Log in

Relevant bibliographies by topics / Fingolimod (FTY720) / Journal articles

To see the other types of publications on this topic, follow the link: Fingolimod (FTY720).

Journal articles on the topic 'Fingolimod (FTY720)'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 July 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Fingolimod (FTY720).'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Balasubramaniam, Sivaraman, Ganapathy Sankaran, and Sneh Badle. "Perspective on FTY720, an Immunosuppressant." Synthesis 50, no. 05 (2018): 968–83. http://dx.doi.org/10.1055/s-0036-1591877.

Full text

Abstract:

FTY720 {fingolimod hydrochloride, 2-amino-2-[2-(4-octylphenyl)ethyl]propane-1,3-diol hydrochloride}, a novel immunosuppressant, was discovered by chemical modification based on the structure activity relationships of ISP-I (myriocin), a metabolite of the fungus Isaria sinclairii. This short perspective provides insights to the various strategies available in the literature for the synthesis of FTY720 and its analogues.1 Introduction2 Classification of Immunosuppressive Drugs3 The Rise of FTY7204 Different Synthetic Strategies for FTY7205 Analogues of FTY7206 Binding Studies of FTY7207 Mode of

APA, Harvard, Vancouver, ISO, and other styles

2

Schröder, Matthias, Olga Arlt, Helmut Schmidt, et al. "Subcellular distribution of FTY720 and FTY720-phosphate in immune cells – another aspect of Fingolimod action relevant for therapeutic application." Biological Chemistry 396, no. 6-7 (2015): 795–802. http://dx.doi.org/10.1515/hsz-2014-0287.

Full text

Abstract:

Abstract FTY720 (Fingolimod; Gilenya®) is an immune-modulatory prodrug which, after intracellular phosphorylation by sphingosine kinase 2 (SphK2) and export, mimics effects of the endogenous lipid mediator sphingosine-1-phosphate. Fingolimod has been introduced to treat relapsing-remitting multiple sclerosis. However, little has been published about the immune cell membrane penetration and subcellular distribution of FTY720 and FTY720-P. Thus, we applied a newly established LC-MS/MS method to analyze the subcellular distribution of FTY720 and FTY720-P in subcellular compartments of spleen cell

APA, Harvard, Vancouver, ISO, and other styles

3

Kipp, M., and S. Amor. "FTY720 on the way from the base camp to the summit of the mountain: relevance for remyelination." Multiple Sclerosis Journal 18, no. 3 (2012): 258–63. http://dx.doi.org/10.1177/1352458512438723.

Full text

Abstract:

FTY720 (fingolimod; Gilenya®), a sphingosine 1-phosphate (S1P) receptor modulator, is the first oral disease-modifying therapy to be approved for the treatment of relapsing–remitting multiple sclerosis. FTY720 is rapidly converted in vivo to the active S-fingolimod-phosphate, which binds to S1P receptors. This action inhibits egress of lymphocytes from the lymph nodes, preventing entry into the blood and thus infiltration into the central nervous system. More recent studies, however, convincingly show that FTY720 crosses the blood–brain barrier, where it is thought to act on S1P receptors on c

APA, Harvard, Vancouver, ISO, and other styles

4

Pitman, M. R., J. M. Woodcock, A. F. Lopez, and S. M. Pitson. "Molecular Targets of FTY720 (Fingolimod)." Current Molecular Medicine 12, no. 10 (2012): 1207–19. http://dx.doi.org/10.2174/156652412803833599.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Budde, Klemens, Manuela Schütz, Petra Glander, et al. "FTY720 (fingolimod) in renal transplantation." Clinical Transplantation 20, s17 (2006): 17–24. http://dx.doi.org/10.1111/j.1399-0012.2006.00596.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Ahmed, Naseer, Humaira Achakzai, M. Naveed Anwar, et al. "Role of Fingolimod in Attenuation of LCL to Reduced Apoptosis in Myocardial Ischemia Reperfusion Injury." Pakistan Journal of Medical and Health Sciences 15, no. 11 (2021): 3080–83. http://dx.doi.org/10.53350/pjmhs2115113080.

Full text

Abstract:

Background: FTY720 (Fingolimod) is a drug having immune-regulatory properties. It is a structurally analogous to Sphingosine-1-phosphate. S1P is a biologically active lipid mediator in various inflammatory pathways. Aim: To investigate the effects of FTY720 on myocardial ischemia reperfusion (IR) injury in cardiac surgery. Study design: Experimental study Place and duration of study: Aga Khan University, Karachi and Khyber Medical University, Peshawar Pakistan from 1st January 2017 to 31st December 2020 with collaboration of University of Verona, Italy. Methodology: Twenty Sprague-Dawley rats

APA, Harvard, Vancouver, ISO, and other styles

7

Gandhi, Roopali, and Maria Mazzola. "Immune regulatory effects of Fingolimod (FTY720) on T cells (THER7P.959)." Journal of Immunology 194, no. 1_Supplement (2015): 208.19. http://dx.doi.org/10.4049/jimmunol.194.supp.208.19.

Full text

Abstract:

Abstract FTY720 is the functional analogue of sphingosine and is the first oral treatment for relapsing remitting MS. We investigated the immune regulatory effects of Fingolimod (FTY720) on T cells in Multiple Sclerosis (MS) and controls. FTY720 function by blocking immune cell trafficking and prevents relapses in Multiple Sclerosis. We found that T cells activated in the presence of FTY-720 were less inflammatory with decreased proliferation and cytokines expression. FTY720 treated T cells have decreased expression of granzyme B and induced less neuronal cytotoxicity. We showed, FTY720 treate

APA, Harvard, Vancouver, ISO, and other styles

8

Chun, Jerold, Yasuyuki Kihara, Deepa Jonnalagadda, and Victoria A. Blaho. "Fingolimod: Lessons Learned and New Opportunities for Treating Multiple Sclerosis and Other Disorders." Annual Review of Pharmacology and Toxicology 59, no. 1 (2019): 149–70. http://dx.doi.org/10.1146/annurev-pharmtox-010818-021358.

Full text

Abstract:

Fingolimod (FTY720, Gilenya) was the first US Food and Drug Administration–approved oral therapy for relapsing forms of multiple sclerosis (MS). Research on modified fungal metabolites converged with basic science studies that had identified lysophospholipid (LP) sphingosine 1-phosphate (S1P) receptors, providing mechanistic insights on fingolimod while validating LP receptors as drug targets. Mechanism of action (MOA) studies identified receptor-mediated processes involving the immune system and the central nervous system (CNS). These dual actions represent a more general theme for S1P and li

APA, Harvard, Vancouver, ISO, and other styles

9

Horga, Alejandro, and Xavier Montalban. "FTY720 (fingolimod) for relapsing multiple sclerosis." Expert Review of Neurotherapeutics 8, no. 5 (2008): 699–714. http://dx.doi.org/10.1586/14737175.8.5.699.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Aoki, Masayo, Akatsuki Kondo, Noriko Matsunaga, et al. "The Immunosuppressant Fingolimod (FTY720) for the Treatment of Mechanical Force-Induced Abnormal Scars." Journal of Immunology Research 2020 (January 7, 2020): 1–11. http://dx.doi.org/10.1155/2020/7057195.

Full text

Abstract:

Aim. Abnormal scars such as hypertrophic scars (HSs) and keloids are excessively growing scars that exhibit chronic inflammation and capillary vasculogenesis. The lipid mediator sphingosine-1-phosphate (S1P) is important in inflammatory cell recruitment and angiogenesis. Fingolimod (FTY720) is an analog of S1P and thus functionally antagonizes S1P receptors and inhibits the enzyme that produces S1P. We examined the effects of topical FTY720 injections on mechanical force-induced HS progression. Methods. Mechanical force-induced HSs were generated in C57BL6/J mice by suturing a dorsal incision

APA, Harvard, Vancouver, ISO, and other styles

11

Kalhori, Veronica, Melissa Magnusson, Muhammad Yasir Asghar, Ilari Pulli, and Kid Törnquist. "FTY720 (Fingolimod) attenuates basal and sphingosine-1-phosphate-evoked thyroid cancer cell invasion." Endocrine-Related Cancer 23, no. 5 (2016): 457–68. http://dx.doi.org/10.1530/erc-16-0050.

Full text

Abstract:

The bioactive lipid sphingosine-1-phosphate (S1P) is a potent inducer of ML-1 thyroid cancer cell migration and invasion. It evokes migration and invasion by activating S1P receptor 1 and 3 (S1P1,3) and downstream signaling intermediates as well as through cross-communication with vascular endothelial growth factor receptor 2 (VEGFR2). However, very little is known about the role of S1P receptors in thyroid cancer. Furthermore, the currently used treatments for thyroid cancer have proven to be rather unsuccessful. Thus, due to the insufficiency of the available treatments for thyroid cancer, n

APA, Harvard, Vancouver, ISO, and other styles

12

Saida, T., S. Kikuchi, Y. Itoyama, et al. "A randomized, controlled trial of fingolimod (FTY720) in Japanese patients with multiple sclerosis." Multiple Sclerosis Journal 18, no. 9 (2012): 1269–77. http://dx.doi.org/10.1177/1352458511435984.

Full text

Abstract:

Background: Fingolimod (FTY720) has previously shown clinical efficacy in phase II/III studies of predominantly Caucasian populations with multiple sclerosis (MS). Objectives: To report six-month efficacy and safety outcomes in Japanese patients with relapsing MS treated with fingolimod. Methods: In this double-blind, parallel-group, phase II study, 171 Japanese patients with relapsing MS were randomized to receive once-daily fingolimod 0.5 mg or 1.25 mg, or matching placebo for six months. The primary and secondary endpoints were the percentages of patients free from gadolinium (Gd)-enhanced

APA, Harvard, Vancouver, ISO, and other styles

13

Jones, Amy J., Marcel Kaiser, and Vicky M. Avery. "Identification and Characterization of FTY720 for the Treatment of Human African Trypanosomiasis." Antimicrobial Agents and Chemotherapy 60, no. 3 (2015): 1859–61. http://dx.doi.org/10.1128/aac.02116-15.

Full text

Abstract:

The screening of a focused library identified FTY720 (Fingolimod; Gilenya) as a potent selective antitrypanosomal compound active againstTrypanosoma brucei gambienseandT. brucei rhodesiense, the causative agents of human African trypanosomiasis (HAT). This is the first report of trypanocidal activity for FTY720, an oral drug registered for the treatment of relapsing multiple sclerosis, and the characterization of sphingolipids as a potential new class of compounds for HAT.

APA, Harvard, Vancouver, ISO, and other styles

14

Tackenberg, B., H. Strik, and M. Ocker. "Fingolimod." Nervenheilkunde 30, no. 05 (2011): 345–49. http://dx.doi.org/10.1055/s-0038-1627821.

Full text

Abstract:

ZusammenfassungProzesse der Signaltransduktion (Kommunikation von extra- nach intrazellulär) sind an einer Vielzahl physiologischer und pathologischer Prozesse beteiligt. Durch molekulare Analysen konnten in den vergangenen Jahren verschiedene Moleküle identifiziert werden, die zu neuen Therapiestrategien bei soliden und hämatologischen Tumoren geführt haben. Dieses Verständnis von Signaltransduktionskaskaden führte in vielen Bereichen zur Entwicklung neuer Wirksubstanzen, z. B. Fingolimod (FTY720), das bei der Therapie der Multiplen Sklerose erfolgreich in Phase-III-Studien getestet wurde. Fi

APA, Harvard, Vancouver, ISO, and other styles

15

Comi, G., P. O'Connor, X. Montalban, et al. "Phase II study of oral fingolimod (FTY720) in multiple sclerosis: 3-year results." Multiple Sclerosis Journal 16, no. 2 (2009): 197–207. http://dx.doi.org/10.1177/1352458509357065.

Full text

Abstract:

In a 6-month, placebo-controlled trial, oral fingolimod (FTY720) 1.25 or 5.0 mg, once daily, significantly reduced MRI inflammatory activity and annualized relapse rate compared with placebo in patients with relapsing multiple sclerosis (MS). The objectives were to monitor the 36-month, interim efficacy and safety results of the ongoing extension of this study. In the extension (months 7—36), placebo-treated patients were re-randomized to either dose of fingolimod; fingolimod-treated patients continued at the same dose. During months 15—24, all patients receiving fingolimod 5.0 mg switched to

APA, Harvard, Vancouver, ISO, and other styles

16

Spanu, Alessandra, Hélène E. Aschmann, Jürg Kesselring, and Milo A. Puhan. "Fingolimod versus interferon beta 1-a: Benefit–harm assessment approach based on TRANSFORMS individual patient data." Multiple Sclerosis Journal - Experimental, Translational and Clinical 8, no. 3 (2022): 205521732211177. http://dx.doi.org/10.1177/20552173221117784.

Full text

Abstract:

Background Fingolimod is a disease-modifying drug approved for multiple sclerosis but its benefit–harm balance has never been assessed compared to other active treatments. Objectives Our aim was to compare the benefits and harms of fingolimod with interferon beta-1a using individual patient data from TRial Assessing injectable interferon versus FTY720 Oral in RRMS trial. Methods We modelled the health status of patients over time including Expanded Disability Status Scale measurements, relapses and any adverse events. We assessed the mean health status between arms and the proportion of patien

APA, Harvard, Vancouver, ISO, and other styles

17

Tachibana, Koki, Kohshi Kusumoto, Mai Ogawa, et al. "FTY720 Reduces Lipid Accumulation by Upregulating ABCA1 through Liver X Receptor and Sphingosine Kinase 2 Signaling in Macrophages." International Journal of Molecular Sciences 23, no. 23 (2022): 14617. http://dx.doi.org/10.3390/ijms232314617.

Full text

Abstract:

Formation of foam cells as a result of excess lipid accumulation by macrophages is a pathological hallmark of atherosclerosis. Fingolimod (FTY720) is an immunosuppressive agent used in clinical settings for the treatment of multiple sclerosis and has been reported to inhibit atherosclerotic plaque development. However, little is known about the effect of FTY720 on lipid accumulation leading to foam cell formation. In this study, we investigated the effects of FTY720 on lipid accumulation in murine macrophages. FTY720 treatment reduced lipid droplet formation and increased the expression of ATP

APA, Harvard, Vancouver, ISO, and other styles

18

Min, Ju-Hong, Byoung Joon Kim, and Kwang Ho Lee. "Development of extensive brain lesions following fingolimod (FTY720) treatment in a patient with neuromyelitis optica spectrum disorder." Multiple Sclerosis Journal 18, no. 1 (2011): 113–15. http://dx.doi.org/10.1177/1352458511431973.

Full text

Abstract:

We report the case of a patient who developed extensive brain lesions during fingolimod (FTY720) treatment in the TRANSFORMS study. His initial diagnosis was multiple sclerosis, but after encephalopathy anti-aquaporin4 antibody (anti-AQP4 Ab) was detected, it was changed to neuromyelitis optica spectrum disorder. After treatment with fingolimod, he developed bilateral extensive brain lesions. The brain MRI showed lesions predominantly involving the right frontal and parietal lobes, with vasogenic edema and enhancement. He had residual encephalomalacia and no recurrence with steroid treatment o

APA, Harvard, Vancouver, ISO, and other styles

19

Tan, Botao, Zeruxin Luo, Yan Yue, et al. "Effects of FTY720 (Fingolimod) on Proliferation, Differentiation, and Migration of Brain-Derived Neural Stem Cells." Stem Cells International 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/9671732.

Full text

Abstract:

Insufficient proliferation, differentiation, and migration are the main pitfalls of neural stem cells (NSCs) in reparative therapeutics for the central nervous system (CNS) diseases. The potent lipid mediator sphingosine-1-phosphate (S1P) regulates cells’ biological behavior broadly in the CNS. However, the effects of activating S1P on NSCs are not quite clear. In the current study, FTY720 (Fingolimod), an analog of S1P, was employed to induce the proliferation, differentiation, and migration of cultured brain-derived NSCs. The results indicated that proliferation and migration ability of NSCs

APA, Harvard, Vancouver, ISO, and other styles

20

Mack, Heather Gwen, Melissa Chih-Hui Tien, and Owen Bruce White. "Acute Anterior Uveitis in a Patient Taking Fingolimod (FTY720) for Multiple Sclerosis." Case Reports in Ophthalmology 7, no. 3 (2016): 562–66. http://dx.doi.org/10.1159/000453392.

Full text

Abstract:

Fingolimod is an oral sphingosine-1-phosphate (S1P) receptor modulator and the first oral therapy for relapsing-remitting multiple sclerosis. Its use has been complicated by a low rate of cystoid macular edema usually in the first 3 months after commencement of the medication. We report the case of a 34-year-old male with relapsing-remitting multiple sclerosis, who developed acute anterior uveitis on day 5 of fingolimod treatment. He responded to appropriate treatment and cessation of drug, but developed low-grade chronic anterior uveitis without cystoid macular edema. We discuss possible mech

APA, Harvard, Vancouver, ISO, and other styles

21

Najarzadegan, Niloofar, Mahboobeh Madani, Masoud Etemadifar, and Nahad Sedaghat. "Immunomodulatory drug fingolimod (FTY720) restricts the growth of opportunistic yeast Candida albicans in vitro and in a mouse candidiasis model." PLOS ONE 17, no. 12 (2022): e0278488. http://dx.doi.org/10.1371/journal.pone.0278488.

Full text

Abstract:

Fingolimod (FTY720) is a drug derived from the fungicidal compound myriocin. As it was unclear whether FTY720 has antifungal effects as well, we aimed to characterize its effect on Candida albicans in vitro and in a mouse candidiasis model. First, antifungal susceptibility testing was performed in vitro. Then, a randomized, six-arm, parallel, open-label trial was conducted on 48 mice receiving oral FTY720 (0.3 mg/kg/day), intraperitoneal C. albicans inoculation, or placebo with different combinations and chorological patterns. The outcome measures of the trial included serum concentrations of

APA, Harvard, Vancouver, ISO, and other styles

22

Davis, Carter Thomas, Arati V. Rao, Eross Guadalupe, Dale J. Christensen, and J. Brice Weinberg. "Fingolimod Is Cytotoxic in Acute Myeloid Leukemia Independent of Additional Chemotherapeutic Agents." Blood 128, no. 22 (2016): 5126. http://dx.doi.org/10.1182/blood.v128.22.5126.5126.

Full text

Abstract:

Abstract INTRODUCTION: Conventional treatment of acute myeloid leukemia (AML) remains largely unchanged for over thirty years. With poor overall survival and disease cure rates, novel therapies are needed. The SET oncoprotein has been implicated in AML as essential for proliferation through inhibition of the tumor suppressor protein phosphatase 2A (PP2A). Interaction between SET and PP2A leads to inactivation of PP2A, leaving cell survival and proliferation signals unchecked. PP2A has been postulated to be an important target in AML. Fingolimod (FTY720), an FDA approved drug for relapsing-remi

APA, Harvard, Vancouver, ISO, and other styles

23

Kappos, Ludwig, Jack Antel, Giancarlo Comi, et al. "Oral Fingolimod (FTY720) for Relapsing Multiple Sclerosis." New England Journal of Medicine 355, no. 11 (2006): 1124–40. http://dx.doi.org/10.1056/nejmoa052643.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Delgado, S. "Oral Fingolimod (FTY720) for Relapsing Multiple Sclerosis." Yearbook of Neurology and Neurosurgery 2008 (January 2008): 92–97. http://dx.doi.org/10.1016/s0513-5117(08)79032-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Stockman, J. A. "Oral Fingolimod (FTY720) for Relapsing Multiple Sclerosis." Yearbook of Pediatrics 2008 (January 2008): 366–68. http://dx.doi.org/10.1016/s0084-3954(08)70473-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Zhang, Dong Dong, Bona Linke, Jing Suo, et al. "Antinociceptive effects of FTY720 during trauma-induced neuropathic pain are mediated by spinal S1P receptors." Biological Chemistry 396, no. 6-7 (2015): 783–94. http://dx.doi.org/10.1515/hsz-2014-0276.

Full text

Abstract:

Abstract FTY720 (fingolimod) is, after its phosphorylation by sphingosine kinase (SPHK) 2, a potent, non-selective sphingosine-1-phosphate (S1P) receptor agonist. FTY720 has been shown to reduce the nociceptive behavior in the paclitaxel model for chemotherapy-induced neuropathic pain through downregulation of S1P receptor 1 (S1P1) in microglia of the spinal cord. Here, we investigated the mechanisms underlying the antinociceptive effects of FTY720 in a model for trauma-induced neuropathic pain. We found that intrathecal administration of phosphorylated FTY720 (FTY720-P) decreased trauma-induc

APA, Harvard, Vancouver, ISO, and other styles

27

Swain, Jitendriya, Santosh R. Borkar, Indrapal Singh Aidhen, and Ashok Kumar Mishra. "A molecular level understanding of interaction between FTY720 (Fingolimod hydrochloride) and DMPC multilamellar vesicles." RSC Adv. 4, no. 33 (2014): 17347–53. http://dx.doi.org/10.1039/c4ra02404d.

Full text

Abstract:

This work focuses on the molecular level understanding of interaction between FTY720 (Fingolimod hydrochloride) and dimyristoylphosphatidylcholine (DMPC) multilamellar vesicles (MLVs) as a drug molecule carrier by investigating the structural changes, solubilisation effect and thermotropic phase behaviour.

APA, Harvard, Vancouver, ISO, and other styles

28

Al Alam, Nadine, and Sawsan Ibrahim Kreydiyyeh. "FTY720P inhibits hepatic Na+–K+ ATPase via S1PR2 and PGE2." Biochemistry and Cell Biology 94, no. 4 (2016): 371–77. http://dx.doi.org/10.1139/bcb-2016-0025.

Full text

Abstract:

Sphingosine-1-phosphate (S1P) was found previously to inhibit Na+–K+ ATPase in HepG2 cells. Whether fingolimod (FTY720), a S1P receptor (S1PR) agonist, similarly inhibits the ATPase is a question that needs to be addressed. The aim of this work was to study the effect of FTY720P, the active form of the drug, on the activity of Na+–K+ ATPase in HepG2 cells and determine its mechanism of action. The activity of the ATPase was assayed by measuring the amount of inorganic phosphate liberated in the presence and the absence of ouabain. FTY720-P (7.5 nmol/L, 15 min) significantly reduced the activit

APA, Harvard, Vancouver, ISO, and other styles

29

Gupta, Pankaj, Rosana Michel, David M. Goldenberg, and Chien-Hsing Chang. "Combination Therapy with FTY720 (Fingolimod) and Bispecific Anti-CD20/CD74 Antibodies in Mantle Cell Lymphoma,." Blood 118, no. 21 (2011): 3736. http://dx.doi.org/10.1182/blood.v118.21.3736.3736.

Full text

Abstract:

Abstract Abstract 3736 Introduction: Mantle cell lymphoma (MCL) is one of the most challenging B-cell lymphomas to treat. Although the response rates with first-line conventional or high-dose chemotherapy, with or without stem-cell transplantation, are high, most patients relapse, after which their prognosis is considered poor. Thus, new therapeutic interventions in MCL are needed, among which targeted therapy with a variety of monoclonal antibodies (mAbs), either alone or in combination with other biological agents or drugs, is a major focus of ongoing clinical studies. FTY720 (fingolimod), a

APA, Harvard, Vancouver, ISO, and other styles

30

Chen, Chongwei, Sujing Zong, Zhenyu Wang та ін. "FTY720 Attenuates LPS-Induced Inflammatory Bone Loss by Inhibiting Osteoclastogenesis via the NF-κB and HDAC4/ATF Pathways". Journal of Immunology Research 2023 (6 січня 2023): 1–14. http://dx.doi.org/10.1155/2023/8571649.

Full text

Abstract:

Osteoclast (OC) abnormalities lead to many osteolytic diseases, such as osteoporosis, inflammatory bone erosion, and tumor-induced osteolysis. Exploring effective strategies to remediate OCs dysregulation is essential. FTY720, also known as fingolimod, has been approved for the treatment of multiple sclerosis and has anti-inflammatory and immunosuppressive effects. Here, we found that FTY720 inhibited osteoclastogenesis and OC function by inhibiting nuclear factor kappa-B (NF-κB) signaling. Interestingly, we also found that FTY720 inhibited osteoclastogenesis by upregulating histone deacetylas

APA, Harvard, Vancouver, ISO, and other styles

31

Ahmed, Naseer, Javeria Farooq, Soban Sadiq, et al. "Fingolimod (FTY720) Preserves High Energy Phosphates and Improves Cardiac Function in Heterotopic Heart Transplantation Model." International Journal of Molecular Sciences 21, no. 18 (2020): 6548. http://dx.doi.org/10.3390/ijms21186548.

Full text

Abstract:

During heart transplantation, donor heart leads to reduced oxygen supply resulting in low level of high energy phosphate (HEP) reserves in cardiomyocyte. Lower HEP is one of the underlying reasons of cell death due to ischemia. In this study we investigated the role of Fingolimod (FTY720) in heart transplantation ischemia. Eight groups of Sprague-Dawley rats (n = 5 for each subgroup) were made, A1 and C1 were given FTY720 1 mg/kg while B1 and D1 were given normal saline. The hearts were implanted into another set of similar rats after preservation period of 1 h at 4–8 °C. Significantly higher

APA, Harvard, Vancouver, ISO, and other styles

32

Li, Xiaoli, Hua Guo, and Yaze Du. "Usage of fingolimod combined with polyacetone system in the treatment of mouse kidney transplantation model." Materials Express 12, no. 1 (2022): 64–73. http://dx.doi.org/10.1166/mex.2022.2131.

Full text

Abstract:

A kidney transplantation model was established with mouse subjects, which was treated with the fingolimod (FTY720) combined with polyacetone (PCL) membrane controlled release system to analyze its therapeutic effect on kidney transplantation. 45 C57BL/6 (H-2b) mice were randomly enrolled into 3 groups, 9 in the Sham group did not receive any treatment, 18 in the model group and FTY720-PCL group, with 9 donors and recipients, respectively. The mice in model group were treated with kidney transplantation, and those in the FTY720-PCL group were treated with FTY720-PCL based on the model group. Th

APA, Harvard, Vancouver, ISO, and other styles

33

Hirata, Naoya, Shigeru Yamada, Shota Yanagida, Atsushi Ono, and Yasunari Kanda. "FTY720 Inhibits Expansion of Breast Cancer Stem Cells via PP2A Activation." International Journal of Molecular Sciences 22, no. 14 (2021): 7259. http://dx.doi.org/10.3390/ijms22147259.

Full text

Abstract:

Growing evidence suggests that breast cancer originates from a minor population of cancer cells termed cancer stem cells (CSCs), which can be identified by aldehyde dehydrogenase (ALDH) activity-based flow cytometry analysis. However, novel therapeutic drugs for the eradication of CSCs have not been discovered yet. Recently, drug repositioning, which finds new medical uses from existing drugs, has been expected to facilitate drug discovery. We have previously reported that sphingosine kinase 1 (SphK1) induced proliferation of breast CSCs. In the present study, we focused on the immunosuppressi

APA, Harvard, Vancouver, ISO, and other styles

34

Manley, Paul W., Sandra W. Cowan-Jacob, Robert Cozens, et al. "Fingolimod (FTY720) Inhibits BCR-ABL Signaling Allosterically by Binding to the Myristate Binding Site." Blood 118, no. 21 (2011): 2746. http://dx.doi.org/10.1182/blood.v118.21.2746.2746.

Full text

Abstract:

Abstract Abstract 2746 Background: The tyrosine kinase (TK) activity of the ABL protein is normally tightly regulated, with the N-terminal cap (NCap) region (≈ 80 amino-acid residues) of the SH3 domain playing an important role. One regulatory mechanism involves the NCap Gly-2 residue being myristoylated and then interacting with a myristate binding site within the SH1 catalytic domain. Chronic myeloid leukemia (CML) results from a chromosome translocation leading to expression of the chimeric BCR-ABL oncoprotein, which lacks the NCap and has constitutively active TK activity. Although drugs t

APA, Harvard, Vancouver, ISO, and other styles

35

Luessi, Felix, Stefan Kraus, Bettina Trinschek, et al. "FTY720 (fingolimod) treatment tips the balance towards less immunogenic antigen-presenting cells in patients with multiple sclerosis." Multiple Sclerosis Journal 21, no. 14 (2015): 1811–22. http://dx.doi.org/10.1177/1352458515574895.

Full text

Abstract:

Objective: We aimed to clarify whether fingolimod has direct effects on antigen-presenting cells in multiple sclerosis patients. Methods: Frequency and phenotype of directly ex vivo dendritic cells and monocytes were analyzed in 43 individuals, including fingolimod-treated and untreated multiple sclerosis patients as well as healthy subjects. These cells were further stimulated with lipopolysaccharide to determine functional effects of fingolimod treatment. Results: Absolute numbers of CD1c+ dendritic cells and monocytes were not significantly reduced in fingolimod-treated patients indicating

APA, Harvard, Vancouver, ISO, and other styles

36

Béchet, Sibylle, and Kumlesh K. Dev. "The Effects of the S1P Receptor Agonist Fingolimod (FTY720) on Central and Peripheral Myelin in Twitcher Mice." Biomedicines 12, no. 3 (2024): 594. http://dx.doi.org/10.3390/biomedicines12030594.

Full text

Abstract:

Krabbe’s disease (KD) is caused by mutations in the lysosomal enzyme galactocerebrosidase and is associated with psychosine toxicity. The sphingosine 1-phosphate receptor (S1PR) agonist fingolimod (FTY720) attenuates psychosine-induced cell death of human astrocytes, demyelination in cerebellar slices, as well as demyelination in the central nervous system of twitcher mice. Psychosine also accumulates in the peripheral nervous system in twitcher mice; however, effects of fingolimod on this peripheral myelin have not been examined. The aim of this study was to investigate the effects of fingoli

APA, Harvard, Vancouver, ISO, and other styles

37

Wang, Zifeng, Masahito Kawabori, and Kiyohiro Houkin. "FTY720 (Fingolimod) Ameliorates Brain Injury through Multiple Mechanisms and is a Strong Candidate for Stroke Treatment." Current Medicinal Chemistry 27, no. 18 (2020): 2979–93. http://dx.doi.org/10.2174/0929867326666190308133732.

Full text

Abstract:

FTY720 (Fingolimod) is a known sphingosine-1-phosphate (S1P) receptor agonist that exerts strong anti-inflammatory effects and was approved as the first oral drug for the treatment of multiple sclerosis by the US Food and Drug Administration (FDA) in 2010. FTY720 is mainly associated with unique functional “antagonist” and “agonist” mechanisms. The functional antagonistic mechanism is mediated by the transient down-regulation and degradation of S1P receptors on lymphocytes, which prevents lymphocytes from entering the blood stream from the lymph node. This subsequently results in the developme

APA, Harvard, Vancouver, ISO, and other styles

38

Cartwright, Tara A., Christopher R. Campos, Ronald E. Cannon, and David S. Miller. "Mrp1 is Essential for Sphingolipid Signaling to P-Glycoprotein in Mouse Blood–Brain and Blood–Spinal Cord Barriers." Journal of Cerebral Blood Flow & Metabolism 33, no. 3 (2012): 381–88. http://dx.doi.org/10.1038/jcbfm.2012.174.

Full text

Abstract:

At the blood–brain and blood–spinal cord barriers, P-glycoprotein, an ATP-driven drug efflux pump, is a major obstacle to central nervous system (CNS) pharmacotherapy. Recently, we showed that signaling through tumor necrosis factor-α (TNF-α), sphingolipids, and sphingosine-1-phosphate receptor 1 (S1PR1) rapidly and reversibly reduced basal P-glycoprotein transport activity in the rat blood–brain barrier. The present study extends those findings to the mouse blood–brain and blood–spinal cord barriers and, importantly, identifies multidrug resistance-associated protein 1 (Mrp1, Abcc1) as the tr

APA, Harvard, Vancouver, ISO, and other styles

39

Montalban, X., G. Comi, P. O’Connor, et al. "Oral fingolimod (FTY720) in relapsing multiple sclerosis: impact on health-related quality of life in a phase II study." Multiple Sclerosis Journal 17, no. 11 (2011): 1341–50. http://dx.doi.org/10.1177/1352458511411061.

Full text

Abstract:

Background: Health-related quality of life (HRQoL) worsens with multiple sclerosis (MS) relapses and disease progression. Common symptoms including depression and fatigue may contribute to poor HRQoL. Objectives: To report exploratory analyses assessing the impact of fingolimod (FTY720) on HRQoL and depression in a phase II study of relapsing MS. Methods: The Hamburg Quality of Life Questionnaire in MS (HAQUAMS) and Beck Depression Inventory second edition (BDI-II) scores were assessed during a 6-month, placebo-controlled study and optional extension. Results: HAQUAMS total score improved with

APA, Harvard, Vancouver, ISO, and other styles

40

Takasaki, Teruaki, Kanako Hagihara, Ryosuke Satoh, and Reiko Sugiura. "More than Just an Immunosuppressant: The Emerging Role of FTY720 as a Novel Inducer of ROS and Apoptosis." Oxidative Medicine and Cellular Longevity 2018 (March 28, 2018): 1–13. http://dx.doi.org/10.1155/2018/4397159.

Full text

Abstract:

Fingolimod hydrochloride (FTY720) is a first-in-class of sphingosine-1-phosphate (S1P) receptor modulator approved to treat multiple sclerosis by its phosphorylated form (FTY720-P). Recently, a novel role of FTY720 as a potential anticancer drug has emerged. One of the anticancer mechanisms of FTY720 involves the induction of reactive oxygen species (ROS) and subsequent apoptosis, which is largely independent of its property as an S1P modulator. ROS have been considered as a double-edged sword in tumor initiation/progression. Intriguingly, prooxidant therapies have attracted much attention due

APA, Harvard, Vancouver, ISO, and other styles

41

Haghikia, Aiden, and Ralf Gold. "The Impact of Fingolimod (FTY720) in Neuroimmunologic Diseases." American Journal of Pathology 176, no. 6 (2010): 2599–601. http://dx.doi.org/10.2353/ajpath.2010.100200.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Klatt, J., H. P. Hartung, and R. Hohlfeld. "FTY720 (Fingolimod) als neue Therapiemöglichkeit der Multiplen Sklerose." Der Nervenarzt 78, no. 10 (2007): 1200–1208. http://dx.doi.org/10.1007/s00115-007-2298-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Miron, Veronique E., Anna Schubart, and Jack P. Antel. "Central nervous system-directed effects of FTY720 (fingolimod)." Journal of the Neurological Sciences 274, no. 1-2 (2008): 13–17. http://dx.doi.org/10.1016/j.jns.2008.06.031.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Pinki and Vijay Thawani. "Fingolimod (Gileyna, FTY720): Innovative treatment for multiple sclerosis." Journal of Pharmacology and Pharmacotherapeutics 2, no. 3 (2011): 207. http://dx.doi.org/10.4103/0976-500x.83296.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Oh, Yoon Sin, Taeho Lee, Sang Mi Shin, et al. "Synthesis of FTY720 (Fingolimod) Derivatives Containing Serine Structure." Bulletin of the Korean Chemical Society 39, no. 2 (2018): 261–64. http://dx.doi.org/10.1002/bkcs.11370.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Shi, Zu-an, Ting-ting Li, Dao-ling Kang, Hang Su, and Fa-ping Tu. "Fingolimod attenuates renal ischemia/reperfusion-induced acute lung injury by inhibiting inflammation and apoptosis and modulating S1P metabolism." Journal of International Medical Research 49, no. 8 (2021): 030006052110328. http://dx.doi.org/10.1177/03000605211032806.

Full text

Abstract:

Objective This study examined whether the immunomodulator fingolimod (FTY720) could alleviate renal ischemia/reperfusion (I/R)-induced lung injury and explored the potential mechanisms. Methods Renal I/R was established in a rat model, and FTY720 (0.5, 1, or 2 mg/kg) was injected intraperitoneally after 15 minutes of ischemia. Pro-inflammatory cytokine levels, oxidative stress, apoptosis, and the mRNA expression of the sphingosine-1-phosphate (S1P)-related signaling pathway genes sphingosine kinase-1 (SphK1) and sphingosine kinase-2 were analyzed in lung tissue. Results Increased pro-inflammat

APA, Harvard, Vancouver, ISO, and other styles

47

LeBlanc, Francis Roland, Hong-Gang Wang, David J. Feith, and Thomas P. Loughran. "FTY720 (Fingolimod) Targets the Sphingolipid Pathway and Induces Autophagy-Related Apoptosis in Human Natural Killer Large Granular Lymphocyte Leukemia." Blood 126, no. 23 (2015): 1288. http://dx.doi.org/10.1182/blood.v126.23.1288.1288.

Full text

Abstract:

Abstract Introduction: Natural killer large granular lymphocytic leukemia (NK-LGL) and chronic lymphoproliferative disorder of NK cells (CLPD-NK) are rare disorders of cytotoxic CD3-/CD56+ natural killer cells. Aggressive NK-LGL leukemia patients present with a malignant clinical course and a fatal outcome with median survival time of two months from diagnosis. Aggressive NK-LGL is refractory to conventional chemotherapy and pathogenetic mechanisms remain undefined. The 'sphingolipid rheostat' has been identified as a key player in determining cell fate. The balance between pro-apoptotic ceram

APA, Harvard, Vancouver, ISO, and other styles

48

Oaks, Joshua J., Ramasamy Santhanam, Christopher J. Walker, et al. "Antagonistic activities of the immunomodulator and PP2A-activating drug FTY720 (Fingolimod, Gilenya) in Jak2-driven hematologic malignancies." Blood 122, no. 11 (2013): 1923–34. http://dx.doi.org/10.1182/blood-2013-03-492181.

Full text

Abstract:

Key Points The tumor suppressor PP2A is repressed in Jak2V617F-driven myleoproliferative neoplasms by a Jak2/PI3K/PKC/SET signaling pathway. PP2A-activating (eg, FTY720, OSU-2S) but not sphingosine-1-phosphate agonistic (eg, FTY720-P) drugs selectively kill Jak2V617F+ cells.

APA, Harvard, Vancouver, ISO, and other styles

49

Kiyota, Miki, Junya Kuroda, Mio Yamamoto-Sugitani, et al. "Fingolimod (FTY720) Overcomes the Resistance to Tyrosine Kinase Inhibitors Via Dual Activation of BIM and BID in Chronic Myelogenous Leukemia." Blood 120, no. 21 (2012): 3744. http://dx.doi.org/10.1182/blood.v120.21.3744.3744.

Full text

Abstract:

Abstract Abstract 3744 [Introduction] Tyrosine kinase inhibitors (TKIs) for BCR-ABL have dramatically improved the treatment outcome of chronic myelogenous leukemia (CML) during this decade, however, the resistance to TKIs due to various molecular mechanisms, such as BCR-ABL mutations, dysfunction of cell killing mechanisms like BIM deregulation, or the supports by leukemia microenvironment factors, has remained to be overcome. We have identified that BIM, a member of BH3-only proteins, is the essential pro-apoptotic mediator under the blockade of BCR-ABL signaling (Kuroda J, PNAS, 2006). One

APA, Harvard, Vancouver, ISO, and other styles

50

Chang, Wei-Ting, Ping-Yen Liu, and Sheng-Nan Wu. "Actions of FTY720 (Fingolimod), a Sphingosine-1-Phosphate Receptor Modulator, on Delayed-Rectifier K+ Current and Intermediate-Conductance Ca2+-Activated K+ Channel in Jurkat T-Lymphocytes." Molecules 25, no. 19 (2020): 4525. http://dx.doi.org/10.3390/molecules25194525.

Full text

Abstract:

FTY720 (fingolimod), a modulator of sphingosine-1-phosphate receptors, is known to produce the immunomodulatory actions and to be beneficial for treating the relapsing multiple sclerosis. However, whether it exerts any effects on membrane ion currents in immune cells remains largely unknown. Herein, the effects of FTY720 on ionic currents in Jurkat T-lymphocytes were investigated. Cell exposure to FTY720 suppressed the amplitude of delayed-rectifier K+ current (IK(DR)) in a time- and concentration-dependent manner with an IC50 value of 1.51 μM. Increasing the FTY720 concentration not only decr

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!