ライフサイエンスコーパス: nM

1 e of 0.006 and an outstanding potency of 1.0 nM.

2 ent linear dynamic range of 100.0 pM to 10.0 nM Hg(2+) concentration with R(2) = 0.982.

3 d 100 muM to 2 mM), low detection limit (2.0 nM), and good selectivity for applications in real sampl

4 2,4-benzothiadiazine 1,1-dioxide, EC50 = 2.0 nM).

5 signaling in macrophages ( approximately 2.0 nM).

6 genase type 1 (11beta-HSD1) enzyme (IC50 3.0 nM) with >10000-fold selectivity over human 11beta-hydro

7 ndole-3-yl)methane (38, PSB-15160, EC50 80.0 nM) and di(5,7-difluoro-1H-indole-3-yl)methane (57, PSB-

8 FI-402257, a potent (Mps1 Ki = 0.09 +/- 0.02 nM; cellular Mps1 EC50 = 6.5 +/- 0.5 nM), highly selecti

9 evolved by phage display (Ki = 0.84 +/- 0.03 nM).

10 its of 1.53 (MERS-CoV), 1.27 (MTB), and 1.03 nM (HPV).

11 has high affinity at human 5-HT6R (Ki = 2.04 nM) and selectivity over 100 target sites which include

12 pound, has an excellent in vitro IC50 (0.056 nM) and improved aqueous solubility as well as good effi

13 t, nematodes treated with the peptide at 0.1 nM are completely resistant to killing by C. albicans Th

14 SW033291 (1) inhibits 15-PGDH with Ki = 0.1 nM in vitro, doubles PGE2 levels in vivo, and shows effi

15 ti-PD-L1 (dissociation constant, 0.6 +/- 0.1 nM) demonstrated increased uptake in B16F10 tumors at pr

16 reciably increased potency (GI50 5.4 +/- 0.1 nM), but lacked ion leakage capabilities associated with

17 detect pheromone gradients as shallow as 0.1 nM/mum.

18 equipotent in both assays (EC50 1.5 and 1.1 nM, respectively).

19 tiomer retaining all the affinity (Ki = 15.1 nM), as predicted earlier by molecular modeling.

20 e proliferation in vitro with an EC50 of 2.1 nM.

21 of CHO-GCGR cells with a K d of 52.7 +/- 5.1 nM.

22 Exposure to 0.1 pM, 10 pM, and 1 nM 17 beta-estradiol (E2) resulted in monotonic inhibiti

23 etabolites at final concentrations between 1 nM and 10 muM, and they are sufficiently robust to analy

24 biosensor presents a linear range between 1 nM and 100 nM of tenofovir and a limit of detection of 1

25 5 with an IC50 value of 0.90 nM (Ki value <1 nM) and inhibits the MLL H3K4 methyltransferase (HMT) ac

26 rsible inhibitor 45a with an IC50 value of 1 nM against the EGFR L858R/T790M double mutant.

27 NOTA-conjugated ligand binding affinity of 1 nM.

28 ysis at ultralow concentrations (less than 1 nM).

29 -hP2X7R cells were 0.2312 +/- 0.01542 min(-1)nM(-1), 0.2547 +/- 0.0155 min(-1), and 1.0277 +/- 0.207,

30 cury in drinking water is 0.002 mg L(-1) (10 nM).

31 250-500 nM and by 1alpha,25-(OH)2D3 at 1-10 nM.

32 omolar affinity for the hA2A AR (Ki = 2.9-10 nM) and some, very interestingly, also showed high selec

33 n SHMT1/2 (biochemical IC50 approximately 10 nM).

34 his method can be deployed with as low as 10 nM enzyme to determine activity against S/T/Y-containing

35 ibitor venetoclax was highly active below 10 nM in B-cell precursor ALL (BCP-ALL) subsets, including

36 fibrin matrix (0.1-0.4 mg/mL fibrinogen, 10 nM thrombin) under a variety of venous flow conditions w

37 s of the excitatory amino acid glutamate (10 nM-1 mM) elicited reproducible and reversible transient

38 The highly potent (IC50 = 10 nM) inhibitor N-(3,4-dimethoxyphenyl)ethyl amide (WOBE43

39 stic effect with excellent affinity (Ki < 10 nM) and outstanding selectivity profiles, providing an a

40 ow nanomolar dissociation constants (KD < 10 nM) for GII.4 VLP.

41 selective antagonist for P2X7Rs (IC50 of 10 nM) and ineffective at the P2X1R (at 10 muM).

42 fter intracerebroventricular injection of 10 nM oxytocin in dependent rats.

43 A detection limit of 10 nM was found using human blood serum, which is well belo

44 miRNA concentration for the range of 0.1-100 nM.

45 n derivatives with excellent potency (50-100 nM) as modulators for cancer invasion and metastasis.

46 presents a linear range between 1 nM and 100 nM of tenofovir and a limit of detection of 1.2 nM.

47 T3 was also observed (IC50 approximately 100 nM).

48 l compounds exhibiting EC50 values below 100 nM.

49 alciparum strains with 5/6 having IC50 < 100 nM against the NF54 strain.

50 with high CXCR7 binding affinities (Ki < 100 nM) and measurable passive permeability (Papp > 5 x 10(-

51 with IC50 values of less than 20 nM, is <100 nM potent against JAK2 and HDAC11, and is selective for

52 tance decreases 40-60% with EC50 values <100 nM propofol without an effect on velocity.

53 s) quickly decays to resting Ca levels (<100 nM) at high Pup, but remained elevated during slower dec

54 robe VH298, with dissociation constants <100 nM, which induced marked HIF-1alpha intracellular stabil

55 tructures that exhibited EC50 values of <100 nM.

56 LPRs, containing 50 nM or 100 nM siRNA, showed high levels of silencing, particularly

57 on intrinsic excitability, we found that 100 nM 2-AG accelerated pacemaking and steepened the frequen

58 anging cytosolic [Ca(2+)] from 50 muM to 100 nM when the toxin occupied the vestibule.

59 atment of HT22 cultures with Ex-4 (25 to 100 nM), prior to injury, attenuated the cytotoxic effects o

60 ad optimization identified selective sub-100-nM inhibitors of the enzyme which significantly reduced

61 the PA ratio, with a dynamic range of 0-1000 nM and a limit of detection of 112 nM.

62 or Cu(2+) detection in the range of 0.5-1000 nM, with a detection limit of 0.18 nM, which is 5 orders

63 mpounds that were MC3R agonists (EC50 < 1000 nM) and MC4R antagonists (5.7 < pA2 < 7.8).

64 in A (EC50 = 0.6 +/- 0.2 nM at kappa; >10000 nM at mu and delta).

65 nM for BRPF2 BD, 8 nM for TAF1 BD2, and 106 nM for TAF1L BD2.

66 cocaine at inhibiting DA uptake (IC50 = 107 nM).

67 ociation constant for CysK:CdiA-CT (K d 11 nM) is comparable to that of the E. coli cysteine syntha

68 e inhibitor structure to achieve a Ki of 110 nM, with 15-60-fold selectivity across a series of phosp

69 of 0-1000 nM and a limit of detection of 112 nM.

70 s: 18 nM (2.0 mug L(-1)); E. verrucosus: 115 nM (12.9 mug L(-1)); 4 weeks exposure; 6 degrees C), Cd

71 at the DAT (Ki=3 muM) than JJC8-016 (Ki=116 nM).

72 IMP288 (dissociation constant, 0.53 +/- 0.12 nM).

73 1 and DCN2 proteins with K i values of 10-12 nM, and disrupts the DCN1-UBC12 interaction in cells.

74 binding were 73 +/- 30 nmol/kg and 28 +/- 12 nM, respectively.

75 Compound 3i is a potent hit (TBK1 DC50 = 12 nM, Dmax = 96%) with excellent selectivity against a rel

76 Pol epsilon binds CMG with a Kd value of 12 nM, but Pol delta binding CMG is undetectable.

77 inhibitor 20l (SLC4011540) (hSphK1 Ki = 120 nM, hSphK2 Ki = 90 nM) and SphK2 inhibitor 20dd (SLC4101

78 s mechanosensory hair cells with HC50 of 120 nM and demonstrates 100% protection in the zebrafish ass

79 ) and selective (N/C interaction EC50 = 1206 nM) modulator.

80 affinity (apparent KD-values of 663 +/- 121 nM and 231 +/- 63 nM for Ca(2+)-free GCAP1 and GCAP2, re

81 Compound 1 displayed a TarO IC50 of 125 nM in an enzyme assay and possessed very high lipophilic

82 nM), P-nAChRs activated by pyrantel (Kb 126 nM), and L-nAChRs activated by levamisole (Kb 0.96 micro

83 ealed to be the most potent inhibitor (KD 13 nM for Bacteroides xylanisolvens GH99 enzyme) of these e

84 e highest methane concentrations (up to 1302 nM).

85 use C3d with mouse FH (3.85 muM), FHR-A (136 nM), FHR-B (546 nM), and FHR-C (1.04 muM), which directl

86 n limits of 18.1 +/- 1.22 and 1.38 +/- 0.139 nM, respectively.

87 th the Kd strengthening to approximately 140 nM for the full lyase domain (residues 2-87).

88 nM, and MDR Mtb patient isolates IC50 = 140 nM) and favorable pharmacokinetic and toxicological prof

89 r studying the stability of thrombin (0-1400 nM) adhered to a fibrin matrix (0.1-0.4 mg/mL fibrinogen

90 2-naphthyl)-imidazole with a Ki value of 143 nM against human liver GPa.

91 a 50% inhibitory concentration (PSMA) of 15 nM and a dissociation constant (HSA) of 11.2 muM, cleare

92 However, at 75-150 nM concentrations, IB was highly effective at killing mu

93 are 262 +/- 4 nM for iMVP/INT, 1800 +/- 160 nM for iMVP/INTDeltaC15 at pH 7.4.

94 ed in compound 2 with biochemical IC50 = 160 nM.

95 respectively, with an estimated IC50 of 160 nM; no statistically significant inhibition of SULT acti

96 ared with the G alphai-activation assay (167 nM), whereas ponesimod, a S1P1 modulator that is current

97 27-219 nM) for hbeta4 nAChR subtypes and 169 nM for halpha7 nAChR.

98 was obtained that binds Shh with a KD of 170 nM, which corresponds to a 120-fold affinity improvement

99 good stability in plasma (Ki = 1.63 +/- 0.18 nM, >27000-fold selectivity, t1/2(plasma) =16 +/- 4 h).

100 0.5-1000 nM, with a detection limit of 0.18 nM, which is 5 orders of magnitude lower than the U.S. E

101 concentrations (nominal LC1; E. cyaneus: 18 nM (2.0 mug L(-1)); E. verrucosus: 115 nM (12.9 mug L(-1

102 cellular IC50 values of 29 nM, 6.3 nM and 19 nM, respectively, and high selectivity toward other poly

103 Compound 2 (Ki = 19 nM) binds within the aldehyde-binding site of the free e

104 ectivity to salvinorin A (EC50 = 0.6 +/- 0.2 nM at kappa; >10000 nM at mu and delta).

105 (half maximal inhibitory concentration, 1-2 nM).

106 of tenofovir and a limit of detection of 1.2 nM.

107 IC50 values of 0.35-4.6 nM (4g) and 0.5-20.2 nM (4i), which are similar to those obtained with CA-4.

108 fication and detection limits of 1.3 and 5.2 nM, respectively.

109 y, proved to be a potent inhibitor (Ki = 8.2 nM) of the Thermotoga maritima TmGH1 beta-glucosidase.

110 of a water stable synthetic antigen (EC50 2 nM).

111 -3-yl)methyl)-3-phenylisoxazole 25 (IC50 = 2 nM, 14-fold selectivity over CYP11B2), exhibiting a supe

112 3-yl)methyl)-2-phenylpyridine Ref 7 (IC50= 2 nM) exhibited promutagenic potential as well as very low

113 (18)F-FHNP had a dissociation constant of 2 nM and maximum binding capacity of 18 fmol/10(6) cells,

114 mpound 22a inhibited SphK1 with an IC50 of 2 nM and was more than 100-fold selective for SphK1 over t

115 nhibit SULT1A3 with high affinity, 23 (+/-2) nM, and to bind weakly, if at all, to the four other maj

116 E-1) cells treated with variable doses (0-20 nM) of vitamin D for 24 h demonstrated that low levels (

117 n for the brain-expressed hCA VII (Ki = 0.20 nM) and selectivity over wider distributed hCA I and hCA

118 IMP288 (dissociation constant, 0.45 +/- 0.20 nM) to TF2-pretargeted LS174T cells were similar to thos

119 tease (IC50 = 390 +/- 20 nM, Ki = 365 +/- 20 nM) and a weak inhibitor of other mammalian metalloprote

120 thal factor (LF) protease (IC50 = 390 +/- 20 nM, Ki = 365 +/- 20 nM) and a weak inhibitor of other ma

121 posure to vasoconstrictors (50 mM KCl and 20 nM Endothelin-1).

122 In contrast, vitamin D at 20 nM concentration suppressed the expression of both TRAIL

123 mal inhibitory concentration values below 20 nM was detected in 2 independent T-ALL cohorts, which co

124 le based infectivity inhibitors (EC50 </= 20 nM).

125 xhibited a wide range of linear response (20 nM to 20 muM and 100 muM to 2 mM), low detection limit (

126 , 6, and 10 with IC50 values of less than 20 nM, is <100 nM potent against JAK2 and HDAC11, and is se

127 ld be distinguished, and affinities up to 20 nM were obtained for biologically active oligopeptides i

128 centration of (18)F-GP1 to GPIIb/IIIa was 20 nM.

129 Dabigatran (20 and 200 nM) inhibits (50 and 93%) clot-bound thrombin reversibly

130 activator with an EC50 of approximately 200 nM and demonstrated its therapeutic efficacy in mouse mo

131 affinity had increased (Kd approximately 200 nM) and was maintained in further speciation.

132 e of pregnant women: mono-n-butyl (MnBP, 200 nM), monobenzyl (MBzP, 3muM), mono-2-ethylhexyl (MEHP, 7

133 of the average diastolic [Ca] nadir to 200 nM (at Pup = 24 mM/s).

134 ration, yielding an IC50 value of 356 +/- 21 nM in neuroblastoma SHSY5Y cells and proved even to effi

135 voltammetry (ASV) of Pb, our sensor shows 21 nM (4.4 ppb) limit of detection, resistance to interferi

136 n potency compared to 4 with EC50 down to 21 nM and with greater metabolic stability.

137 pha4beta2 (0.83 nM) nAChR but weaker (27-219 nM) for hbeta4 nAChR subtypes and 169 nM for halpha7 nAC

138 most potent inhibitors of SGLT2 (IC50 = 9-23 nM) were considerably weaker inhibitors of SGLT1 (IC50 =

139 pound (+)-15a, which displayed an EC50 of 23 nM in the calcium flux assay while showing no beta-arres

140 ne transcription in living cells (IC50 = 230 nM), providing the most potent inhibitor of the sonic he

141 SB-16133, 61) exhibited an IC50 value of 233 nM, selectivity versus other P2Y receptor subtypes, and

142 ibits stronger affinity to iMVP (K Dapp = 24 nM) and dissociates at a slower rate than wild-type INT

143 ifically inhibits URAT1 with a potency of 25 nM.

144 TCRs (KD values of approximately 50 and 250 nM) against MART1/HLA-A2 or WT1/HLA-A2 were used, allowi

145 t activated CFTR with EC50 approximately 250 nM, which when delivered topically increased tear fluid

146 ic H2O2 sensor with a detection limit of 250 nM and a broad linear range of 250 nM to 7 mM.

147 it of 250 nM and a broad linear range of 250 nM to 7 mM.

148 t 12b for its high affinity value (Ki = 0.27 nM) and for its anxiolytic-like and ability to relieve n

149 r inhibitor of AmpC beta-lactamase (K i = 27 nM), we have identified and characterized a set of BZB a

150 h biochemical and cellular IC50 values of 29 nM, 6.3 nM and 19 nM, respectively, and high selectivity

151 ization (EC50: 41.9 +/- 29.8 vs. 455 +/- 299 nM) than Cu-DA(IR800)-TOC.

152 e JNK3 in the subnanomolar range (IC50 = 0.3 nM), shows high metabolic stability in human liver micro

153 t inhibitor of Clk1 and -4 (IC50 = 7 and 2.3 nM, respectively), exhibiting an unprecedented selectivi

154 ve ligand of the series [(+/-)16b, Ki = 24.3 nM] was resolved into its two enantiomers by chiral HPLC

155 Dissociation constant, 3.3 nM (+/-0.58), and receptor density, 10.1 fmol/mg (+/-0.6

156 nanomolar GI50 values (16o, mean GI50 of 3.3 nM) against a large number (93) of cancer cell lines.

157 ndole-3-yl)methane (57, PSB-16671, EC50 41.3 nM).

158 mical and cellular IC50 values of 29 nM, 6.3 nM and 19 nM, respectively, and high selectivity toward

159 (3+) = 167 +/- 5 nM and Kd Sm(3+) = 63 +/- 3 nM), but in nominally 0 [Ca(2+)], low [Eu(3+)] activated

160 ts exhibited insulin detection limits of 9.3 nM or 190 amol (1.9 x 10(-16) mol).

161 d (18)F-FES had a dissociation constant of 3 nM and maximum binding capacity 83 fmol/10(6) SKOV3 cell

162 ene 2-position, had IC50 of approximately 30 nM, approximately 3.6-fold more potent than the most pot

163 oride conductance with EC50 approximately 30 nM, without causing cAMP or calcium elevation.

164 s excellent potency with human nNOS (Ki = 30 nM) and very high selectivity over other NOS isoforms, e

165 ive GRK2 inhibitor, 14as, with an IC50 of 30 nM against GRK2 and greater than 230-fold selectivity ov

166 active concentrations of CXCL12 with 100-300 nM CXCL14 resulted in chemotaxis responses that exceeded

167 activate PKA, which measures in the 100-300 nM range.

168 potent small molecule inhibitors (IC50 < 300 nM).

169 Ki = 0.45 nM) and A3AR antagonist (Ki = 0.31 nM) and highly selective versus A2A; 11 and 26 were most

170 ric binding site (apparent Kd: 0.87 and 0.31 nM, respectively).

171 The high potency (IC50 of 31 nM [MMP-10] and 5 nM [MMP-13]) and selectivity over MMP-

172 potent analogues (3a, IC50 approximately 32 nM; 3b, IC50 approximately 9 nM; and 14, IC50 approximat

173 rum laboratory-adapted strains (mean IC50 32 nM), Ugandan field isolates (mean ex vivo IC50 64 nM), a

174 opment of compound 32, with a Kd value of 32 nM and an EC50 value of 0.67 muM in a surrogate cellular

175 s in HeLa cells under basal conditions is 33 nM/h within the cell.

176 ied compound 7, a potent AR (ARE EC50 = 0.34 nM) and selective (N/C interaction EC50 = 1206 nM) modul

177 bnanomolar affinities for halpha2beta2 (0.34 nM), halpha3beta2 (0.80 nM) and halpha4beta2 (0.83 nM) n

178 sins B, K, and L ( Ki = 6.87, 0.49, and 0.34 nM, respectively).

179 hanced binding at DAT (EC50 approximately 35 nM) and at the norepinephrine transporter (NET).

180 ximately 9 nM; and 14, IC50 approximately 35 nM) inhibit ATX-dependent invasion of A2058 human melano

181 icity for alpha V beta 3 in HUVECs (K d 35 nM).

182 n of [Ru(bpy)3](2+), a detection limit of 36 nM was observed.

183 Protamine displays a 390-nM affinity for APJ and behaves as a full antagonist wit

184 ed A. fumigatus biofilms with an EC50 of 0.4 nM.

185 nce (SPR) biosensor technology are 262 +/- 4 nM for iMVP/INT, 1800 +/- 160 nM for iMVP/INTDeltaC15 at

186 inding studies established a Ki value of 4.4 nM at a known allosteric binding site.

187 d when deep-ocean Fe-concentrations were > 4 nM.

188 to the inactive Ras GDP form with a Kd of 4 nM and structural studies support its selectivity for in

189 The 4 nM binding affinity requires phosphorylation at Rpb1 S14

190 rated affinity for PSMA on the order of 4-40 nM and affinity for HSA in the range of 1-53 muM.

191 ectly detected at concentration as low as 40 nM.

192 , PDGF-AB:R2 KD = 110 pM, PDGF-BB:R2 KD = 40 nM, and PDGF-CC:R2 KD = 70 pM.

193 onsumption of 1.8 W, a detection limit of 40 nM, a dynamic range of 0.14-10 muM, and an infield accur

194 d at 1 kHz and yield detection limits of 400 nM for fluorescein in water.

195 ual acting human (h) A1AR agonist (Ki = 0.45 nM) and A3AR antagonist (Ki = 0.31 nM) and highly select

196 16) displayed potent inhibition (Ki = 11.45 nM) and was 84-fold more selective toward the N-domain.

197 ely 6.2 pM vs Kd, Adnectin2 approximately 46 nM).

198 /- 0.02 nM; cellular Mps1 EC50 = 6.5 +/- 0.5 nM), highly selective, and orally active small-molecule

199 nt Plasmodium falciparum parasites (IC50 1-5 nM) as well as against gametocytes.

200 yR's open probability (Kd Eu(3+) = 167 +/- 5 nM and Kd Sm(3+) = 63 +/- 3 nM), but in nominally 0 [Ca(

201 in (RF) conjugation], and concentration (2.5 nM) of AuNRs and the PPTT laser power (2 W/cm(2)) to ach

202 16-fold selective for the hMC1R (EC50 = 4.5 nM) versus other melanocortin receptors.

203 e high potency (IC50 of 31 nM [MMP-10] and 5 nM [MMP-13]) and selectivity over MMP-1, -2, -3, -7, -8,

204 22 in mouse brain and kidney being 1.3 and 5 nM, respectively.

205 Ta toxin), with IC50 down to approximately 5 nM.

206 d SK1 and VEGF expression, while low dose (5 nM) docetaxel had no significant effect.

207 ional potency profiles with EC50 values </=5 nM against major drug resistant HCV variants.

208 dynamic ranges over 4 orders of magnitude (5 nM-50 muM, R(2) > 0.99) were obtained.

209 euronal activity at a low concentration of 5 nM.

210 ese methods allow detection limits down to 5 nM for the neutral amino acids and 500 nM for acidic ami

211 24 h demonstrated that low levels (0.5 to 5 nM) significantly increased the TRAIL alpha but no chang

212 ately 90% knockdown of miRNA levels by 30-50 nM small RNA zippers.

213 emely different EC50 values of 1 pM and 50 nM, respectively.

214 imidazole (42) with IC50 values of 44 and 50 nM, respectively.

215 ma concentrations peaked at approximately 50 nM (Cmax) and remained elevated for several hours.

216 LPRs, containing 50 nM or 100 nM siRNA, showed high levels of silencing, par

217 nt blockers of TGF-beta1 responses (IC50 50 nM), Snail1 expression, and collagen deposition in vivo

218 oxyvitamin D3 < 20 ng/mL (equivalent to < 50 nM) before alloSCT and was assessed using accredited lab

219 The primary exposures were VDI (25(OH)D3 <50 nM) at birth and 6 months of age.

220 The most potent inhibitors (IC50 </= 50 nM) significantly decreased viability, clonogenic surviv

221 at pepcan-12 acts as a potent (K i value 50 nM) hCB2 receptor positive allosteric modulator (PAM).

222 ssion is up-regulated by 25(OH)D3 at 250-500 nM and by 1alpha,25-(OH)2D3 at 1-10 nM.

223 gs provide evidence that 25(OH)D3 at 250-500 nM can induce osteogenic differentiation and that 25(OH)

224 to 5 nM for the neutral amino acids and 500 nM for acidic amino acids and were used to analyze sampl

225 d this population is saturable at loads >500 nM and sensitive to the initial fibrinogen concentration

226 ulated by HG or high hydrocortisone (HC: 500 nM hydrocortisone) and was lower in heavier animals.

227 bound A*0101 with high affinity (IC50 < 500 nM).

228 ellular antitubercular activity (MIC50 = 500 nM).

229 ich bound to BoHV-1 with a Kd value of 3.519 nM and demonstrated the greatest virus binding as shown

230 s, of which ST3 has a binding affinity of 52 nM at GluN1/2A and 782 nM at GluN1/2B receptors.

231 le antituberculosis activity (Mtb IC50 = 525 nM, Mtb Wayne IC50 = 76 nM, and MDR Mtb patient isolates

232 ill not potent enough (IC50 approximately 53 nM) to enter preclinical studies.

233 VEGFR2 interactions with PDGF-AA:R2 KD = 530 nM, PDGF-AB:R2 KD = 110 pM, PDGF-BB:R2 KD = 40 nM, and P

234 tion [EC50]: 0.21 +/- 0.18 vs. 1.38 +/- 0.54 nM) and receptor internalization (EC50: 41.9 +/- 29.8 vs

235 se FH (3.85 muM), FHR-A (136 nM), FHR-B (546 nM), and FHR-C (1.04 muM), which directly correlate with

236 th values in the low nanomolar range (3.2-55 nM).

237 phenylalanine) to produce a potent (Ki = 1.6 nM) and the most selective (>/=360-fold) engineered cath

238 s raised with a dissociation constant of 1.6 nM.

239 evealed favorable D3R affinity (Ki = 12-25.6 nM) and were highly selective for D3R vs D3R (ranging fr

240 ative activity, with IC50 values of 0.35-4.6 nM (4g) and 0.5-20.2 nM (4i), which are similar to those

241 ed out to possess an IC50 of 93.7 and of 4.6 nM on MDM2 and MDM4, respectively.

242 selective NS5A inhibitor of HCV (EC50 = 4.6 nM), with greater therapeutic index (CC50/EC50 > 10000).

243 nd (human 50% inhibitory concentration = 9.6 nM) for the PAM site of mGluR2, was evaluated as a selec

244 -3 are within nanomolar range (14, 12, and 6 nM, respectively).

245 e E. coli cysteine synthase complex (K d 6 nM), and both complexes bind through a two-step mechanis

246 ntration giving 50% inhibition of 361 +/- 60 nM).

247 g a potent EGFR kinase inhibition (IC50 = 60 nM).

248 inhibit telomerase activity with IC50 of 600 nM.

249 e ring was identified as a potent (Ki = 0.63 nM) and highly selective kappa agonist (EC50 = 1.8 nM) s

250 t KD-values of 663 +/- 121 nM and 231 +/- 63 nM for Ca(2+)-free GCAP1 and GCAP2, respectively).

251 Ugandan field isolates (mean ex vivo IC50 64 nM), and murine P. berghei and P. falciparum infections

252 rminal segment of FHA with approximately 650 nM affinity.

253 labeled trastuzumab (0.016-0.368 MBq/mug, 67 nM) for 18 h versus the absorbed dose followed a linear

254 ry potent, dual inhibitor with an IC50 of 67 nM for BRPF2 BD, 8 nM for TAF1 BD2, and 106 nM for TAF1L

255 t FXIa clinical candidate, 55 (FXIa Ki = 0.7 nM), with excellent preclinical efficacy in thrombosis m

256 EC50 values in the low nanomolar range (1.7 nM at GluN1/2C).

257 ligand had a binding affinity of 6.7 +/- 1.7 nM for PSMA and an exceptionally high internalization ra

258 se (HMT) activity with an IC50 value of 12.7 nM.

259 phonic acid, exhibited Ki values of 6 and 70 nM for human HGPRT and Pf HGXPRT, respectively.

260 detection for certain metals is as low as 70 nM, and highly similar metals such as lanthanides and ac

261 itavancin against drug-resistant targets (70 nM) was found to be 11,000 times stronger than for vanco

262 l (MBzP, 3muM), mono-2-ethylhexyl (MEHP, 700 nM), and monoethyl (MEP, 1.5muM) phthalates.

263 he-DNal(2')-NH2] were more potent (EC50 < 73 nM) than the melanocortin tetrapeptide Ac-His-DPhe-Arg-T

264 vity (Mtb IC50 = 525 nM, Mtb Wayne IC50 = 76 nM, and MDR Mtb patient isolates IC50 = 140 nM) and favo

265 as the most potent analogue with a KD of 76 nM against BioA and a minimum inhibitory concentration o

266 inding affinity of 52 nM at GluN1/2A and 782 nM at GluN1/2B receptors.

267 d highly selective kappa agonist (EC50 = 1.8 nM) selective for the periphery with dose-dependent anti

268 h a dissociation constant of 436.5 +/- 104.8 nM, although much higher concentrations are needed to tr

269 ibitor with an IC50 of 67 nM for BRPF2 BD, 8 nM for TAF1 BD2, and 106 nM for TAF1L BD2.

270 ve with affinities that ranged from 0.5 to 8 nM.

271 aggregated tau (inhibition constant value, 8 nM) and high (>/=500x) in vitro selectivity for tau over

272 r halpha2beta2 (0.34 nM), halpha3beta2 (0.80 nM) and halpha4beta2 (0.83 nM) nAChR but weaker (27-219

273 Inhibitor 36 (IC50 = 80 nM) was identified to be highly selective for MBLs when

274 well below the diagnostic cutoff point of 80 nM.

275 alpha3beta2 (0.80 nM) and halpha4beta2 (0.83 nM) nAChR but weaker (27-219 nM) for hbeta4 nAChR subtyp

276 compounds, 3b and 3f (IC50 approximately 84 nM), lack inhibitory action on ENPP6 and ENPP7 but posse

277 tified 4b (GS-5734) with anti-EBOV EC50 = 86 nM in macrophages as the clinical candidate.

278 ed a potent cathepsin G inhibitor (Ki = 0.89 nM).

279 he beta-arrestin recruitment assay (EC50 0.9 nM) compared with the G alphai-activation assay (167 nM)

280 gricolor, potently inhibits NaV1.7 (IC50 0.9 nM) with at least 40-1000-fold selectivity over all othe

281 shed M-nAChRs activated by morantel (Kb 13.9 nM), P-nAChRs activated by pyrantel (Kb 126 nM), and L-n

282 III by >80% in Hep3B cells with an EC50 2.9 nM.

283 pproximately 32 nM; 3b, IC50 approximately 9 nM; and 14, IC50 approximately 35 nM) inhibit ATX-depend

284 Moreover, bioactive peptide 25 (Ki = 9 nM) achieved oral bioavailability of 18% in rats, which

285 89) binds to WDR5 with an IC50 value of 0.90 nM (Ki value <1 nM) and inhibits the MLL H3K4 methyltran

286 4011540) (hSphK1 Ki = 120 nM, hSphK2 Ki = 90 nM) and SphK2 inhibitor 20dd (SLC4101431) (Ki = 90 nM, 1

287 new submicromolar KOR binders (best Ki = 90 nM).

288 d SphK2 inhibitor 20dd (SLC4101431) (Ki = 90 nM, 100-fold SphK2 selectivity).

289 a dramatic increase in activity (EC50 = 0.92 nM).

290 zole 18, a modest HCV inhibitor (EC50 = 9440 nM), a series of structurally related thiazole derivativ

291 es, of human RIPK1 enzymatic activity with a nM Kd; has a non-ATP competitive mode of action and a no

292 ow muM) and the oxidant is very dilute (high nM-low mM).

293 Lead compounds such as 63 exhibit low nM inhibition of both LDHA and LDHB, submicromolar inhib

294 1g-i revealed low nM IC50 values for HDAC6 with up to 15-fold preference o

295 uld be detected at concentrations in the low nM range.

296 st characterization of smFRET-samples at sub-nM-concentrations.

297 n layer can be tuned by adding very low (sub-nM) concentrations of redox species to the solution via

298 omplex media (milk or blood plasma) with sub-nM detection ability.

299 es the release of tOmpA from Skp despite the nM affinity of the Skp:tOmpA complex.

300 Polymer NPs with nM affinity to a key vascular endothelial growth factor