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Relevant bibliographies by topics / Tenapanor

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Journal articles

Academic literature on the topic 'Tenapanor'

Author: Grafiati

Published: 4 June 2025

Last updated: 1 August 2025

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Journal articles on the topic "Tenapanor"

1

Block, Geoffrey A., David P. Rosenbaum, Andrew Yan, and Glenn M. Chertow. "Efficacy and Safety of Tenapanor in Patients with Hyperphosphatemia Receiving Maintenance Hemodialysis: A Randomized Phase 3 Trial." Journal of the American Society of Nephrology 30, no. 4 (2019): 641–52. http://dx.doi.org/10.1681/asn.2018080832.

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BackgroundGuidelines recommend reducing elevated serum phosphate in patients with CKD. Tenapanor, a minimally absorbed inhibitor of gastrointestinal sodium/hydrogen exchanger 3 (NHE3), reduces paracellular phosphate transport.MethodsIn this phase 3 randomized, double-blind trial, we randomly assigned patients with hyperphosphatemia receiving maintenance hemodialysis to receive twice-daily oral tenapanor (3, 10, or 30 mg [the latter down-titrated, if needed]) for 8 weeks. Patients were then rerandomized 1:1 to receive either their previously assigned dose or placebo for a 4-week ‘withdrawal’ pe

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2

Yuan, Gang, Yili Chen, Li Li, et al. "Pharmacokinetics, Safety, and Tolerability of Tenapanor in Healthy Chinese and Caucasian Volunteers: A Randomized, Open-Label, Single-Center, Placebo-Controlled Phase 1 Study." International Journal of Clinical Practice 2024 (March 6, 2024): 1–10. http://dx.doi.org/10.1155/2024/1386980.

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Background. Tenapanor is a locally acting selective sodium-hydrogen exchanger 3 inhibitor with the potential to treat sodium/phosphorus and fluid overload in various cardiac-renal diseases, which has been approved for constipation-predominant irritable bowel syndrome in the US. The pharmacokinetics (PK) of tenapanor and its metabolite tenapanor-M1 (AZ13792925), as well as the safety and tolerability of tenapanor, were investigated in healthy Chinese and Caucasian subjects. Methods. This randomized, open-label, single-center, placebo-controlled phase 1 study (https://www.chinadrugtrials.org.cn;

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3

Suzuki, Naoki, Yuuki Takeda, Akie Kabuto, et al. "Efficacy of tenapanor in managing hyperphosphatemia and constipation in hemodialysis patients: A randomized controlled trial." PLOS One 20, no. 6 (2025): e0319319. https://doi.org/10.1371/journal.pone.0319319.

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Introduction Tenapanor is a minimally absorbed, small-molecule inhibitor of sodium/hydrogen exchanger 3 and thus suppresses sodium absorption in the gastrointestinal tract. It is approved by the FDA for the treatment of hyperphosphatemia in dialysis patients. This randomized controlled trial evaluated its efficacy in the treatment of hyperphosphatemia and constipation in hemodialysis patients. Methods Ninety hemodialysis patients were randomized 1:1 to receive either tenapanor or standard care. Randomization was performed using a computer-generated sequence stratified by baseline serum phospho

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4

Dos Santos, Denise Francisca, Aloisio Pêgo Palacios Luz, Marly Sousa De Araújo, et al. "Tenapanor como terapia para hiperfosfatemia refratária em pacientes submetidos à diálise: revisão sistemática." Brazilian Journal of Health Review 7, no. 1 (2024): 7327–40. http://dx.doi.org/10.34119/bjhrv7n1-599.

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A hiperfosfatemia é uma complicação desafiadora em pacientes em diálise, associada a complicações vasculares e ósseas. O tenapanor, um inibidor do cotransportador de sódio-fósforo no intestino, surge como uma promissora intervenção farmacológica. O presente estudo tem como objetivo avaliar a eficácia do tenapanor como agente terapêutico para hiperfosfatemia refratária em pacientes submetidos à diálise. Este estudo, baseado em uma revisão sistemática da literatura científica, abrange o período de 2014 a 2024, utilizando as bases de dados PubMed (Medline), Cochrane Library e Scientific Electroni

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5

Tan, Xinjie, Archana Kini, Dorothee Römermann, and Ursula Seidler. "The NHE3 Inhibitor Tenapanor Prevents Intestinal Obstructions in CFTR-Deleted Mice." International Journal of Molecular Sciences 23, no. 17 (2022): 9993. http://dx.doi.org/10.3390/ijms23179993.

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Mutations in the CFTR chloride channel result in intestinal obstructive episodes in cystic fibrosis (CF) patients and in CF animal models. In this study, we explored the possibility of reducing the frequency of obstructive episodes in cftr−/− mice through the oral application of a gut-selective NHE3 inhibitor tenapanor and searched for the underlying mechanisms involved. Sex- and age-matched cftr+/+ and cftr−/− mice were orally gavaged twice daily with 30 mg kg− 1 tenapanor or vehicle for a period of 21 days. Body weight and stool water content was assessed daily and gastrointestinal transit t

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6

Stamatopoulos, Konstantinos, Nena Mistry, Nikoletta Fotaki, David B. Turner, and Brandon Swift. "Physiologically Based Biopharmaceutics Model (PBBM) of Minimally Absorbed Locally Acting Drugs in the Gastrointestinal Tract—Case Study: Tenapanor." Pharmaceutics 15, no. 12 (2023): 2726. http://dx.doi.org/10.3390/pharmaceutics15122726.

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A physiologically based biopharmaceutics model (PBBM) was developed to predict stool and urine sodium content in response to tenapanor administration in healthy subjects. Tenapanor is a minimally absorbed small molecule that inhibits the sodium/hydrogen isoform 3 exchanger (NHE3). It is used to treat irritable bowel syndrome with constipation (IBS-C). Its mode of action in the gastrointestinal tract reduces the uptake of sodium, resulting in an increase in water secretion in the intestinal lumen and accelerating intestinal transit time. The strategy employed was to perform drug–drug interactio

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7

Shigematsu, Takashi, Yotaro Une, Kazuaki Ikejiri, Hironori Kanda, Masafumi Fukagawa, and Tadao Akizawa. "Therapeutic Effects of Add-On Tenapanor for Hemodialysis Patients with Refractory Hyperphosphatemia." American Journal of Nephrology 52, no. 6 (2021): 496–506. http://dx.doi.org/10.1159/000516156.

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<b><i>Introduction:</i></b> Phosphate binders are used to treat hyperphosphatemia. Some patients have inappropriately controlled serum phosphorus levels, which may occur for many reasons, including a high pill burden and adverse events (AEs). Tenapanor selectively inhibits the passive paracellular transfer of phosphate in the gastrointestinal tract, thereby reducing serum phosphorus levels. This novel mechanism of action may contribute to improved phosphate management. The efficacy and safety of tenapanor have not been evaluated in Japanese patients with high serum phos

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8

Pergola, Pablo E., David P. Rosenbaum, Yang Yang, and Glenn M. Chertow. "A Randomized Trial of Tenapanor and Phosphate Binders as a Dual-Mechanism Treatment for Hyperphosphatemia in Patients on Maintenance Dialysis (AMPLIFY)." Journal of the American Society of Nephrology 32, no. 6 (2021): 1465–73. http://dx.doi.org/10.1681/asn.2020101398.

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BackgroundHyperphosphatemia is associated with cardiovascular morbidity and mortality in patients receiving maintenance dialysis. It is unknown whether combining two therapies with different mechanisms of action—tenapanor, an inhibitor of paracellular phosphate absorption, and phosphate binders—is safe and effective for the management of hyperphosphatemia in patients receiving maintenance dialysis.MethodsThis double-blind phase 3 trial enrolled 236 patients undergoing maintenance dialysis with hyperphosphatemia (defined in this trial as serum phosphorus 5.5–10 mg/dl inclusive) despite receivin

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9

Markham, Anthony. "Tenapanor: First Approval." Drugs 79, no. 17 (2019): 1897–903. http://dx.doi.org/10.1007/s40265-019-01215-9.

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10

Lin, Tiffany, Akram Al-Makki, and Brian Shepler. "Tenapanor: A new treatment option for hyperphosphatemia in end stage kidney disease." Journal of Pharmacy & Pharmaceutical Sciences 25 (January 16, 2022): 77–83. http://dx.doi.org/10.18433/jpps32284.

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Purpose: This narrative review explores the currently published studies that have evaluated tenapanor for the treatment of hyperphosphatemia in end-stage kidney disease (ESKD) patients on hemodialysis. This medication’s new phosphate lowering mechanism of action reduces intestinal phosphate absorption predominantly through reduction of passive paracellular phosphate flux by inhibition of the sodium/hydrogen exporter isoform 3 (NHE3). Tenapanor additionally prevents active transcellular phosphate absorption compensation by decreasing the expression of sodium phosphorus 2b transport protein (NaP

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