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https://www.readbyqxmd.com/read/28218904/the-protumorigenic-potential-of-fty720-by-promoting-extramedullary-hematopoiesis-and-mdsc-accumulation
#1
Y Li, T Zhou, Y Wang, C Ning, Z Lv, G Han, J C Morris, E N Taylor, R Wang, H Xiao, C Hou, Y Ma, B Shen, J Feng, R Guo, Y Li, G Chen
FTY720 (also called fingolimod) is recognized as an immunosuppressant and has been approved by the Food and Drug Administration to treat refractory multiple sclerosis. However, long-term administration of FTY720 potentially increases the risk for cancer in recipients. The underlying mechanisms remain poorly understood. Herein, we provided evidence that FTY720 administration potentiated tumor growth. Mechanistically, FTY720 enhanced extramedullary hematopoiesis and massive accumulation of myeloid-derived suppressor cells (MDSCs), which actively suppressed antitumor immune responses...
February 20, 2017: Oncogene
https://www.readbyqxmd.com/read/28212923/multiple-sclerosis-in-the-real-world-a-systematic-review-of-fingolimod-as-a-case-study
#2
REVIEW
Tjalf Ziemssen, Jennie Medin, C Anne-Marie Couto, Catherine R Mitchell
INTRODUCTION: The aim of our study was to systematically review the growing body of published literature reporting on one specific multiple sclerosis (MS) treatment, fingolimod, in the real world to assess its effectiveness in patients with MS, evaluate methodologies used to investigate MS in clinical practice, and describe the evidence gaps for MS as exemplified by fingolimod. METHODS: We conducted a PRISMA-compliant systematic review of the literature (cut-off date: 4 March 2016)...
February 13, 2017: Autoimmunity Reviews
https://www.readbyqxmd.com/read/28211024/comparative-effectiveness-research-of-disease-modifying-therapies-for-the-management-of-multiple-sclerosis-analysis-of-a-large-health-insurance-claims-database
#3
Aaron Boster, Jacqueline Nicholas, Ning Wu, Wei-Shi Yeh, Monica Fay, Michael Edwards, Ming-Yi Huang, Andrew Lee
INTRODUCTION: Limited data are available on the real-world effectiveness of newer oral disease-modifying therapies (DMTs) in multiple sclerosis. The purpose of this study was to retrospectively compare the real-world effectiveness of dimethyl fumarate (DMF), fingolimod, teriflunomide, and injectable DMTs in routine clinical practice based on US claims data. METHODS: Patients newly-initiating DMF, interferon beta (IFNβ), glatiramer acetate (GA), teriflunomide, or fingolimod in 2013 were identified in the Truven MarketScan Commercial Claims Databases (N = 6372)...
February 16, 2017: Neurology and Therapy
https://www.readbyqxmd.com/read/28209440/severe-disease-exacerbations-in-patients-with-multiple-sclerosis-after-discontinuing-fingolimod
#4
REVIEW
Anna Członkowska, Łukasz Smoliński, Tomasz Litwin
Discontinuation of fingolimod in patients with multiple sclerosis (MS) can lead to disease reactivation. In this review, we describe cases of severe exacerbations in patients with MS following discontinuation of fingolimod, including three cases from our center. We consider potential mechanisms of disease reactivation after cessation of fingolimod, and the evidence supporting this rebound effect. We conclude that discontinuation of fingolimod results in the return of disease activity, which then leads to severe exacerbations (i...
February 2, 2017: Neurologia i Neurochirurgia Polska
https://www.readbyqxmd.com/read/28209331/treatment-effectiveness-of-alemtuzumab-compared-with-natalizumab-fingolimod-and-interferon-beta-in-relapsing-remitting-multiple-sclerosis-a-cohort-study
#5
Tomas Kalincik, J William L Brown, Neil Robertson, Mark Willis, Neil Scolding, Claire M Rice, Alastair Wilkins, Owen Pearson, Tjalf Ziemssen, Michael Hutchinson, Christopher McGuigan, Vilija Jokubaitis, Tim Spelman, Dana Horakova, Eva Havrdova, Maria Trojano, Guillermo Izquierdo, Alessandra Lugaresi, Alexandre Prat, Marc Girard, Pierre Duquette, Pierre Grammond, Raed Alroughani, Eugenio Pucci, Patrizia Sola, Raymond Hupperts, Jeannette Lechner-Scott, Murat Terzi, Vincent Van Pesch, Csilla Rozsa, François Grand'Maison, Cavit Boz, Franco Granella, Mark Slee, Daniele Spitaleri, Javier Olascoaga, Roberto Bergamaschi, Freek Verheul, Steve Vucic, Pamela McCombe, Suzanne Hodgkinson, Jose Luis Sanchez-Menoyo, Radek Ampapa, Magdolna Simo, Tunde Csepany, Cristina Ramo, Edgardo Cristiano, Michael Barnett, Helmut Butzkueven, Alasdair Coles
BACKGROUND: Alemtuzumab, an anti-CD52 antibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitting multiple sclerosis, but its efficacy relative to more potent immunotherapies is unknown. We compared the effectiveness of alemtuzumab with natalizumab, fingolimod, and interferon beta in patients with relapsing-remitting multiple sclerosis treated for up to 5 years. METHODS: In this international cohort study, we used data from propensity-matched patients with relapsing-remitting multiple sclerosis from the MSBase and six other cohorts...
February 10, 2017: Lancet Neurology
https://www.readbyqxmd.com/read/28203061/herding-a-new-phenomenon-affecting-medical-decision-making-in-multiple-sclerosis-care-lessons-learned-from-discutir-ms
#6
Gustavo Saposnik, Jorge Maurino, Angel P Sempere, Christian C Ruff, Philippe N Tobler
PURPOSE: Herding is a phenomenon by which individuals follow the behavior of others rather than deciding independently on the basis of their own private information. A herding-like phenomenon can occur in multiple sclerosis (MS) when a neurologist follows a therapeutic recommendation by a colleague even though it is not supported by best practice clinical guidelines. Limited information is currently available on the role of herding in medical care. The objective of this study was to determine the prevalence (and its associated factors) of herding in the management of MS...
2017: Patient Preference and Adherence
https://www.readbyqxmd.com/read/28191684/sequence-of-cardiovascular-autonomic-alterations-after-fingolimod-initiation
#7
Sakari Simula, Tomi P Laitinen, Tiina M Laitinen, Päivi Hartikainen, Juha E K Hartikainen
BACKGROUND: Homeostasis between heart rate and blood pressure is based on several interacting regulatory reflexes, which become influenced by fingolimod initiation. The aim of this study was to determine the sequence of changes in cardiovascular autonomic regulation after fingolimod initiation. METHODS: Twenty-seven patients with relapsing-remitting multiple sclerosis underwent continuous electrocardiogram recording during the first 6 hr after the first dose of fingolimod...
February 13, 2017: Annals of Noninvasive Electrocardiology
https://www.readbyqxmd.com/read/28180112/oral-multiple-sclerosis-drugs-inhibit-the-in-vitro-growth-of-epsilon-toxin-producing-gut-bacterium-clostridium-perfringens
#8
Kareem R Rumah, Timothy K Vartanian, Vincent A Fischetti
There are currently three oral medications approved for the treatment of multiple sclerosis (MS). Two of these medications, Fingolimod, and Teriflunomide, are considered to be anti-inflammatory agents, while dimethyl fumarate (DMF) is thought to trigger a robust antioxidant response, protecting vulnerable cells during an MS attack. We previously proposed that epsilon toxin from the gut bacterium, Clostridium perfringens, may initiate newly forming MS lesions due to its tropism for blood-brain barrier (BBB) vasculature and central nervous system myelin...
2017: Frontiers in Cellular and Infection Microbiology
https://www.readbyqxmd.com/read/28167760/sphingosine-1-phosphate-receptor-modulation-suppresses-pathogenic-astrocyte-activation-and-chronic-progressive-cns-inflammation
#9
Veit Rothhammer, Jessica E Kenison, Emily Tjon, Maisa C Takenaka, Kalil Alves de Lima, Davis M Borucki, Chun-Cheih Chao, Annabel Wilz, Manon Blain, Luke Healy, Jack Antel, Francisco J Quintana
Multiple sclerosis (MS) is an autoimmune inflammatory demyelinating disease of the CNS that causes disability in young adults as a result of the irreversible accumulation of neurological deficits. Although there are potent disease-modifying agents for its initial relapsing-remitting phase, these therapies show limited efficacy in secondary progressive MS (SPMS). Thus, there is an unmet clinical need for the identification of disease mechanisms and potential therapeutic approaches for SPMS. Here, we show that the sphingosine 1-phosphate receptor (S1PR) modulator fingolimod (FTY720) ameliorated chronic progressive experimental autoimmune encephalomyelitis in nonobese diabetic mice, an experimental model that resembles several aspects of SPMS, including neurodegeneration and disease progression driven by the innate immune response in the CNS...
February 6, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28165320/cutaneous-cryptococcosis-in-a-patient-taking-fingolimod-for-multiple-sclerosis-here-come-the-opportunistic-infections
#10
Adam F Carpenter, Shikha J Goodwin, Peter F Bornstein, Andrew J Larson, Christine K Markus
BACKGROUND: Fingolimod is an oral disease-modifying therapy for relapsing forms of multiple sclerosis, which acts by sequestering lymphocytes within lymph nodes. OBJECTIVE: To describe a case of extrapulmonary cryptococcosis in a patient taking fingolimod. METHODS: Case report. RESULTS: A 47-year-old man developed a non-healing skin lesion approximately 16 months after starting treatment with fingolimod. Biopsy revealed cryptococcosis...
February 2017: Multiple Sclerosis: Clinical and Laboratory Research
https://www.readbyqxmd.com/read/28162947/fty720-supplementation-partially-improves-erectile-dysfunction-in-rats-with-streptozotocin-induced-type-1-diabetes-through-inhibition-of-endothelial-dysfunction-and-corporal-fibrosis
#11
Kai Cui, Yajun Ruan, Tao Wang, Ke Rao, Zhong Chen, Shaogang Wang, Jihong Liu
INTRODUCTION: Erectile dysfunction (ED) in patients with diabetes mellitus (DM) seriously affects their quality of life. However, these patients show a poor effect rate for oral phosphodiesterase type 5 inhibitors. Thus, new treatment methods are urgently needed. Fingolimod hydrochloride (FTY720) was approved in 2010 for the treatment of patients with the relapsing-remitting form of multiple sclerosis. AIM: To investigate whether FTY720 supplementation could ameliorate ED induced by DM (DMED)...
February 2, 2017: Journal of Sexual Medicine
https://www.readbyqxmd.com/read/28161400/memory-b-cells-are-major-targets-for-effective-immunotherapy-in-relapsing-multiple-sclerosis
#12
REVIEW
David Baker, Monica Marta, Gareth Pryce, Gavin Giovannoni, Klaus Schmierer
Although multiple sclerosis (MS) is considered to be a CD4, Th17-mediated autoimmune disease, supportive evidence is perhaps circumstantial, often based on animal studies, and is questioned by the perceived failure of CD4-depleting antibodies to control relapsing MS. Therefore, it was interestingly to find that current MS-treatments, believed to act via T cell inhibition, including: beta-interferons, glatiramer acetate, cytostatic agents, dimethyl fumarate, fingolimod, cladribine, daclizumab, rituximab/ocrelizumab physically, or functionally in the case of natalizumab, also depleted CD19+, CD27+ memory B cells...
January 31, 2017: EBioMedicine
https://www.readbyqxmd.com/read/28161158/fingolimod-fty720-attenuates-social-deficits-learning-and-memory-impairments-neuronal-loss-and-neuroinflammation-in-the-rat-model-of-autism
#13
Hongmei Wu, Xuelai Wang, Jingquan Gao, Shuang Liang, Yanqiu Hao, Caihong Sun, Wei Xia, Yonggang Cao, Lijie Wu
AIMS: To investigate the effect of FTY720 on the valproic acid (VPA) rat model of autism. MAIN METHODS: As an animal model of autism, we used intraperitoneal injection of VPA on embryonic day 12.5 in Wistar rats. The pups were given FTY720 orally at doses of 0.25, 0.5 and 1mg/kg daily from postnatal day 15 to 35. Social behavior, spatial learning and memory were assessed at the end of FTY720 treatment. The histological change, oxidative stress, neuroinflammatory responses, and apoptosis-related proteins in the hippocampus were evaluated...
February 1, 2017: Life Sciences
https://www.readbyqxmd.com/read/28155899/fingolimod-alters-the-transcriptome-profile-of-circulating-cd4-cells-in-multiple-sclerosis
#14
Jörg Friess, Michael Hecker, Luisa Roch, Dirk Koczan, Brit Fitzner, Ines Charlotte Angerer, Ina Schröder, Kristin Flechtner, Hans-Jürgen Thiesen, Alexander Winkelmann, Uwe Klaus Zettl
Multiple sclerosis is a demyelinating disease affecting the central nervous system. T cells are known to contribute to this immune-mediated condition. Fingolimod modulates sphingosine-1-phosphate receptors, thereby preventing the egress of lymphocytes, especially CCR7-expressing CD8+ and CD4+ T cells, from lymphoid tissues. Using Affymetrix Human Transcriptome Arrays (HTA 2.0), we performed a transcriptome profiling analysis of CD4+ cells obtained from the peripheral blood of patients with highly active relapsing-remitting multiple sclerosis...
February 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28153532/fty720-fingolimod-reverses-%C3%AE-synuclein-induced-downregulation-of-brain-derived-neurotrophic-factor-mrna-in-oln-93-oligodendroglial-cells
#15
Ismael Segura-Ulate, Barbara Yang, Javier Vargas-Medrano, Ruth G Perez
Multiple system atrophy (MSA) is a demyelinating neurodegenerative disorder characterized by accumulation of aggregated α-synuclein (aSyn) inside oligodendrocyte precursors, mature oligodendroglia, and neurons. MSA dysfunction is associated with loss of trophic factor production by glial and neuronal cells. Here, we report that recombinant wild type human aSyn uptake by OLN-93, an oligodendroglia cell-line, reduced brain-derived neurotrophic factor (BDNF) expression. Furthermore, OLN-93 cells stably transfected with human wild type or an MSA-associated mutant aSyn, A53E that produces neuronal and glial inclusions, reduced BDNF mRNA to nearly unmeasurable qPCR levels...
January 31, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28153091/effect-of-fingolimod-on-neural-stem-cells-a-novel-mechanism-and-broadened-application-for-neural-repair
#16
Yuan Zhang, Xing Li, Bogoljub Ciric, Cun-Gen Ma, Bruno Gran, Abdolmohamad Rostami, Guang-Xian Zhang
Inflammatory demyelination and axonal damage of the CNS are hallmarks of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Fingolimod (FTY720), the first FDA-approved oral medication for MS, suppresses acute disease but is less effective at the chronic stage, and whether it has a direct effect on neuroregeneration in MS and EAE remains unclear. Here we show that FTY720, at nanomolar concentrations, effectively protected survival of neural stem cells (NSCs) and enhanced their development into mature oligodendrocytes (OLGs) in vitro, primarily through the S1P3 and S1P5 receptors...
February 1, 2017: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/28150133/impact-of-age-and-polytherapy-on-fingolimod-induced-bradycardia-a-preclinical-study
#17
Christian Ritter, Martin K R Svačina, Ilja Bobylev, Abhijeet Joshi, Toni Schneider, Helmar C Lehmann
Fingolimod is a an oral disease modifying drug for relapsing remitting multiple sclerosis (MS) preventing egress of B and T cells from lymph nodes. Relevant first dose adverse events include bradycardia and atrioventricular conduction slowing. Cardiac side effects of fingolimod and combinational pharmacotherapy including duloxetine and tolterodine were monitored in mice of different age using implantable ECG telemetric systems. Cardiac tissue was assessed for S1P-receptor subtype (1 and 3), and for GIRK1 expression...
February 1, 2017: Journal of Neuroimmune Pharmacology: the Official Journal of the Society on NeuroImmune Pharmacology
https://www.readbyqxmd.com/read/28148838/fingolimod-treatment-abrogates-chikungunya-virus-induced-arthralgia
#18
Teck-Hui Teo, Yi-Hao Chan, Wendy W L Lee, Fok-Moon Lum, Siti Naqiah Amrun, Zhisheng Her, Ravisankar Rajarethinam, Andres Merits, Olaf Rötzschke, Laurent Rénia, Lisa F P Ng
Chikungunya virus (CHIKV) is one of the many rheumatic arthropod-borne alphaviruses responsible for debilitating joint inflammation in humans. Despite the severity in many endemic regions, clinically approved intervention targeting the virus remains unavailable. CD4(+) T cells have been shown to mediate CHIKV-induced joint inflammation in mice. We demonstrate here that transfer of splenic CD4(+) T cells from virus-infected C57BL/6 mice into virus-infected T cell receptor-deficient (TCR(-/-)) mice recapitulated severe joint pathology including inflammation, vascular leakages, subcutaneous edema, and skeletal muscle necrosis...
February 1, 2017: Science Translational Medicine
https://www.readbyqxmd.com/read/28143860/hepatitis-e-virus-infection-in-a-patient-with-suspected-drug-induced-liver-injury
#19
Ashfaque Memon, Jose Miranda
A 58 years old woman, known case of multiple sclerosis, was referred to the acute medical assessment unit for worsening liver function. She was recently started on a new drug (fingolimod) for multiple sclerosis. After excluding common causes of acute hepatitis in the community, a working diagnosis of drug-induced liver injury was made. When liver enzymes kept rising, further investigations were carried out, which revealed acute hepatitis E virus (HEV) infection. This finding was unexpected, as this patient had no risk factor to acquire HEV infection and there was not a single case of HEV diagnosed in our hospital since long time...
January 31, 2017: BMJ Case Reports
https://www.readbyqxmd.com/read/28134307/fingolimod-limits-acute-a%C3%AE-neurotoxicity-and-promotes-synaptic-versus-extrasynaptic-nmda-receptor-functionality-in-hippocampal-neurons
#20
Pooja Joshi, Martina Gabrielli, Luisa Ponzoni, Silvia Pelucchi, Matteo Stravalaci, Marten Beeg, Sonia Mazzitelli, Daniela Braida, Mariaelvina Sala, Enrica Boda, Annalisa Buffo, Marco Gobbi, Fabrizio Gardoni, Michela Matteoli, Elena Marcello, Claudia Verderio
Fingolimod, also known as FTY720, is an analogue of the sphingolipid sphingosine, which has been proved to be neuroprotective in rodent models of Alzheimer's disease (AD). Several cellular and molecular targets underlying the neuroprotective effects of FTY720 have been recently identified. However, whether the drug directly protects neurons from toxicity of amyloid-beta (Aβ) still remains poorly defined. Using a combination of biochemical assays, live imaging and electrophysiology we demonstrate that FTY720 induces a rapid increase in GLUN2A-containing neuroprotective NMDARs on the surface of dendritic spines in cultured hippocampal neurons...
January 30, 2017: Scientific Reports
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