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Your search keyword '"CHEN Xuejun"' showing total 39 results
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39 results on '"CHEN Xuejun"'

1. Lysine 2‐hydroxyisobutyrylation proteomics analyses reveal the regulatory mechanism of CaMYB61‐CaAFR1 module in regulating stem development in Capsicum annuum L.

Author

Li, Qing, primary, Fu, Canfang, additional, Hu, Bowen, additional, Yang, Bozhi, additional, Yu, Huiyang, additional, He, Huan, additional, Xu, Qing, additional, Chen, Xuejun, additional, Dai, Xiongze, additional, Fang, Rong, additional, Xiong, Xingyao, additional, Zhou, Kunhua, additional, Yang, Sha, additional, Zou, Xuexiao, additional, Liu, Zhoubin, additional, and Ou, Lijun, additional

Published
2024
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2. PD‐1 inhibition with retifanlimab and/or arginase inhibition with INCB001158 in Japanese patients with solid tumors: A phase I study

Author

Kuboki, Yasutoshi, primary, Koyama, Takafumi, additional, Matsubara, Nobuaki, additional, Naito, Yoichi, additional, Kondo, Shunsuke, additional, Harano, Kenichi, additional, Yonemori, Kan, additional, Yoh, Kiyotaka, additional, Gu, Yuan, additional, Mita, Tetsuya, additional, Chen, Xuejun, additional, Ueda, Eiji, additional, Yamamoto, Noboru, additional, Doi, Toshihiko, additional, and Shimizu, Toshio, additional

Published
2024
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21. A phase 1 dosing study of ruxolitinib in children with relapsed or refractory solid tumors, leukemias, or myeloproliferative neoplasms: A Children's Oncology Group phase 1 consortium study (ADVL1011)

Author

Loh, Mignon L., primary, Tasian, Sarah K., additional, Rabin, Karen R., additional, Brown, Patrick, additional, Magoon, Daniel, additional, Reid, Joel M., additional, Chen, Xuejun, additional, Ahern, Charlotte H., additional, Weigel, Brenda J., additional, and Blaney, Susan M., additional

Published
2015
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28. The Effect of CYP3A4 Inhibition or Induction on the Pharmacokinetics and Pharmacodynamics of Orally Administered Ruxolitinib (INCB018424 Phosphate) in Healthy Volunteers

Author

Shi, Jack G., primary, Chen, Xuejun, additional, Emm, Thomas, additional, Scherle, Peggy A., additional, McGee, Ryan F., additional, Lo, Yvonne, additional, Landman, Robert R., additional, McKeever, Edward G., additional, Punwani, Naresh G., additional, Williams, William V., additional, and Yeleswaram, Swamy, additional

Published
2012
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37. Evaluation of Clinical Cardiac Safety of Itacitinib, a JAK1 Inhibitor, in Healthy Participants.

Author

Gong X, Darpo B, Xue H, Punwani N, He K, Barbour AM, Epstein N, Landman R, Chen X, and Yeleswaram S

Subjects
Acetonitriles adverse effects, Adolescent, Adult, Dose-Response Relationship, Drug, Female, Heart Rate drug effects, Humans, Janus Kinase 1 antagonists & inhibitors, Janus Kinase Inhibitors adverse effects, Male, Middle Aged, Pyrazoles adverse effects, Pyrimidines adverse effects, Pyrroles adverse effects, Young Adult, Acetonitriles administration & dosage, Electrocardiography, Janus Kinase Inhibitors administration & dosage, Pyrazoles administration & dosage, Pyrimidines administration & dosage, Pyrroles administration & dosage
Abstract

Itacitinib is a JAK1-selective inhibitor in phase 3 development in graft-versus-host disease. A post hoc electrocardiogram (ECG) analysis and a plasma concentration-QTc (C-QTc) analysis were performed to assess cardiac safety using data from the first-in-human itacitinib study. The study included 2 cohorts of 12 healthy participants each in an interleaving dosing design with single doses of 10-300 mg or placebo; 500 and 1000 mg doses were subsequently added with 12 participants randomized to itacitinib or placebo. Continuous Holter recordings were collected from 1 hour predose to 8 hours postdose on each dosing day, and ECG intervals were blindly extracted to match timed pharmacokinetic samples. Data showed no hysteresis, and a prespecified linear mixed-effects C-QTc model was used with change-from-baseline QTcF (QT interval corrected for heart rate by Fridericia's method) as the dependent variable, plasma itacitinib concentrations and centered baseline QTcF as continuous covariates, treatment and time as categorical factors, and a random intercept per participant. The estimated slope of the C-QTc relationship was not significantly different from zero: 0.0002 milliseconds per nM (90%CI, -0.00019 to 0.00054 milliseconds). No clinically meaningful effects on cardiac conduction (PR and QRS intervals) or any categorical PR or QRS outliers were observed. A QTc effect exceeding the threshold of concern (10 milliseconds) can be excluded for itacitinib plasma concentrations up to ∼13 000 nM (∼7200 ng/mL), which is well above the maximum concentration expected with the highest proposed therapeutic dose of itacitinib either with concomitant use of cytochrome P450 3A4 inhibitors or in patients with impaired hepatic function., (© 2019, The American College of Clinical Pharmacology.)

Published
2020
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38. Population Pharmacokinetic and Pharmacodynamic Modeling of Epacadostat in Patients With Advanced Solid Malignancies.

Author

Shi JG, Bowman KJ, Chen X, Maleski J, Leopold L, and Yeleswaram S

Subjects
Adult, Aged, Female, Humans, Indoleamine-Pyrrole 2,3,-Dioxygenase metabolism, Kynurenine blood, Male, Middle Aged, Neoplasms blood, Oximes blood, Sulfonamides blood, Tryptophan blood, Indoleamine-Pyrrole 2,3,-Dioxygenase antagonists & inhibitors, Models, Biological, Neoplasms metabolism, Oximes pharmacokinetics, Oximes pharmacology, Sulfonamides pharmacokinetics, Sulfonamides pharmacology
Abstract

Epacadostat (EPA, INCB024360) is a selective inhibitor of the enzyme indoleamine 2,3-dioxygenase 1 (IDO1) and is being developed as an orally active immunotherapy to treat advanced malignancies. In the first clinical study investigating the safety, tolerability, pharmacokinetics (PK), and pharmacodynamics (PD) of EPA in oncology patients, increasing doses of EPA ranging from 50 mg once daily to 700 mg twice daily were administered as a monotherapy to 52 subjects with advanced solid tumors. The EPA plasma concentration-time profiles were adequately described by a population PK model comprised of the first-order kinetics of oral absorption with 2-compartment distribution and constant clearance from the central compartment. Body weight was the only significant covariant to influence EPA PK. Determination of EPA's on-target potency, ie, its half-maximal inhibitory concentration (IC 50 ) against IDO1, is important for dose selection but complicated by the bioconversion of tryptophan (TRP) to kynurenine (KYN) catalyzed by both IDO1 and TRP 2,3-dioxygenase (TDO). In vitro and ex vivo, the IC 50 was estimated following the selective induction of IDO1, rendering the TDO activity relatively insignificant; however, it was desirable to determine the in vivo IC 50 without inducing an IDO1 abundance. A mechanistic population PD model was developed based on time-matched EPA, TRP, and KYN plasma concentrations in 44 oncology patients, and EPA in vivo IC 50 was estimated to be ∼70 nM, consistent with the ex vivo value independently determined. The model suggests that ∼60% and 40% of TRP→KYN bioconversion was mediated by IDO1 and TDO, respectively, in the cancer patients at baseline. For this study population of limited numbers of subjects, neither age nor sex was a significant covariate for EPA PK or PD., (© 2016, The American College of Clinical Pharmacology.)

Published
2017
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39. Pharmacokinetics and pharmacodynamics of orally administered ruxolitinib (INCB018424 phosphate) in renal and hepatic impairment patients.

Author

Chen X, Shi JG, Emm T, Scherle PA, McGee RF, Lo Y, Landman RR, Punwani NG, Williams WV, and Yeleswaram S

Abstract

Hepatic and renal impairment studies were conducted with ruxolitinib, a JAK1&2 inhibitor that is cleared predominantly by metabolism. Both studies were open label, single-dose studies. Ruxolitinib area under the curve (AUC) was increased by 87%, 28%, and 65%, respectively, in subjects with mild, moderate, and severe hepatic impairment compared to healthy subjects with no correlation between exposure of ruxolitinib and the degree of hepatic impairment. The pharmacodynamics (PD) data were consistent with ruxolitinib pharmacokinetics (PK). The renal impairment study showed a surprising finding. While there was no change in ruxolitinib PK with varying degrees of renal impairment, the PD showed increasing pharmacological activity with increased severity of renal impairment. Analysis of the metabolite exposures revealed that active metabolites contributed to the observed incremental increase in PD activity. The recovery of ruxolitinib in dialysate was negligible. The starting dose of ruxolitinib in subjects with any hepatic impairment or moderate or severe renal impairment should be decreased to 10 mg twice daily (BID) if their platelet counts are between 100 × 10(9) /L and 150 × 10(9) /L. Subjects on dialysis should initiate dosing with a single dose of 15 or 20 mg, based on platelet counts, with dosing only on the days of dialysis., (© 2013, The American College of Clinical Pharmacology.)

Published
2014
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