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Статті в журналах з теми "Fingolimod hydrochloride"

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Автор: Grafiati

Опубліковано: 22 червня 2024

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1

Kaduk, James A., Kai Zhong, Amy M. Gindhart, and Thomas N. Blanton. "Crystal structure of fingolimod hydrochloride, C19H34ClNO2." Powder Diffraction 30, no. 3 (August 12, 2015): 205–10. http://dx.doi.org/10.1017/s0885715615000317.

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The crystal structure of fingolimod hydrochloride (C19H34ClNO2) has been solved and refined using synchrotron X-ray powder diffraction data, and optimized using density functional techniques. Fingolimod hydrochloride crystallizes in space group P21/n (#14) with a = 7.137 53(5), b = 5.957 98(4), c = 49.5196(4) Å, β = 91.0808(7)°, V = 2105.46(2) Å3, and Z = 4. The structure consists of a “lipid bilayer” packing. The polar ends of the molecules make O–H···Cl and N–H···Cl hydrogen bonds to the chloride anion, and the octyl side chains pack adjacent to each other. The hydrogen bonds form three types of chains with graph sets C1,2(7), C1,2(7), and C1,2(8). The result is a complex chain of hydrogen bonds parallel to the b-axis. The powder pattern has been submitted to ICDD for inclusion in future releases of the Powder Diffraction File™.

2

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.

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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.

3

Ganhadeiro, Flaviane Maximino Bitencourt, Carla Resende Vaz Oliveira, and Bruno Cezario Costa Reis. "O benefício do uso de fingolimode em pacientes portadores de Esclerose Múltipla." Revista Eletrônica Acervo Médico 23, no. 4 (April 15, 2023): e12504. http://dx.doi.org/10.25248/reamed.e12504.2023.

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Objetivo: Avaliar os benefícios do uso de Fingolimode no tratamento do Esclerose Múltipla de acordo com cada faixa etária. Métodos: A parte metodológica é formada pelo National Library of Medicine, Biblioteca Virtual em Saúde e Directory of Open Access Journals que foram as bases de dados usadas para formar o compilado bibliográfico dessa revisão de literatura. Os descritores utilizados foram “Multiple Sclerosis”, “Drug Therapy” e “Fingolimod Hydrochloride”. Os critérios de inclusão foram artigos de ensaios clínicos, randomizados ou não randomizados, estudos de caso-controle, estudo de coorte, livre acesso, publicados em inglês, português, espanhol e no intervalo de 2018 a 2023. Resultados: Dos cinco artigos selecionados, foi relatado a redução das recidivas com o uso do Fingolimode, a melhor eficácia sustentada a longo prazo, melhor resultado no tratamento de pacientes afro-americanos com EM quando comparados aos outros e também que foi encontrado maior custo-efetividade no tratamento com Fingolimode quando comparado aos outros medicamentos. Considerações finais: Dessa forma, com o uso do Fingolimode relatam a redução das recidivas e também apresenta melhor eficácia sustentada a longo prazo. Além disso, a idade média abordada para esse tratamento é 37,5 anos.

4

Balasubramaniam, Sivaraman, Ganapathy Sankaran, and Sneh Badle. "Perspective on FTY720, an Immunosuppressant." Synthesis 50, no. 05 (January 24, 2018): 968–83. http://dx.doi.org/10.1055/s-0036-1591877.

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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 Action8 Conclusion

5

Hussar, Daniel A., and David E. Zimmerman. "New drugs: Dabigatran etexilate mesylate, fingolimod hydrochloride, and ulipristal acetate." Journal of the American Pharmacists Association 51, no. 1 (January 2011): 122–26. http://dx.doi.org/10.1331/japha.2011.11506.

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6

Vinigari, Krishna, Krishna Jonnada, Noorjahan Mohammed, and Girija Mangatayaru Kotu. "An alternative efficient approach for the synthesis of Fingolimod hydrochloride." Synthetic Communications 49, no. 1 (January 2, 2019): 39–48. http://dx.doi.org/10.1080/00397911.2018.1536788.

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7

Thomas, Katja, Undine Proschmann, and Tjalf Ziemssen. "Fingolimod hydrochloride for the treatment of relapsing remitting multiple sclerosis." Expert Opinion on Pharmacotherapy 18, no. 15 (September 4, 2017): 1649–60. http://dx.doi.org/10.1080/14656566.2017.1373093.

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8

Ward, Melanie D., David E. Jones, and Myla D. Goldman. "Overview and safety of fingolimod hydrochloride use in patients with multiple sclerosis." Expert Opinion on Drug Safety 13, no. 7 (June 16, 2014): 989–98. http://dx.doi.org/10.1517/14740338.2014.920820.

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9

Tamakuwala, Mayurkumar, Warren Ratna, Amit Joshi, and Grazia Stagni. "Fingolimod hydrochloride gel shows promising therapeutic effects in a mouse model of atopic dermatitis." Journal of Pharmacy and Pharmacology 68, no. 10 (July 27, 2016): 1268–77. http://dx.doi.org/10.1111/jphp.12588.

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10

Suresh Kumar, Ramdoss, Hariram Balasubramanian, Kalyanaraman Lakshminarayanan, Srinivasu K. Mullapudi, Katkam Srinivas, and Rajeswar Reddy Sagyam. "A systematic approach for reversed phase liquid chromatographic method development of fingolimod hydrochloride via design augmentation." Arabian Journal of Chemistry 12, no. 8 (December 2019): 3289–301. http://dx.doi.org/10.1016/j.arabjc.2015.08.012.

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11

Wang, Jian-Rong, Sha Li, Bingqing Zhu, and Xuefeng Mei. "Insight into the conformational polymorph transformation of a block-buster multiple sclerosis drug fingolimod hydrochloride (FTY 720)." Journal of Pharmaceutical and Biomedical Analysis 109 (May 2015): 45–51. http://dx.doi.org/10.1016/j.jpba.2015.02.018.

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12

Chiba, Kenji, and Narihiko Yoshii. "Pharmacological properties and clinical efficacy of fingolimod hydrochloride (Imusera^|^reg;/Gilenya^|^reg;) for the treatment of multiple sclerosis." Folia Pharmacologica Japonica 139, no. 6 (2012): 265–74. http://dx.doi.org/10.1254/fpj.139.265.

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13

Swain, Jitendriya, Monalisa Mohapatra, Santosh R. Borkar, Indrapal Singh Aidhen, and Ashok Kumar Mishra. "Study of aqueous phase aggregation of FTY720 (fingolimod hydrochloride) and its effect on DMPC liposomes using fluorescent molecular probes." Physical Chemistry Chemical Physics 15, no. 41 (2013): 17962. http://dx.doi.org/10.1039/c3cp53148a.

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14

Tamakuwala, M., and G. Stagni. "Fingolimod Hydrochloride Gel for Dermatological Applications: Optimization of Formulation Strength and Effect of Colloidal Oatmeal (Aveeno®) as Penetration Enhancer." AAPS PharmSciTech 17, no. 4 (September 29, 2015): 907–14. http://dx.doi.org/10.1208/s12249-015-0415-9.

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15

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.

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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 to its efficacy in cancer treatment. These strategies include diverse chemotherapeutic agents and molecular targeted drugs such as sulfasalazine which inhibits the CD44v-xCT (cystine transporter) axis. In this review, we introduce our recent discoveries using a chemical genomics approach to uncover a signaling network relevant to FTY720-mediated ROS signaling and apoptosis, thereby proposing new potential targets for combination therapy as a means to enhance the antitumor efficacy of FTY720 as a ROS generator. We extend our knowledge by summarizing various measures targeting the vulnerability of cancer cells’ defense mechanisms against oxidative stress. Future directions that may lead to the best use of FTY720 and ROS-targeted strategies as a promising cancer treatment are also discussed.

16

Rajan, N., and K. Anver Basha. "Rapid Determination of Fingolimod Hydrochloride-Related Substances and Degradation Products in API and Pharmaceutical Dosage Forms by Use of a Stability-Indicating UPLC Method." Chromatographia 77, no. 21-22 (October 15, 2014): 1545–52. http://dx.doi.org/10.1007/s10337-014-2751-4.

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17

Ostroumova, O. D., M. S. Cherniaeva, D. I. Bakhteeva, N. A. Arablinskiy, and D. A. Sychyov. "Some groups of drugs which use is associated with development of drug-induced atrial fibrillation." Medical alphabet 1, no. 11 (June 15, 2021): 20–28. http://dx.doi.org/10.33667/2078-5631-2021-11-20-28.

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Recently, more and more attention has been paid to the problem of drug‑induced (DI) atrial fibrillation (AF). It is known that the development of DI AF can be associated with the intake of cardiovascular and anticancer drugs, drugs that affect the central nervous system or respiratory organs. However, there are other drugs that can provoke DI AF, which practitioners are less aware of. This article is a review of the current literature on DI AF associated with the intake of other groups of drugs and individual drugs that are not included in the above groups. Analysis of the available literature has shown that the incidence of DI AF reaches 6.9% when taking zoledronic acid and 1.5% when taking alendronate, although data from different authors regarding the causal relationship between bisphosphonate therapy and the development of AF are ambiguous. The use of high doses of glucocorticosteroids (at a daily dose of ≥ 7.5 mg in terms of prednisolone) is also associated with an increased risk of AF (OR = 6.07; 95% CI: 3.90–9.42). Treatment with non‑steroidal anti‑inflammatory drugs is also associated with a higher risk of developing DI AF compared to those who do not use it – the incidence rate is 1.17 (95% CI: 1.10–1.24) for nonselective and 1.27 (95% CI: 1.20–1.34) for cyclooxygenase‑2 inhibitors. The literature contains a description of clinical cases of DI AF while taking immunosuppressants (azathioprine, methotrexate + etanercept, fingolimod, cyclosporine), drugs that affect the genitourinary system (vardenafil, sildenafil, yohimbine hydrochloride, hexoprenaline), local anesthetics, bupacaero testosterone, stanozolol, testosterone cypionate, nandrolone decanoate extraboline) and nicotine‑containing products (nicotine‑containing chewing gum).

18

Buylova, I. A., N. G. Sakhno, G. M. Bulgakova, and O. V. Gunar. "ELIMINATION OF FALSE RESULTS OF MEDICINES MICROBIOLOGICAL TESTING." Bulletin of the Scientific Centre for Expert Evaluation of Medicinal Products 8, no. 3 (September 26, 2018): 187–92. http://dx.doi.org/10.30895/1991-2919-2018-8-3-187-192.

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The validity of medicines microbial quality testing relies on the adequacy of the test procedure employed. The aim of the study was to analyse factors triggering false results during microbial quality testing of non-sterile medicinal products, as well as to find ways of their elimination. Materials and methods: the study was focused on non-sterile medicinal products tested for microbial quality: N-methylglucamine, L-Malic acid, Xeroform, Fingolimod hydrochloride, Succinic acid, Streptocide, Aripiprazole, Doxazosin, Clopidogrel, Moxonidine, Tilorone, Mycophenolic acid, Folic acid, Gabapentin, Dutasteride, Imatinib, Temozolomide. The study involved the use of the following test strains: Bacillus subtilis, Bacillus cereus, Candida albicans, Escherichia coli, Aspergillus brasiliensis, as well as of reagents and growth media. The methods used were determination of antimicrobial activity under conditions of microbial quality testing, and modified in-depth testing of microbial quality of medicinal products according to the requirements of the State Pharmacopoeia of the Russian Federation, 13th edition. Results: the analysis of literature sources helped reveal the main factors causing false results of microbiological testing and determine ways of their elimination. The article sets forth the results of experimental comparison of two ways of sample preparation for solid formulations: the standard one described in the State Pharmacopoeia of the Russian Federation, 13th edition, and the one involving the use of a laboratory shaker. The article provides experimental data on specific aspects of elimination of antimicrobial activity against B. subtilis and B. cereus and the use of specific inactivators for particular medicinal products. Conclusions: a set of measures aimed at prevention of false-positive and false-negative testing results should include: sterility control of the growth media and reagents used, monitoring of facilities; control of growth promotion properties and selectivity of the growth media; selection of adequate incubation conditions and inoculation procedure with due regard to the dosage form; justification of the amount of sample, diluents and dilution factor used; consideration of the antimicrobial activity of a medicinal product.

19

"New drugs: Fingolimod hydrochloride." Australian Prescriber 34, no. 5 (October 1, 2011): 153–59. http://dx.doi.org/10.18773/austprescr.2011.081.

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20

Hussain, Afzal, Ashfaq Hussain, and Chandan Kumar Verma. "COVID-19 infection: A review of summarized Clinical trials study for the treatment." Coronaviruses 01 (September 25, 2020). http://dx.doi.org/10.2174/2666796701999200925204309.

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Background: Coronavirus Disease 2019 (COVID-19) is a widely infectious and pathogenic viral infection due to Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) that has arisen in Wuhan, China, and spread throughout the world. Coronavirus is indeed an enveloped RNA virus of the genus Betacoronavirus, which is transmitted to birds, humans as well as other mammals. The fastest human to human transition has been generally established. On July 19, 2020, WHO has been reported total confirmed cases: 1,40, 43,176, total confirmed new cases: 1,66,735, total deaths: 5,97,583, total new deaths: 4,496 globally. Material & Methods: In this review, the Clinical trial database is analyzed and systematically summarized drugs which are in the recruiting phase and the completion phase of the clinical trial. Results: Total 383 clinical trials are listed, involving more than 350 medicines such as Deferoxamine, Favipiravir, DAS181, Tocilizumab Injection, Sarilumab, Placebo, Sildenafil citrate tablets, Sargramostim, Lopinavir/ritonavir, Remdesivir, Bevacizumab, Tetrandrine, Fingolimod, Methylprednisolone, Plaquenil, Tocilizumab, Hydroxychloroquine, Abidol hydrochloride, Bevacizumab Injection, Methylprednisolone, Amoxicillin-clavulanate, Moxifloxacin, Sarilumab, Darunavir, and Cobicistat, etc. Conclusion: There is no commercially authorized antiviral treatment or vaccine suitable for use against COVID-19. However, Clinical trials represent an effective approach because they facilitate the development of new types of pharmaceutical drugs.

21

Ye, Min, Yongkang Gai, Hao Ji, Yaqun Jiang, Pengxin Qiao, Wenxia Wang, Yongxue Zhang, Xiaotian Xia, and Xiaoli Lan. "A Novel Radioimmune 99mTc-Labeled Tracer for Imaging Sphingosine 1-Phosphate Receptor 1 in Tumor Xenografts: An In Vitro and In Vivo Study." Frontiers in Immunology 12 (August 18, 2021). http://dx.doi.org/10.3389/fimmu.2021.660842.

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Sphingosine-1-phosphate (S1P) is a phospholipid that regulates pleiotropic biological activities and exerts extracellular functions by binding to five specific G-protein-coupled receptors, S1P receptors (S1PR) 1–5. When activated by S1P, S1PR promote the proliferation and invasion of tumor cells by inducing the formation of new blood vessels. We developed and assessed a new monoclonal antibody imaging probe 99mTc-HYNIC-S1PR1mAb, to explore the feasibility of targeting the S1PR1 in vitro and in vivo. S1PR1mAb was prepared and followed by technetium-99m labeling with succinimidyl 6-hydraziniumnicotinate hydrochloride. Cell uptake and blocking studies were performed to investigate the binding specificity of 99mTc-HYNIC-S1PR1mAb in vitro. 99mTc-HYNIC-S1P1mAb was also tested in vivo in mice xenografted with SK-HEP-1 (high-expression of S1PR1) and MCF-7 (low-expression of S1PR1) using single-photon emission-computed tomography (SPECT). Ex vivo gamma counting of tissues from tumor-bearing mice was used to evaluate 99mTc-HYNIC-S1PR1mAb biodistribution. The biodistribution study results showed significantly higher uptake in SK-HEP-1 tumors than in MCF-7 tumors (P < 0.001). Reduced uptake of 99mTc-HYNIC-S1PR1mAb in SK-HEP-1 was observed in tumor-bearing nude mice pretreated with fingolimod, which binds competitively to the receptors, especially S1PR1. 99mTc-HYNIC-S1PR1mAb can be synthesized and specifically targeted to S1PR1 in vitro and in vivo, allowing S1PR1 expression assessment with SPECT imaging.