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1 PK analyses showed a >3-fold faster absorption with crus
2 PK analysis of selinexor revealed a clinically insignifi
3 PK analysis was performed under fasting and fed states (
4 PK for 400 mg (day 7) showed Cmax 3.07 muM, Tmax 3.0 hou
5 PK of MFG were determined on day 7 by high-performance l
6 PK parameters were markedly improved: a 16.4-times highe
7 PK-PD modeling of tenofovir (TFV) in plasma, female repr
8 PK/PD analyses using MARS identified isoniazid Cmax and
9 PK/PD analyses were performed at 7 time points.
10 PK/PD analysis predicts that minocycline would be expect
11 PKs had significantly higher postoperative refractive co
20 ties, and in vitro dose-response data into a PK/pharmacodynamic (PD) model to allow for placement of
21 d model of RNA to describe the response of a PK over a range of mechanical forces (fs) and monovalent
22 ed an in vivo preclinical model to perform a PK-PD analysis of systemic TDF PrEP for vaginal HIV acqu
23 nstrating target engagement in vivo and ADME-PK properties that are suitable for further evaluation.
24 olism, excretion, and pharmacokinetics (ADME-PK) properties of new chemical entities are an integral
26 efits, caveats, and impact of in silico ADME-PK should serve as a resource for medicinal chemists, co
34 ce interval [CI], 2.05-5.33; P < 0.001), and PK was more likely to fail compared with endothelial ker
37 demonstrated a critical role for the CH and PK regions in promoting cell migration and Stat3 activat
44 ion units and platelet reactivity index, and PK by plasma levels of prasugrel's active metabolite.
45 ty vs the human GLP-1 and GCG receptors, and PK profile in rats were determined for the new analogues
46 taining both proteinase K (PK)-sensitive and PK-resistant PrP(Sc) and samples containing only the PK-
47 ncentrations after 7-8 weeks of therapy, and PK parameters determined using nonlinear mixed-effects m
48 Identification of these virulence-associated PKs provides new insights into T. brucei-host interactio
50 ivo response, and that physiologically based PK models can assist in the prioritization of leading pr
51 efficacy, we generated physiologically based PK models to simulate systemic and gastrointestinal drug
53 age (P = 0.261) or gender (P = 0.78) between PK and DSAEK groups in our predominantly Chinese (76.6%)
57 %) in magnetic cation content at the central PK layers engenders up to a 90% increase in potential fe
58 inhibitors along with the in vivo mouse CNS PK profile of PF-DcpSi (compound 24), one of the analogs
63 Ri induces moderate ssDNA and triggers a DNA-PK and Chk1-mediated backup pathway to suppress origin f
66 entified HDAC1/HDAC9 as well as BRD8 and DNA-PK as important regulators of Golgi breakdown mediated b
68 otherapeutic regimen targeting CD133 and DNA-PK in combination with traditional protocols may increas
74 on analysis (GEMA) to identify BRCA- and DNA-PK-deficient leukemias either directly, using reverse tr
79 icient quiescent leukemia cells and BRCA/DNA-PK-deficient proliferating leukemia cells were sensitive
82 interactome, which includes NONO, Dhx9, DNA-PK and Stau1, further supports the protein's diverse fun
83 naling pathway consisting of histone H4, DNA-PK, RIP1 and IAPs that attenuates ROS-mediated apoptosis
85 stone H4 knockdown cells, and inhibiting DNA-PK reduced expression of RIP1 and IAPs in cisplatin-trea
86 pendent on DNA-dependent protein kinase (DNA-PK) and Ataxia telangiectasia mutated (ATM) signaling.
87 ugh CD133, DNA-dependent protein kinase (DNA-PK), and MDR1 are elevated in CD133+ GCSCs, the relation
88 (TORK) and DNA-dependent protein kinase (DNA-PK), was evaluated in primary CLL cells in vitro and in
89 tosis when DNA-dependent protein kinase (DNA-PK)-mediated non-homologous end joining is inhibited.
92 d DNA-dependent protein kinase-mediated (DNA-PK-mediated) nonhomologous end-joining, whereas DNA repa
94 tment led to enhanced phosphorylation of DNA-PK, a non-homologous end joining repair protein, in Hec-
95 the inhibition of either caspase-3/7 or DNA-PK during mitotic arrest, promotes subsequent cell survi
96 ered protein that binds Ku, Ku/DNA-PKcs (DNA-PK), and X4L4 within an extended flexible NHEJ core comp
97 complex and result in activation of the DNA-PK and ATM kinases, which play key roles in regulating t
99 knockdown of Ku80 and inhibition of the DNA-PK enzyme, which are involved in nonhomologous end joini
101 was developed to incorporate absorbed doses, PK properties, and in vitro dose-response data into a PK
102 , an inducer of contact activation, enhances PK activation by FXII-T, and facilitates FXII-T activati
104 a steady-state TCL level, present stable EVL-PK parameters without significant changes in dose or exp
107 ology approach, we have extended an existing PK-PD model of tumor growth with a mechanistic model of
109 ribed compounds of the class, show favorable PK properties, and demonstrate efficacy in an in vivo St
113 the hypothesis that reported indications for PK significantly vary between global regions and over ti
118 d using a modified classification system for PK indications and analyzed via multivariate regression.
119 y, about 39% of the antibodies evaluated for PKs in cynos have fast nonspecific (or non-target-mediat
120 s surrogate discovery approach needs further PK studies but in the meantime can be used as an intelli
121 med to provide a thorough overview of global PK indications as reported in peer-reviewed manuscripts.
124 Subgroup analysis showed that eyes that had PK or EK for failed TPK conducted for Aspergillus kerati
126 cal candidate for COPD, with predicted human PK properties suitable for once daily human dosing.
130 ll density loss was significantly greater in PK compared with DSAEK (60.9% vs. 48.7%; P = 0.007).
131 ere explored with substantial improvement in PK through modifications at the P1 site, while potency g
132 eplication of CSFV was markedly inhibited in PK-15 cells treated with U0126, a specific inhibitor for
135 ith its two main catabolites, the individual PK profiles of all three components could be derived by
136 t the transcriptional level in CSFV-infected PK-15 cells and in various organs of CSFV-infected pigs.
138 ue for samples containing both proteinase K (PK)-sensitive and PK-resistant PrP(Sc) and samples conta
141 1.56; P < 0.001), penetrating keratoplasty (PK) (adjusted HR, 1.12 vs. ALK and 1.10 vs. EK; P < 0.00
142 plasty (DSAEK) and penetrating keratoplasty (PK) for Fuchs endothelial dystrophy (FED) or bullous ker
144 ho had undergone a penetrating keratoplasty (PK), endothelial keratoplasty (EK), or deep anterior lam
147 r glycolytic ATP-generating pyruvate kinase (PK) directly into the viral replicase complex to boost p
148 ity (dimeric) M2 isoform of pyruvate kinase (PK) over its constitutively active splice variant M1 iso
150 e PKM1 and PKM2 isoforms of pyruvate kinase (PK), and PKM2 expression is closely linked to embryogene
152 preclinical PK and clinical human microdose PK data are described leading to the discovery of the fi
153 but low plasma and brain exposure in a mouse PK experiment due to short plasma stability; this was ov
154 nt in vitro properties and a promising mouse PK profile, making it suitable for in vivo testing.
156 ther PKM1 or PKM2 differentially affects net PK activity, viability, and cellular ATP levels of the l
165 coneogenesis; however, in vivo regulation of PK flux by gluconeogenic hormones and substrates is poor
166 eovascularization was present at the time of PK in 44.6% of eyes with prior hydrops and 7.6% without
170 e pulling experiments have been performed on PKs to decipher the mechanism of programmed ribosomal fr
173 yzed 828 consecutive cases of DSAEK (423) or PK (405) for FED and BK from the Singapore Cornea Transp
174 ties in predicted exposure concentrations or PK behaviors can significantly influence the prioritizat
176 e HFS-TB model offers the ability to perform PK/PD studies including humanlike drug exposures, to ide
177 to the central three of the five perovskite (PK) layers is presented, which reveals a marked preferen
178 in-host pharmacokinetic and pharmacodynamic (PK/PD) models with mathematical models for the populatio
179 use of this pharmacokinetic-pharmacodynamic (PK-PD) approach we demonstrate that the killing dynamics
180 mechanistic pharmacokinetic-pharmacodynamic (PK-PD) modeling is increasingly used for antimicrobial d
181 and in vivo pharmacokinetic-pharmacodynamic (PK-PD) properties gave a compound with low predicted dos
184 sed whether pharmacokinetic/pharmacodynamic (PK/PD) parameters could predict 2-month culture conversi
185 re we use pharmacokinetics/pharmacodynamics (PK/PD) analysis to rationally develop an anti-Wolbachia
187 xposure concentrations, and pharmacokinetic (PK) characteristics provide the foundation for HT risk p
188 ve biophysical analyses and pharmacokinetic (PK) studies in mouse, rat, and monkey further confirmed
189 tuximab concentrations, and pharmacokinetic (PK) variability could be influenced by tumor burden.
190 ort of molecules; available pharmacokinetic (PK) data; protein sequences of ADME-related molecular ta
192 Compound 10 had the desired pharmacokinetic (PK) and pharmacodynamic (PD) profile and demonstrated ma
193 knowledge as to which drug pharmacokinetic (PK) characteristics are key to generate an in vivo respo
194 lable, displaying favorable pharmacokinetic (PK) properties and remarkable antitumor efficacy in the
196 t recipients has increased, pharmacokinetic (PK) studies of immunosuppressants rarely include older p
197 in avian medicine, limited pharmacokinetic (PK) data in domestic and companion birds are available.
201 o 2, but with a preclinical pharmacokinetic (PK) profile that was predictive of once-daily dosing.
202 monized in vivo human serum pharmacokinetic (PK) studies to evaluate the potential in vitro-in vivo c
203 target with mucosal tissue pharmacokinetic (PK) data and mathematical modeling to determine the numb
204 red by their unsatisfactory pharmacokinetic (PK) properties along with the rapid development of drug-
205 zed in vitro and by in vivo pharmacokinetic (PK) and pharmacological studies to unveil its potential
207 rocessing: terfenadine for pharmacokinetics (PK) and toxicity; trimethylamine (TMA) as a potentially
208 ellular uptake mechanisms, pharmacokinetics (PK), administration routes and major challenges in FR-ta
213 s of safety, tolerability, pharmacokinetics (PK), and by mRNA expression of the p53 target gene pleck
214 First, we examined the pharmacokinetics (PKs) of methylone and its metabolites after subcutaneous
216 tween drug concentrations (pharmacokinetics [PK]) and protective efficacy (pharmacodynamics [PD]).
219 howed, after i.p. dosing, encouraging plasma PK profile and brain exposure, as well as efficacy in a
222 s using a general linear model showed plasma PK to be significantly associated with progression of bo
223 T levels were higher in subjects with plasma PK levels in the highest 10th percentile compared with s
224 ercentile compared with subjects with plasma PK levels in the lower 10th percentile (P = 0.048).
225 ious episodes (47.8%) in the first year post-PK and 35 episodes (52.2%) after the first year post-PK.
230 MPS) was devised that correlated preclinical PK results with cLogD, number of rotatable bonds, and nu
231 sign strategies and results from preclinical PK and clinical human microdose PK data are described le
232 The hypothesis that plasma prekallikrein (PK) is a risk factor for the development of vascular com
234 frameshifting and response of a pseudoknot (PK) RNA to force, a number of single-molecule pulling ex
235 tients aged >18 years who underwent a repeat PK or EK following a failed TPK with a follow-up of at l
238 ing 20/200 or better at 2 years after repeat PK, compared with an 80% (95% CI, 68%-88%) probability w
239 years was 47% (95% CI, 40%-54%) after repeat PK, whereas the probability of retention of the KPro at
242 The proportion of clear grafts in the repeat PK group, device retention in the KPro group, and the de
243 opulation model allowed describing rituximab PK and calculating rituximab exposure (area under the co
244 metabolic tumor volume (TMTV0) on rituximab PK and of TMTV0 and rituximab exposure on outcome in pat
245 DX/MS revealed that catalytically active rM1-PK undergoes significant rigidification in the active si
246 me rigidification was seen upon exposing rM1-PK to substrates or products in the absence of turnover.
247 ach using rabbit muscle pyruvate kinase (rM1-PK) which catalyzes the conversion of phosphoenolpyruvat
248 ries exhibited high oral exposures in rodent PK studies and demonstrated significant tumor growth inh
249 e OEP40 channel is slightly cation-selective PK+/PCl- approximately 4:1 and rectifying (i/i congruent
253 of TER is the template/pseudoknot domain (t/PK) which includes the template, for adding telomeric re
255 brate TR contains the template/pseudoknot (t/PK) and CR4/5 domains required for telomerase activity i
262 of the test molecule at any point along the PK profile within a coefficient of variation of approxim
263 Other objectives were to characterize the PK/pharmacodynamic (PD) relationship, correlate biomarke
266 gained graft clarity after regrafting in the PK group (P < .01) but not in the EK group (P = .205) at
269 be useful for overcoming limitations in the PK properties of proof-of-concept (POC) compounds to acc
270 ose-dependent effect was demonstrated in the PK/PD model as well as in secondary efficacy outcomes.
271 ce rates and absorbed doses were used in the PK/PD model to evaluate the impact of their uncertaintie
284 Among the compounds assessed in the in vivo PK experiments, 14i showed, after i.p. dosing, encouragi
299 ied 5 and 3 modules of genes correlated with PK parameters and a portion of these were enriched for b
300 K, the 1-year graft survival was higher with PK (90.6%) than with ELK (60.8%) (P = .0025) but no sign
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