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Article ; Online: Elexacaftor/Tezacaftor/Ivacaftor Treatment and Depression-related Events.

Ramsey, Bonnie / Correll, Christoph U / DeMaso, David R / McKone, Edward / Tullis, Elizabeth / Taylor-Cousar, Jennifer L / Chu, Chenghao / Volkova, Nataliya / Ahluwalia, Neil / Waltz, David / Tian, Simon / Mall, Marcus A

American journal of respiratory and critical care medicine

2024 Volume 209, Issue 3, Page(s) 299–306

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Humans ; Cystic Fibrosis Transmembrane Conductance Regulator ; Depression/drug therapy ; Cystic Fibrosis/drug therapy ; Benzodioxoles ; Indoles ; Aminophenols ; Pyrazoles ; Pyridines ; Pyrrolidines ; Quinolones
Chemical Substances	elexacaftor (RRN67GMB0V) ; ivacaftor (1Y740ILL1Z) ; tezacaftor ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; Benzodioxoles ; Indoles ; Aminophenols ; Pyrazoles ; Pyridines ; Pyrrolidines ; Quinolones
Language	English
Publishing date	2024-03-19
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202308-1525OC
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Article ; Online: Real-world safety and effectiveness of elexacaftor/tezacaftor/ivacaftor in people with cystic fibrosis: Interim results of a long-term registry-based study.

Bower, Julie K / Volkova, Nataliya / Ahluwalia, Neil / Sahota, Gurvaneet / Xuan, Fengjuan / Chin, Anna / Weinstock, Tanya G / Ostrenga, Josh / Elbert, Alexander

Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society

2023 Volume 22, Issue 4, Page(s) 730–737

Abstract: Background: Phase 3 clinical trials showed elexacaftor/tezacaftor/ivacaftor (ELX/TEZ/IVA) was safe and efficacious in people with cystic fibrosis (CF) with ≥1 F508del-CFTR allele. To assess long-term effects of ELX/TEZ/IVA under real-world conditions of ...

Abstract	Background: Phase 3 clinical trials showed elexacaftor/tezacaftor/ivacaftor (ELX/TEZ/IVA) was safe and efficacious in people with cystic fibrosis (CF) with ≥1 F508del-CFTR allele. To assess long-term effects of ELX/TEZ/IVA under real-world conditions of use, a 5-year observational registry-based study is being conducted. We report interim results from the first 2 years of follow-up. Methods: The study included people with CF in the US Cystic Fibrosis Foundation Patient Registry (CFFPR) who initiated ELX/TEZ/IVA between October 2019 and December 2020. Pulmonary exacerbations (PEx), percent predicted forced expiratory volume in 1 second (ppFEV Results: 16,116 people with CF were included (mean treatment duration 20.4 months). Among those with 5 years of pre-treatment data, mean PEx/patient/year declined to 0.18 (95% CI: 0.17, 0.19) in Years 1 and 2 post-treatment from 0.86 (95% CI: 0.83, 0.88) in the baseline year (79% reduction), after a continued increase observed pre-treatment. Similarly, a decline in mean hospitalizations/patient/year was observed in Year 1 that was sustained in Year 2 (74% reduction from baseline year). The mean absolute change in ppFEV Conclusions: ELX/TEZ/IVA treatment was associated with sustained improvements in lung function, reduced frequency of PEx and all-cause hospitalization, increased BMI, and lower prevalence of positive bacterial cultures. Additionally, there was a 72% lower rate of death and 85% lower rate of lung transplantation relative to the year before ELX/TEZ/IVA availability. These results, from the largest cohort of ELX/TEZ/IVA-treated people to date, extend our understanding of the broad clinical benefits of ELX/TEZ/IVA.
MeSH term(s)	Humans ; Cystic Fibrosis/diagnosis ; Cystic Fibrosis/drug therapy ; Cystic Fibrosis/epidemiology ; Cystic Fibrosis Transmembrane Conductance Regulator ; Aminophenols/adverse effects ; Benzodioxoles/adverse effects ; Registries ; Mutation ; Chloride Channel Agonists/adverse effects
Chemical Substances	elexacaftor (RRN67GMB0V) ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; ivacaftor (1Y740ILL1Z) ; tezacaftor ; Aminophenols ; Benzodioxoles ; Chloride Channel Agonists
Language	English
Publishing date	2023-03-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2084724-5
ISSN	1873-5010 ; 1569-1993
ISSN (online)	1873-5010
ISSN	1569-1993
DOI	10.1016/j.jcf.2023.03.002
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Article: Impact of frailty on endoscopic retrograde cholangiopancreatography outcomes in nonagenarians: A United States national experience.

Basida, Sanket Dhirubhai / Dahiya, Dushyant Singh / Yousaf, Muhammad Nadeem / Basida, Brinda / Pinnam, Bhanu Siva Mohan / Gangwani, Manesh Kumar / Ali, Hassam / Singh, Sahib / Shah, Yash R / Ahluwalia, Daksh / Shah, Mihir Prakash / Chandan, Saurabh / Sharma, Neil R / Thakkar, Shyam

World journal of gastrointestinal endoscopy

2024 Volume 16, Issue 3, Page(s) 148–156

Abstract: Background: Endoscopic retrograde cholangiopancreatography (ERCP) is an essential therapeutic tool for biliary and pancreatic diseases. Frail and elderly patients, especially those aged ≥ 90 years are generally considered a higher-risk population for ... ...

Abstract	Background: Endoscopic retrograde cholangiopancreatography (ERCP) is an essential therapeutic tool for biliary and pancreatic diseases. Frail and elderly patients, especially those aged ≥ 90 years are generally considered a higher-risk population for ERCP-related complications. Aim: To investigate outcomes of ERCP in the Non-agenarian population (≥ 90 years) concerning Frailty. Methods: This is a cohort study using the 2018-2020 National Readmission Database. Patients aged ≥ 90 were identified who underwent ERCP, using the international classification of diseases-10 code with clinical modification. Johns Hopkins's adjusted clinical groups frailty indicator was used to classify patients as frail and non-frail. The primary outcome was mortality, and the secondary outcomes were morbidity and the 30 d readmission rate related to ERCP. We used univariate and multivariate regression models for analysis. Results: A total of 9448 patients were admitted for any indications of ERCP. Frail and non-frail patients were 3445 (36.46%) and 6003 (63.53%) respectively. Indications for ERCP were Choledocholithiasis (74.84%), Biliary pancreatitis (9.19%), Pancreatico-biliary cancer (7.6%), Biliary stricture (4.84%), and Cholangitis (1.51%). Mortality rates were higher in frail group [adjusted odds ratio (aOR) = 1.68, Conclusion: There was a significantly higher mortality risk and healthcare burden amongst nonagenarian frail patients undergoing ERCP compared to non-frail. Larger studies are warranted to investigate and mitigate modifiable risk factors.
Language	English
Publishing date	2024-04-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2573698-X
ISSN	1948-5190
ISSN	1948-5190
DOI	10.4253/wjge.v16.i3.148
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Article ; Online: Melatonin ameliorates aging-related impaired angiogenesis in gastric endothelial cells via local actions on mitochondria and VEGF-survivin signaling.

Ahluwalia, Amrita / Patel, Khushin / Hoa, Neil / Brzozowska, Iwona / Jones, Michael K / Tarnawski, Andrzej S

American journal of physiology. Gastrointestinal and liver physiology

2021 Volume 321, Issue 6, Page(s) G682–G689

Abstract: Tissue injury healing is impaired in aging, and this impairment is caused in part by reduced angiogenesis. Melatonin, a neuroendocrine hormone that regulates sleep and circadian rhythm, is also produced in the gastrointestinal tract. The expression of ... ...

Abstract	Tissue injury healing is impaired in aging, and this impairment is caused in part by reduced angiogenesis. Melatonin, a neuroendocrine hormone that regulates sleep and circadian rhythm, is also produced in the gastrointestinal tract. The expression of melatonin receptors MT1 and MT2 in gastric endothelial cells and their roles in aging-related impairment of gastric angiogenesis have not been examined. We hypothesized that MT1 and MT2 expression is reduced in gastric endothelial cells of aging rats and that melatonin treatment can upregulate their expression and improve angiogenesis. We examined the expression of MT1 and MT2 in gastric endothelial cells (GECs) isolated from young and aging rats. We also examined the effects of melatonin treatment on angiogenesis, GEC mitochondrial function, expression of vascular endothelial growth factor (VEGF), its signaling receptor (VEGFR-2), and the inhibitor of apoptosis protein, survivin. Young and aging GECs expressed MT1 (in the cytoplasm and mitochondria) and MT2 (in nucleus and mitochondria). In aging GECs, MT1 and MT2 levels, in vitro angiogenesis, and mitochondrial membrane potential were significantly reduced (by 1.5-fold, 1.9-fold, 3.1-fold, and 1.63-fold, respectively) compared with young GECs. Melatonin treatment of aging GECs significantly increased MT1 and MT2 expression compared with the controls, induced nuclear translocation of MT1, and significantly ameliorated the aging-related impairment of angiogenesis and mitochondrial function. Aging GECs have significantly reduced MT1 and MT2 expression, angiogenesis, and mitochondrial membrane potential compared with young GECs. Treatment of aging GECs with melatonin increases expression of VEGF receptor and survivin and ameliorates aging-related impaired angiogenesis and mitochondrial function.
MeSH term(s)	Age Factors ; Angiogenesis Inducing Agents/pharmacology ; Animals ; Cells, Cultured ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Gastric Mucosa/blood supply ; Melatonin/pharmacology ; Mitochondria/drug effects ; Mitochondria/metabolism ; Neovascularization, Physiologic/drug effects ; Rats, Inbred F344 ; Receptor, Melatonin, MT1/agonists ; Receptor, Melatonin, MT1/metabolism ; Receptor, Melatonin, MT2/agonists ; Receptor, Melatonin, MT2/metabolism ; Signal Transduction ; Survivin/metabolism ; Vascular Endothelial Growth Factor A/metabolism ; Rats
Chemical Substances	Angiogenesis Inducing Agents ; Birc5 protein, rat ; Receptor, Melatonin, MT1 ; Receptor, Melatonin, MT2 ; Survivin ; Vascular Endothelial Growth Factor A ; vascular endothelial growth factor A, rat ; Melatonin (JL5DK93RCL)
Language	English
Publishing date	2021-10-20
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00101.2021
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Article ; Online: Membrane Estrogen Receptor Beta is Sufficient to Mitigate Cardiac Cell Pathology.

Ahluwalia, Amrita / Hoa, Neil / Moreira, Debbie / Aziz, Daniel / Singh, Karanvir / Patel, Khushin N / Levin, Ellis R

Endocrinology

2022

Abstract: Estrogen acting through estrogen receptor beta has been shown to oppose the stimulation of cardiac myocytes and cardiac fibroblasts that results in cardiac hypertrophy and fibrosis. Previous work has implicated signal transduction from ERβ as being ... ...

Abstract	Estrogen acting through estrogen receptor beta has been shown to oppose the stimulation of cardiac myocytes and cardiac fibroblasts that results in cardiac hypertrophy and fibrosis. Previous work has implicated signal transduction from ERβ as being important to the function of estrogen in these regards. Here we address whether membrane ERβ is sufficient to oppose key mechanisms by which Angiotensin II stimulates cardiac cell pathology. To do this we first defined essential structural elements within ERβ that are necessary for membrane or nuclear localization in cells. We previously determined that cysteine 418 is the site of palmitoylation of ERβ that is required and sufficient for cell membrane localization in mice and is the same site in humans. Here we determined in CHO cells, and mouse and rat myocytes and cardiac fibroblasts, the impact on multiple aspects of signal transduction by expressing wild type or a C418A mutant ERβ. To test the importance of the nuclear receptor, we determined a four amino acid deletion in the E domain of ERβ that strongly blocked nuclear localization. Using these tools, we expressed wild type and mutant ERβ constructs into cardiomyocytes and cardiac fibroblasts from ERβ deleted mice. We determined the ability of estrogen to mitigate cell pathology stimulated by Angiotensin II and whether the membrane ERβ is necessary and sufficient.
Language	English
Publishing date	2022-12-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqac200
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Article ; Online: Phase 1 Study to Assess the Safety and Pharmacokinetics of Elexacaftor/Tezacaftor/Ivacaftor in Subjects Without Cystic Fibrosis With Moderate Hepatic Impairment.

Viswanathan, Lakshmi / Bachman, Eric / Tian, Simon / Ahluwalia, Neil / Zhang, Yaohua / Bernstein, Harold S / Panorchan, Paul

European journal of drug metabolism and pharmacokinetics

2022 Volume 47, Issue 6, Page(s) 817–825

Abstract: Background and objective: Elexacaftor/tezacaftor/ivacaftor is highly effective in treating people with cystic fibrosis (pwCF) who have ≥ 1 responsive mutation. Liver disease occurs in approximately 10%-20% of pwCF. The objective of this study was to ... ...

Abstract	Background and objective: Elexacaftor/tezacaftor/ivacaftor is highly effective in treating people with cystic fibrosis (pwCF) who have ≥ 1 responsive mutation. Liver disease occurs in approximately 10%-20% of pwCF. The objective of this study was to assess the safety and pharmacokinetics of elexacaftor/tezacaftor/ivacaftor in people with moderate hepatic impairment, which is necessary to inform on its use and guide dosing recommendations. Methods: The safety and pharmacokinetics of elexacaftor/tezacaftor/ivacaftor were evaluated in subjects without CF with moderate hepatic impairment versus matched healthy controls. Twenty-two subjects (11 with moderate hepatic impairment and 11 healthy subjects) received half the standard adult daily dose of elexacaftor/tezacaftor/ivacaftor (elexacaftor 100 mg/tezacaftor 50 mg/ivacaftor 150 mg) orally for 10 days. Results: Elexacaftor/tezacaftor/ivacaftor was safe and well tolerated in subjects with moderate hepatic impairment and healthy controls. On day 10, the mean values of the area under the curve during the dosing interval (AUC Conclusions: A dose reduction of elexacaftor/tezacaftor/ivacaftor is warranted in people with moderate hepatic impairment. (Trial registry number 2018-002570-40; registered 2 July 2018.).
MeSH term(s)	Adult ; Humans ; Cystic Fibrosis/drug therapy ; Cystic Fibrosis/genetics ; Cystic Fibrosis/chemically induced ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator/therapeutic use ; Liver Diseases/drug therapy
Chemical Substances	ivacaftor (1Y740ILL1Z) ; tezacaftor ; elexacaftor (RRN67GMB0V) ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6)
Language	English
Publishing date	2022-08-29
Publishing country	France
Document type	Clinical Trial, Phase I ; Journal Article
ZDB-ID	196729-0
ISSN	2107-0180 ; 0398-7639 ; 0378-7966
ISSN (online)	2107-0180
ISSN	0398-7639 ; 0378-7966
DOI	10.1007/s13318-022-00791-8
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Article ; Online: NSAID-induced injury of gastric epithelial cells is reversible: roles of mitochondria, AMP kinase, NGF, and PGE

Ahluwalia, Amrita / Hoa, Neil / Jones, Michael K / Tarnawski, Andrzej S

American journal of physiology. Gastrointestinal and liver physiology

2019 Volume 317, Issue 6, Page(s) G862–G871

Abstract: Nonsteroidal anti-inflammatory drugs (NSAIDs) such as diclofenac (DFN) and indomethacin (INDO) are extensively used worldwide. Their main side effects are injury of the gastrointestinal tract, including erosions, ulcers, and bleeding. Since gastric ... ...

Abstract	Nonsteroidal anti-inflammatory drugs (NSAIDs) such as diclofenac (DFN) and indomethacin (INDO) are extensively used worldwide. Their main side effects are injury of the gastrointestinal tract, including erosions, ulcers, and bleeding. Since gastric epithelial cells (GEPCs) are crucial for mucosal defense and are the major target of injury, we examined the extent to which DFN- and INDO-induced GEPC injury can be reversed by nerve growth factor (NGF), 16,16 dimethyl prostaglandin E
MeSH term(s)	16,16-Dimethylprostaglandin E2/pharmacology ; Aminoimidazole Carboxamide/analogs & derivatives ; Aminoimidazole Carboxamide/pharmacology ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/adverse effects ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Anti-Ulcer Agents/pharmacology ; Cell Death/drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Diclofenac/adverse effects ; Gastric Mucosa/drug effects ; Gastric Mucosa/metabolism ; Gastric Mucosa/pathology ; Indomethacin/adverse effects ; Membrane Potential, Mitochondrial/drug effects ; Mitochondria/drug effects ; Mitochondria/metabolism ; Nerve Growth Factor/pharmacology ; Rats ; Ribonucleosides/pharmacology
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Anti-Ulcer Agents ; Ribonucleosides ; Diclofenac (144O8QL0L1) ; Aminoimidazole Carboxamide (360-97-4) ; acadesine (53IEF47846) ; Nerve Growth Factor (9061-61-4) ; 16,16-Dimethylprostaglandin E2 (M790V82VAC) ; Indomethacin (XXE1CET956)
Language	English
Publishing date	2019-09-23
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00192.2019
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Article ; Online: Mitochondria in gastric epithelial cells are the key targets for NSAIDs-induced injury and NGF cytoprotection.

Ahluwalia, Amrita / Jones, Michael K / Hoa, Neil / Tarnawski, Andrzej S

Journal of cellular biochemistry

2019 Volume 120, Issue 7, Page(s) 11651–11659

Abstract: Gastric epithelial cells are important components of mucosal protection and targets of nonsteroidal anti-inflammatory drugs (NSAIDs)-induced injury. Diclofenac (DFN) is one of the most widely used NSAIDs; however, even its short-term use can induce ... ...

Abstract	Gastric epithelial cells are important components of mucosal protection and targets of nonsteroidal anti-inflammatory drugs (NSAIDs)-induced injury. Diclofenac (DFN) is one of the most widely used NSAIDs; however, even its short-term use can induce gastric erosions and ulcers. Nerve growth factor (NGF) has been reported to act not only on neuronal cells but also on endothelial cells; however, its action on gastric epithelial cells is unknown. This study was aimed to determine, whether NGF can protect gastric epithelial cells against DFN-induced injury, and to determine the underlying molecular mechanisms with a focus on mitochondria, survivin, and insulin-like growth factor 1 (IGF-1). Cultured normal rat gastric mucosal epithelial cells 1 (RGM1) were treated with phosphate-buffered saline (PBS; control), NGF (100 ng/mL) and/or DFN (0.25-1.00 mM) for 4 hours. We examined: (1) cell injury by confocal microscopy; (2) cell death/survival using Calcein AM live cell tracking dye; (3) mitochondrial structure and membrane potential function using MitoTracker in live cells; and (4) expression of NGF, its receptor - tropomyosin receptor kinase A (TrkA), survivin and IGF-1 by immunostaining. DFN treatment of RGM1 cells for 4 hours caused extensive cell injury, mitochondrial disintegration, reduced cell viability (from 94 ± 3% in controls to 14 ± 4% in 0.5 mM DFN-treated cells; P < 0.001), and expression of survivin and IGF-1. NGF treatment significantly increased survivin and IGF-1 expression by 41% and 75%, respectively versus PBS controls. Pretreatment with NGF before DFN treatment reduced mitochondrial damage and cell death by 73% and 82%, respectively versus treatment with DFN alone (all P < 0.001). This study also showed the presence of high-affinity TrkA receptors in the plasma membrane and mitochondria of RGM1 cells indicating novel actions of NGF.
Language	English
Publishing date	2019-02-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.28445
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Article ; Online: Mechanisms by Which Membrane and Nuclear ER Alpha Inhibit Adipogenesis in Cells Isolated From Female Mice.

Ahluwalia, Amrita / Hoa, Neil / Ge, Lisheng / Blumberg, Bruce / Levin, Ellis R

Endocrinology

2020 Volume 161, Issue 11

Abstract: Mesenchymal stem cells can differentiate into mature chondrocytes, osteoblasts, and adipocytes. Excessive and dysfunctional visceral adipocytes increase upon menopause and importantly contribute to altered metabolism in postmenopausal women. We ... ...

Abstract	Mesenchymal stem cells can differentiate into mature chondrocytes, osteoblasts, and adipocytes. Excessive and dysfunctional visceral adipocytes increase upon menopause and importantly contribute to altered metabolism in postmenopausal women. We previously showed both plasma membrane and nuclear estrogen receptors alpha (ERα) with endogenous estrogen are required to suppress adipogenesis in vivo. Here we determined mechanisms by which these liganded ER pools collaborate to inhibit the peroxisome proliferator-activated gamma (PPARγ) gene and subsequent progenitor differentiation. In 3T3-L1 pre-adipocytes and adipose-derived stem cells (ADSC), membrane ERα signaled through phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT) to enhance ERα nuclear localization, importantly at the PPARγ gene promoter. AKT also increased overall abundance and recruitment of co-repressors GATA3, β-catenin, and TCF4 to the PPARγ promoter. Membrane ERα signaling additionally enhanced wingless-integrated (Wnt)1 and 10b expression. The components of the repressor complex were required for estrogen to inhibit rosiglitazone-induced differentiation of ADSC and 3T3-L1 cells to mature adipocytes. These mechanisms whereby ER cellular pools collaborate to inhibit gene expression limit progenitor differentiation to mature adipocytes.
MeSH term(s)	3T3-L1 Cells ; Adipocytes/physiology ; Adipogenesis/genetics ; Animals ; Cell Differentiation/genetics ; Cell Membrane/metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Down-Regulation/genetics ; Estrogen Receptor alpha/metabolism ; Estrogen Receptor alpha/physiology ; Female ; Mice ; Mice, Transgenic ; Signal Transduction/genetics
Chemical Substances	Estrogen Receptor alpha
Language	English
Publishing date	2020-09-25
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqaa175
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Article ; Online: Long-Term Safety and Efficacy of Elexacaftor/Tezacaftor/Ivacaftor in Children Aged ⩾6 Years with Cystic Fibrosis and at Least One

Wainwright, Claire / McColley, Susanna A / McNally, Paul / Powers, Michael / Ratjen, Felix / Rayment, Jonathan H / Retsch-Bogart, George / Roesch, Erica / Ahluwalia, Neil / Chin, Anna / Chu, Chenghao / Lu, Mengdi / Menon, Prema / Waltz, David / Weinstock, Tanya / Zelazoski, Laura / Davies, Jane C

American journal of respiratory and critical care medicine

2023 Volume 208, Issue 1, Page(s) 68–78

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Adult ; Child ; Humans ; Cystic Fibrosis/drug therapy ; Cystic Fibrosis/genetics ; Cystic Fibrosis/diagnosis ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator/therapeutic use ; Alleles ; Chloride Channel Agonists/therapeutic use ; Aminophenols/adverse effects ; Benzodioxoles/adverse effects ; Mutation
Chemical Substances	elexacaftor (RRN67GMB0V) ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; ivacaftor (1Y740ILL1Z) ; tezacaftor ; Chloride Channel Agonists ; Aminophenols ; Benzodioxoles
Language	English
Publishing date	2023-05-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202301-0021OC
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In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito