamide treatment exacerbates the dhm1 pheno

145 s the isolation and characterization of an N-isobutyl decanamide-hypersensitive (dhm1) mutant of Arab

146 hyl, 2-ethyl, 2-n-propyl, 2-isopropyl, and 2-isobutyl derivatives of dihydrotetrabenazine.

147 acetic acid] and pregabalin (PGB) [(S)-(+)-3-isobutyl-GABA or (S)-3-(aminomethyl)-5-methylhexanoic ac

148 Gabapentin (GBP) and S(+)-3-isobutyl-gamma-aminobutyric acid (IBG) are anticonvulsan

149 Attempts to replace the isobutyl group at P1' with small cyclic moieties caused

150 er by replacing the cyclohexane ring with an isobutyl group attached either to position 4 or position

151 n the 3'-pyridyl ring and variation of the 3-isobutyl group gave potent compounds (pK(i) > 9.0) with

152 at with a phenyl group, and an anion with an isobutyl group has the weakest chiral recognition).

153 , the simulations suggest that directing the isobutyl group into the minor groove causes the groove t

154 herein the steric bulk associated with the N-isobutyl groups increases the energy barrier required to

155 For example, the Janus particle with isobutyl groups on one POSS and carboxylic groups on the

156 nt with this, we now report that addition of isobutyl groups to the PNA backbone hinders aggregation

157 was explored with methyl, ethyl, butyl, and isobutyl groups.

158 of the 3-substituent was benzyl > n-butyl > isobutyl > H.

159 From these studies, a new zirconocene isobutyl hydride complex, Cp' '(2)Zr(CH(2)CHMe(2))(H) (C

160 tive elimination for a family of zirconocene isobutyl hydride complexes, Cp(CpR(n)())Zr(CH(2)CHMe(2))

161 e)G and N2-ethyl(Et)G, partially bypassed N2-isobutyl(Ib)G and N2-benzylG, and was blocked at N2-CH2(

162 y bypassed N2-methyl(Me)G, N2-ethyl(Et)G, N2-isobutyl(Ib)G, N2-benzyl(Bz)G, and N2-CH2(2-naphthyl)G b

163 (beta-naphthyl)cyclohexyl auxiliaries, using isobutyl iodide and benzyl bromide as model electrophile

164 Conventional 201TI and hexakis 2-methoxy-2-isobutyl isonitrile studies are less accurate as compare

165 s in the study are ethyl, n-propyl, n-butyl, isobutyl, isopropyl, sec-butyl, and tert-butyl.

166 ase now accepts the analogous ketone, methyl isobutyl ketone (MIBK), which corresponds to exchange of

167 into high volume industrial ketones: methyl isobutyl ketone (MIBK, yield 84%), diisobutyl ketone (DI

168 yed focus on the determination of (1) methyl isobutyl ketone in water over the range of 1-160 ppm, (2

169 e, using azeotropic distillation with methyl isobutyl ketone to drive the dehydration.

170 oroethylene, methyl tert-butyl ether, methyl isobutyl ketone), diffusion-limited (theoretical), R d,

171 y analyzing the standard solutions of methyl isobutyl ketone, heptanone, nonanone, and acetophenone a

172 Samples were diluted in methyl isobutyl ketone.

173 ability is shown for both acetone and methyl isobutyl ketone.

174 ed with 10 microM forskolin and 300 microM 3-isobutyl-L-methylxanthine and voltage-clamped with pipet

175 elimination to a [(C5Me5)2Ln][(mu-Ph)2BPh2]/isobutyl lithium route.

176 st 4.2 LD(50) of S-(2-(diethylamino)ethyl) O-isobutyl methanephosphonothioate without perturbation of

177 (IPMP), secbutyl methoxypyrazine (SBMP) and isobutyl methoxypyrazine (IBMP) in wine.

178 ignificantly influenced by harvest date were isobutyl methoxypyrazine, C(6) alcohols and hexyl acetat

179 sters tested, the hydrolysis product of rVX, isobutyl methyl phosphonate, was the best substrate with

180 The effects of isobutyl methyl xanthine (IBMX), an inhibitor of phospho

181 Addition of forskolin and isobutyl-methyl-xanthine during hypoxia resulted in reve

182 ophenylthio) (8-CPT)-cAMP (100 micromol/L) + isobutyl methylxanthine (100 micromol/L).

183 he nonselective phosphodiesterase inhibitor, isobutyl methylxanthine (IBMX) increased the potency of

184 completely by the nonselective PDE inhibitor isobutyl methylxanthine and also by the selective PDE 3B

185 rapid and sustained response to glucose plus isobutyl-methylxanthine in perifusion studies that is cl

186 depots, under identical culture conditions (isobutyl-methylxanthine, dexamethasone, and insulin), re

187 eincubation with an MMP-3 inhibitor, NNGH [N-isobutyl-N-(4-methoxyphenylsulfonyl)-glycylhydroxamic ac

188 d a MMP inhibitor, (2S:-allyl-N:-hydroxy-3R:-isobutyl-N:-(1S:-methylcarbamoyl-2-ph enylet hyl)-succin

189 but did not show protonated molecules for an isobutyl or benzylic EHNA derivative, suggesting the lat

190 A hydrophobic group such as isobutyl or isopropoxyl was found to be optimal at the 4

191 erally more potent than hydrogen, isopropyl, isobutyl, or benzyl.

192 omparison of rate constant for hydrolysis of isobutyl phenyl carbonate with benzyl phenyl carbonate s

193 amines R' 'NH(2) (R' ' = n-propyl, n-butyl, isobutyl, phenyl, 4-methylphenyl, 4-(dimethylamino)pheny

194 th simulations) for the OIPC diethyl(methyl)(isobutyl)phosphonium hexafluorophosphate ([P(1,2,2,4)][P

195 late (DEHP), di-n-butyl phthalate (DnBP), di-isobutyl phthalate (DiBP), and butyl-benzyl phthalate (B

196 hyl-5-carboxypentyl) phthalate (MECPP), mono-isobutyl phthalate (MiBP), mono-n-butyl phthalate (MBP),

197 evels of mono-n-butyl phthalate (MnBP), mono-isobutyl phthalate (MiBP), monobenzyl phthalate (MBzP),

198 ns of mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP).

199 (mCPP), mono-n-butyl phthalate (mBP), mono(2-isobutyl) phthalate (miBP), monobenzyl phthalate (mBzP),

200 m for para-dichlorobenzene, 6,800 ppm for di(isobutyl) phthalate, 7,700 ppm for diethyl phthalate, an

201 methylphosphonic acid (R = ethyl, isopropyl, isobutyl, pinacolyl (3,3-dimethyl-2-butyl), cyclohexyl,

202 le neopentyl protecting group and the labile isobutyl protecting group were utilized in the synthesis

203 inoethyl methylphosphonothioate) and R-VX (O-isobutyl-S-2-diethylaminoethyl methylphosphonothioate),

204 hobic moiety to the lactam ring to mimic the isobutyl side chain of the leucyl residue of PLG would i

205 ation of the malonylidene unit to include an isobutyl substituent at C3 affords a photosubstrate whic

206 Combination of the optimal 4'-isobutyl substituent with the 2'-amino function afforded

207 , ethyl, propyl, and to a much lesser extent isobutyl substituents at C(2) (R configuration only).

208 In this case, a 2'-isobutyl-substituted spiro[indoline-3,3'-pyrrolenine] re

209 up as well as a short alkyl chain (propyl or isobutyl) which defined the 0/1 molecular binary code.

210 sphodiesterase (PDE) inhibitors, 1-methyl-3- isobutyl xanthine and theophylline and rolipram, a speci