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27 results on '"Carpenter, Thomas O"'

2. Response of enthesopathy in ENPP1 deficiency to enzyme replacement therapy in murine models and enthesopathy comorbidities and quality of life in ENPP1‐deficient adults

Author

Ansh, Anenya J., primary, Nester, Catherine, additional, O'Brien, Christine, additional, Stabach, Paul R., additional, Murtada, Sae‐Il, additional, Lester, Ethan R., additional, Khursigara, Gus, additional, Molloy, Liz, additional, Carpenter, Thomas O., additional, Ferreira, Carlos R., additional, and Braddock, Demetrios T., additional

Published
2022
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3. Musculoskeletal Comorbidities and Quality of Life in ENPP1‐Deficient Adults and the Response of Enthesopathy to Enzyme Replacement Therapy in Murine Models

Author

Ferreira, Carlos R., primary, Ansh, Anenya Jai, additional, Nester, Catherine, additional, O'Brien, Christine, additional, Stabach, Paul R., additional, Murtada, Sae‐Il, additional, Lester, Ethan R., additional, Khursigara, Gus, additional, Molloy, Liz, additional, Carpenter, Thomas O., additional, and Braddock, Demetrios T., additional

Published
2021
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5. Response of the ENPP1 ‐Deficient Skeletal Phenotype to Oral Phosphate Supplementation and/or Enzyme Replacement Therapy: Comparative Studies in Humans and Mice

Author

Ferreira, Carlos R, primary, Kavanagh, Dillon, additional, Oheim, Ralf, additional, Zimmerman, Kristin, additional, Stürznickel, Julian, additional, Li, Xiaofeng, additional, Stabach, Paul, additional, Rettig, R Luke, additional, Calderone, Logan, additional, MacKichan, Colin, additional, Wang, Aaron, additional, Hutchinson, Hunter A, additional, Nelson, Tracy, additional, Tommasini, Steven M, additional, Kroge, Simon, additional, Fiedler, Imke AK, additional, Lester, Ethan R, additional, Moeckel, Gilbert W, additional, Busse, Björn, additional, Schinke, Thorsten, additional, Carpenter, Thomas O, additional, Levine, Michael A, additional, Horowitz, Mark C, additional, and Braddock, Demetrios T, additional

Published
2021
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6. Burosumab for the Treatment of Tumor‐Induced Osteomalacia

Author

Jan de Beur, Suzanne M, primary, Miller, Paul D, additional, Weber, Thomas J, additional, Peacock, Munro, additional, Insogna, Karl, additional, Kumar, Rajiv, additional, Rauch, Frank, additional, Luca, Diana, additional, Cimms, Tricia, additional, Roberts, Mary Scott, additional, San Martin, Javier, additional, and Carpenter, Thomas O, additional

Published
2021
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7. Severity of reduced bone mineral density and risk of fractures in long‐term survivors of childhood leukemia and lymphoma undergoing guideline‐recommended surveillance for bone health

Author

Bloomhardt, Hadley M., primary, Sint, Kyaw, additional, Ross, Wilhelmenia L., additional, Rotatori, Jaime, additional, Ness, Kathryn, additional, Robinson, Cemre, additional, Carpenter, Thomas O., additional, Chow, Eric J., additional, and Kadan‐Lottick, Nina S., additional

Published
2019
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9. Hypophosphatemia promotes lower rates of muscle ATP synthesis

Author

Pesta, Dominik H., primary, Tsirigotis, Dimitrios N., additional, Befroy, Douglas E., additional, Caballero, Daniel, additional, Jurczak, Michael J., additional, Rahimi, Yasmeen, additional, Cline, Gary W., additional, Dufour, Sylvie, additional, Birkenfeld, Andreas L., additional, Rothman, Douglas L., additional, Carpenter, Thomas O., additional, Insogna, Karl, additional, Petersen, Kitt Falk, additional, Bergwitz, Clemens, additional, and Shulman, Gerald I., additional

Published
2016
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10. Pigment epithelium‐derived factor restoration increases bone mass and improves bone plasticity in a model of osteogenesis imperfecta type VI via Wnt3a blockade

Author

Belinsky, Glenn S., primary, Sreekumar, Bharath, additional, Andrejecsk, Jillian W., additional, Saltzman, W. Mark, additional, Gong, Jingjing, additional, Herzog, Raimund I., additional, Lin, Samantha, additional, Horsley, Valerie, additional, Carpenter, Thomas O., additional, and Chung, Chuhan, additional

Published
2016
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12. Pharmacokinetics and pharmacodynamics of a human monoclonal anti‐FGF23 antibody (KRN23) in the first multiple ascending‐dose trial treating adults with X‐linked hypophosphatemia

Author

Zhang, Xiaoping, primary, Imel, Erik A., additional, Ruppe, Mary D., additional, Weber, Thomas J., additional, Klausner, Mark A., additional, Ito, Takahiro, additional, Vergeire, Maria, additional, Humphrey, Jeffrey, additional, Glorieux, Francis H., additional, Portale, Anthony A., additional, Insogna, Karl, additional, Carpenter, Thomas O., additional, and Peacock, Munro, additional

Published
2015
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15. Determination of mesenchymal stem cell fate by pigment epithelium‐derived factor (PEDF) results in increased adiposity and reduced bone mineral content

Author

Gattu, Arijeet K., primary, Swenson, E. Scott, additional, Iwakiri, Yasuko, additional, Samuel, Varman T., additional, Troiano, Nancy, additional, Berry, Ryan, additional, Church, Christopher D., additional, Rodeheffer, Matthew S., additional, Carpenter, Thomas O., additional, and Chung, Chuhan, additional

Published
2013
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25. Severity of reduced bone mineral density and risk of fractures in long-term survivors of childhood leukemia and lymphoma undergoing guideline-recommended surveillance for bone health.

Author

Bloomhardt HM, Sint K, Ross WL, Rotatori J, Ness K, Robinson C, Carpenter TO, Chow EJ, and Kadan-Lottick NS

Subjects
Absorptiometry, Photon, Adolescent, Adult, Bone Density, Bone Neoplasms physiopathology, Bone Neoplasms secondary, Child, Child, Preschool, Cross-Sectional Studies, Female, Fractures, Bone complications, Fractures, Bone diagnostic imaging, Fractures, Bone physiopathology, Humans, Male, Medical Records, Precursor Cell Lymphoblastic Leukemia-Lymphoma complications, Precursor Cell Lymphoblastic Leukemia-Lymphoma diagnostic imaging, Precursor Cell Lymphoblastic Leukemia-Lymphoma physiopathology, Spine, Young Adult, Bone Neoplasms epidemiology, Cancer Survivors, Fractures, Bone epidemiology, Precursor Cell Lymphoblastic Leukemia-Lymphoma epidemiology
Abstract

Background: Survivors of childhood leukemia/lymphoma are at increased risk for reduced bone mineral density (BMD). The authors sought to determine the frequency of reduced BMD detected by off-therapy surveillance, factors associated with reduced BMD, and the association of reduced BMD with fractures., Methods: This cross-sectional study included childhood leukemia/lymphoma survivors attending 2 survivorship clinics who received guideline-recommended BMD surveillance ≥2 years post-therapy with dual-energy x-ray absorptiometry (from January 1, 2004 to August 31, 2016). Lumbar spine BMD z-scores were height-for-age-adjusted. Low and very low BMD were >1 SD and >2 SDs below norms, respectively. Treatment, chronic conditions, and fractures were abstracted from medical records. Logistic regression was used to examine the association of low BMD with patient/treatment factors and fractures., Results: In total, 542 patients (51.5% female) with a mean age of 15.5 years (range, 4.4-52.2 years) who were 6 years post-therapy (range, 2.0-35.1 years) were evaluated, including 116 who reported post-therapy fractures. Lumbar spine low BMD was identified in 17.2% of survivors, and very low BMD was identified in 3.5% of survivors, but frequencies varied considerably between subgroups; 10.8% of survivors aged 15 to 19 years at diagnosis had very low BMD. In multivariable analyses, older age at diagnosis, white race, and being underweight were significantly associated with low BMD. Survivors with low BMD had greater odds of nondigit fractures (odds ratio, 2.2; 95% CI, 1.3-3.7) and specifically long-bone fractures (odds ratio, 2.7; 95% CI, 1.5-4.7)., Conclusions: In this study of childhood leukemia/lymphoma survivors undergoing guideline-recommended dual-energy x-ray absorptiometry surveillance, patients who were older at diagnosis, white, and underweight were at the highest risk for lumbar spine low BMD. Low BMD was associated with a greater risk of fractures, emphasizing the clinical importance of surveillance., (© 2019 American Cancer Society.)

Published
2020
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26. Population pharmacokinetic and pharmacodynamic analyses from a 4-month intradose escalation and its subsequent 12-month dose titration studies for a human monoclonal anti-FGF23 antibody (KRN23) in adults with X-linked hypophosphatemia.

Author

Zhang X, Peyret T, Gosselin NH, Marier JF, Imel EA, and Carpenter TO

Subjects
Adult, Antibodies, Monoclonal, Humanized, Familial Hypophosphatemic Rickets blood, Female, Fibroblast Growth Factor-23, Fibroblast Growth Factors blood, Half-Life, Humans, Male, Middle Aged, Phosphates blood, Vitamin D analogs & derivatives, Vitamin D blood, Antibodies, Monoclonal administration & dosage, Antibodies, Monoclonal pharmacokinetics, Familial Hypophosphatemic Rickets drug therapy
Abstract

X-linked hypophosphatemia (XLH) is an inherited metabolic bone disease with abnormally elevated serum FGF23 resulting in low renal maximum threshold for phosphate reabsorption, low serum phosphate (Pi) and 1,25-dihydroxyvitamin D levels with subsequent development of short stature and skeletal deformities. KRN23 is a novel human anti-FGF23 antibody for the treatment of XLH. The pharmacokinetics (PK) and pharmacodynamics (PD) models of KRN23 were assessed following subcutaneous dosing every 28 days over an initial 4-month dose escalation (0.05-0.6 mg/kg) and a subsequent 12-month titration period (0.1-1.0 mg/kg) in XLH adults. The PK of KRN23 was described by a 1-compartmental model with first-order absorption and elimination at doses ≥0.1 mg/kg. The elimination half-life was 17.8 days. Covariates did not affect KRN23 PK. Mean peak serum Pi was attained 7-10 days after dosing and progressively increased following each of the initial 4 doses with comparable peak values attained following the sixth through tenth doses with a slight decrease thereafter. A PK-PD model with a maximum effect (Emax ) and a time-varying effective concentration to reach 50% of Emax (EC50,t ) described data adequately. Typical Emax was 1.5 mg/dL. Typical EC50,t was 1780 ng/mL and 5999 ng/mL after first and last dose, respectively., (© 2015, The American College of Clinical Pharmacology.)

Published
2016
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27. Pharmacokinetics and pharmacodynamics of a human monoclonal anti-FGF23 antibody (KRN23) in the first multiple ascending-dose trial treating adults with X-linked hypophosphatemia.

Author

Zhang X, Imel EA, Ruppe MD, Weber TJ, Klausner MA, Ito T, Vergeire M, Humphrey J, Glorieux FH, Portale AA, Insogna K, Carpenter TO, and Peacock M

Subjects
Adult, Aged, Antibodies, Monoclonal administration & dosage, Antibodies, Monoclonal, Humanized, Area Under Curve, Biomarkers, Bone and Bones metabolism, Female, Fibroblast Growth Factor-23, Humans, Male, Middle Aged, Phosphorus blood, Young Adult, Antibodies, Monoclonal pharmacokinetics, Antibodies, Monoclonal pharmacology, Familial Hypophosphatemic Rickets drug therapy
Abstract

In X-linked hypophosphatemia (XLH), serum fibroblast growth factor 23 (FGF23) is increased and results in reduced renal maximum threshold for phosphate reabsorption (TmP), reduced serum inorganic phosphorus (Pi), and inappropriately low normal serum 1,25 dihydroxyvitamin D (1,25[OH]2 D) concentration, with subsequent development of rickets or osteomalacia. KRN23 is a recombinant human IgG1 monoclonal antibody that binds to FGF23 and blocks its activity. Up to 4 doses of KRN23 were administered subcutaneously every 28 days to 28 adults with XLH. Mean ± standard deviation KRN23 doses administered were 0.05, 0.10 ± 0.01, 0.28 ± 0.06, and 0.48 ± 0.16 mg/kg. The mean time to reach maximum serum KRN23 levels was 7.0 to 8.5 days. The mean KRN23 half-life was 16.4 days. The mean area under the concentration-time curve (AUCn ) for each dosing interval increased proportionally with increases in KRN23 dose. The mean intersubject variability in AUCn ranged from 30% to 37%. The area under the effect concentration-time curve (AUECn ) for change from baseline in TmP per glomerular filtration rate, serum Pi, 1,25(OH)2 D, and bone markers for each dosing interval increased linearly with increases in KRN23 AUCn . Linear correlation between serum KRN23 concentrations and increase in serum Pi support KRN23 dose adjustments based on predose serum Pi concentration., (© 2015 The Authors. The Journal of Clinical Pharmacology Published by Wiley Periodicals, Inc. on behalf of American College of Clinical Pharmacology.)

Published
2016
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