Artículos de revistas: "Pranlukast"

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&NA;. "Pranlukast". Reactions Weekly &NA;, n.º 695 (abril de 1998): 11. http://dx.doi.org/10.2165/00128415-199806950-00038.

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&NA;. "Pranlukast". Reactions Weekly &NA;, n.º 743 (marzo de 1999): 11–12. http://dx.doi.org/10.2165/00128415-199907430-00034.

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3

&NA;. "Pranlukast". Reactions Weekly &NA;, n.º 747 (abril de 1999): 10. http://dx.doi.org/10.2165/00128415-199907470-00030.

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4

&NA;. "Pranlukast". Reactions Weekly &NA;, n.º 1138 (febrero de 2007): 23. http://dx.doi.org/10.2165/00128415-200711380-00068.

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5

Keam, Susan J., Katherine A. Lyseng-Williamson y Karen L. Goa. "Pranlukast". Drugs 63, n.º 10 (2003): 991–1019. http://dx.doi.org/10.2165/00003495-200363100-00005.

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6

&NA;. "Pranlukast". Reactions Weekly &NA;, n.º 865 (agosto de 2001): 11. http://dx.doi.org/10.2165/00128415-200108650-00032.

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7

&NA;. "Pranlukast". Reactions Weekly &NA;, n.º 876 (noviembre de 2001): 10. http://dx.doi.org/10.2165/00128415-200108760-00032.

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8

&NA;. "Pranlukast". Reactions Weekly &NA;, n.º 987 (febrero de 2004): 13. http://dx.doi.org/10.2165/00128415-200409870-00039.

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9

Kubota, Jun, Sho Takahashi, Takayuki Suzuki, Akira Ito, Naoe Akiyama y Noriko Takahata. "Pranlukast treatment and the use of respiratory support in infants with respiratory syncytial virus infection". PLOS ONE 17, n.º 5 (27 de mayo de 2022): e0269043. http://dx.doi.org/10.1371/journal.pone.0269043.

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Background In infants, respiratory syncytial virus (RSV) infection occasionally causes severe symptoms requiring respiratory support; however, supportive care is the primary treatment. This study compared the use of respiratory support among infants with RSV infection treated with or without pranlukast. Methods This retrospective cohort study included infants aged <10 months with RSV infection who were admitted to three secondary level hospitals in Japan between 2012 and 2019. The infants were divided into two groups depending on whether they were treated with pranlukast. The primary outcome was the receiving respiratory support (high-flow nasal cannula, nasal continuous positive airway pressure, or ventilator). The secondary outcomes were the length of hospital stay, and the Global Respiratory Severity Score (GRSS) on starting respiratory support or at the time of the worst signs during hospitalization. We performed a propensity score-matched analysis. Results A total of 492 infants, including 147 propensity score-matched pairs, were included in the analysis. The use of respiratory support was significantly lower in infants treated with pranlukast (3.4% [5/147]) than those treated without pranlukast (11.6% [17/147]; P = 0.01). In the propensity score-matched analysis, pranlukast use was associated with a significantly lower chance of needing respiratory support (odds ratio: 0.27, 95% confidence interval: 0.08–0.79; P = 0.01); however, the length of hospital stay (median: 4 days) and the GRSS (median: 2.804 and 2.869 for infants treated with and without pranlukast, respectively) did not differ significantly between propensity score-matched pairs. Conclusions Pranlukast use was associated with a reduced likelihood of requiring respiratory support in infants aged <10 months with RSV infection.

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10

Figueroa, Eric E., Meghan Kramer, Kevin Strange y Jerod S. Denton. "CysLT1 receptor antagonists pranlukast and zafirlukast inhibit LRRC8-mediated volume regulated anion channels independently of the receptor". American Journal of Physiology-Cell Physiology 317, n.º 4 (1 de octubre de 2019): C857—C866. http://dx.doi.org/10.1152/ajpcell.00281.2019.

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Volume-regulated anion channels (VRACs) encoded by the leucine-rich repeat containing 8 ( LRRC8) gene family play critical roles in myriad cellular processes and might represent druggable targets. The dearth of pharmacological compounds available for studying VRAC physiology led us to perform a high-throughput screen of 1,184 of US Food and Drug Administration-approved drugs for novel VRAC modulators. We discovered the cysteinyl leukotriene receptor 1 (CysLT1R) antagonist, pranlukast, as a novel inhibitor of endogenous VRAC expressed in human embryonic kidney 293 (HEK293) cells. Pranlukast inhibits VRAC voltage-independently, reversibly, and dose-dependently with a maximal efficacy of only ~50%. The CysLT1R pathway has been implicated in activation of VRAC in other cell types, prompting us to test whether pranlukast requires the CysLT1R for inhibition of VRAC. Quantitative PCR analysis demonstrated that CYSLTR1 mRNA is virtually undetectable in HEK293 cells. Furthermore, the CysLT1R agonist leukotriene D4 had no effect on VRAC activity and failed to stimulate Gq-coupled receptor signaling. Heterologous expression of the CysLT1R reconstituted LTD4-CysLT1R- Gq-calcium signaling in HEK293 cells but had no effect on VRAC inhibition by pranlukast. Finally, we show the CysLT1R antagonist zafirlukast inhibits VRAC with an IC50 of ~17 µM and does so with full efficacy. Our data suggest that both pranlukast and zafirlukast are likely direct channel inhibitors that work independently of the CysLT1R. This study provides clarifying insights into the putative role of leukotriene signaling in modulation of VRAC and identifies two new chemical scaffolds that can be used for development of more potent and specific VRAC inhibitors.

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11

Kim, Seo W., Hunam Kim, Yon J. Ryu, Jin H. Lee, Sung S. Shim, Yoo K. Kim y Jung H. Chang. "Efficacy and Safety of Modified Pranlukast (Prakanon®) Compared with Pranlukast (Onon®): A Randomized, Open-Label, Crossover Study". Open Respiratory Medicine Journal 10, n.º 1 (30 de junio de 2016): 36–45. http://dx.doi.org/10.2174/1874306401610010036.

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Introduction: Pranlukast is a leukotriene receptor antagonist (LTRA) that is used as an additional controller of mild to moderate asthma. This study compared the efficacy and side effects of two bioequivalent preparations of pranlukast: original pranlukast (Onon®; Ono Pharmaceutical, Japan) and a modified formulation of pranlukast (Prakanon®; Yuhan Co, Korea) in patients with mild to moderate asthma. Methods: Of the 34 subjects screened, 30 patients who were using standard medication to control asthma and scored less than 20 points on the Asthma Control Test™ (ACT) were assigned randomly to one of the two groups in a prospective, open label, crossover study: group 1 received Prakanon® (150 mg/day) and group 2 received Onon® (450 mg/day) for 8 weeks each; after a 1-week rest period, the groups were switched to the alternative medication for further 8 weeks and monitored for 2 more weeks without study medication. Evaluation parameters included the ACT, quality of life questionnaire adult Korean asthmatics (QLQAKA), pulmonary function tests, peripheral blood tests, vital signs, and adverse events. Results: Thirty patients were enrolled and 21 completed the trial: 10 in group 1 and 11 in group 2. The baseline data of the two groups did not differ. No statistical significant differences were observed in efficacy and lung function at each time and in changes from baseline value between the two kinds of pranlukast. The final asthma control rate was 81% with Prakanon® and 76% with Onon®. There were no differences in vital signs and laboratory data at each time and in changes from baseline value between the two drugs. There were no differences in adverse events between the two drugs. The most common side effect was abdominal pain. Drug compliance was high, without differences between the two drugs. Conclusion: These findings suggest that Prakanon® which is an improved formulation of pranlukast at a lower dose than the original formulation, Onon®, has a similar efficacy and side effect profile in the control of persistent asthma.

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12

&NA;. "Montelukast/pranlukast/zafirlukast". Reactions Weekly &NA;, n.º 967 (septiembre de 2003): 12. http://dx.doi.org/10.2165/00128415-200309670-00040.

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13

Yelamanchi, Soujanya D., Sumaithangi Thattai Arun Kumar, Archita Mishra, Thottethodi Subrahmanya Keshava Prasad y Avadhesha Surolia. "Metabolite Dysregulation by Pranlukast in Mycobacterium tuberculosis". Molecules 27, n.º 5 (24 de febrero de 2022): 1520. http://dx.doi.org/10.3390/molecules27051520.

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Mycobacterium tuberculosis has been infecting millions of people worldwide over the years, causing tuberculosis. Drugs targeting distinct cellular mechanisms including synthesis of the cell wall, lipids, proteins, and nucleic acids in Mtb are currently being used for the treatment of TB. Although extensive research is being carried out at the molecular level in the infected host and pathogen, the identification of suitable drug targets and drugs remains under explored. Pranlukast, an allosteric inhibitor of MtArgJ (Mtb ornithine acetyltransferase) has previously been shown to inhibit the survival and virulence of Mtb. The main objective of this study was to identify the altered metabolic pathways and biological processes associated with the differentially expressed metabolites by PRK in Mtb. Here in this study, metabolomics was carried out using an LC-MS/MS-based approach. Collectively, 50 metabolites were identified to be differentially expressed with a significant p-value through a global metabolomic approach using a high-resolution mass spectrometer. Metabolites downstream of argJ were downregulated in the arginine biosynthetic pathway following pranlukast treatment. Predicted human protein interactors of pranlukast-treated Mtb metabolome were identified in association with autophagy, inflammation, DNA repair, and other immune-related processes. Further metabolites including N-acetylglutamate, argininosuccinate, L-arginine, succinate, ergothioneine, and L-phenylalanine were validated by multiple reaction monitoring, a targeted mass spectrometry-based metabolomic approach. This study facilitates the understanding of pranlukast-mediated metabolic changes in Mtb and holds the potential to identify novel therapeutic approaches using metabolic pathways in Mtb.

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14

Yonetomi, Y., M. Fujita, N. Nakagawa y T. Obata. "Preclinical pharmacology of pranlukast". Clinical & Experimental Allergy Reviews 1, n.º 3 (noviembre de 2001): 210–17. http://dx.doi.org/10.1046/j.1472-9725.2001.t01-1-00008.x.

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15

&NA;. "Pranlukast protects against deteriorating asthma control". Inpharma Weekly &NA;, n.º 1086 (mayo de 1997): 16. http://dx.doi.org/10.2165/00128413-199710860-00031.

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16

Iikura, Y., K. Miura, Y. Odajima, T. Imai, H. Sugimoto y M. Ebisawa. "Efficacy of pranlukast in childhood asthma". Clinical & Experimental Allergy Reviews 1, n.º 3 (noviembre de 2001): 287–96. http://dx.doi.org/10.1046/j.1472-9725.2001.t01-1-00014.x.

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17

&NA;. "Pranlukast demonstrates long-term efficacy in asthma". Inpharma Weekly &NA;, n.º 1303 (septiembre de 2001): 6. http://dx.doi.org/10.2165/00128413-200113030-00015.

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18

Kim, Sujeong y Jong-Myung Lee. "A Case of Pranlukast-Induced Anaphylactic Shock". Allergy, Asthma & Immunology Research 8, n.º 3 (2016): 276. http://dx.doi.org/10.4168/aair.2016.8.3.276.

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19

Yang, X. X., W. S. Powell, L. J. Xu y J. G. Martin. "Strain dependence of the airway response to dry-gas hyperpnea challenge in the rat". Journal of Applied Physiology 86, n.º 1 (1 de enero de 1999): 152–58. http://dx.doi.org/10.1152/jappl.1999.86.1.152.

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The aim of the study was to investigate strain dependence and mechanisms of airway responses to dry-gas hyperpnea challenge in the rat. We studied responses in a strain that is hyperresponsive to methacholine, Fischer 344 (F-344); in two normoresponsive strains, Lewis and ACI; and in an atopic but normoresponsive strain, Brown Norway (BN). We examined the effects of a neurokinin (NK) 1-receptor (CP-99994), an NK2-receptor (SR-48968), and a leukotriene D4(LTD4)-receptor antagonist (pranlukast) on responses to hyperpnea challenge in BN rats. The animals were ventilated with a tidal volume of 8 ml/kg and a frequency of 150 breaths/min with either a dry or humidified mixture of 5% CO2-95% O2 for 5 min for hyperpnea challenge, whereas responses to challenge were measured during spontaneous breathing. Pulmonary resistance increased after dry-gas challenge in BN and ACI but not in F-344 and Lewis rats. CP-99994, SR-48968, and pranlukast significantly attenuated the increase in pulmonary resistance after dry-gas challenge. There were no significant differences in responsiveness to airway challenge with LTD4 among the BN, F-344 and ACI rats. We conclude that responses to dry-gas hyperpnea challenge are strain dependent in rats and are mediated by NKs and LTD4.

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Tsuji, Yuichirou, Kenji Narui, Takaaki Takayanagi, Hiroshi Chikaoka, Seiji Takita, Youji Iikura y Tadasu Sakai. "Effectiveness of pranlukast hydrate for Henoch-Schoenlein purpura." Nihon Shoni Jinzobyo Gakkai Zasshi 11, n.º 2 (1998): 185–90. http://dx.doi.org/10.3165/jjpn.11.185.

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21

Theron, A. J., H. C. Steel, G. R. Tintinger, C. M. Gravett, R. Anderson y C. Feldman. "Cysteinyl Leukotriene Receptor-1 Antagonists as Modulators of Innate Immune Cell Function". Journal of Immunology Research 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/608930.

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Cysteinyl leukotrienes (cysLTs) are produced predominantly by cells of the innate immune system, especially basophils, eosinophils, mast cells, and monocytes/macrophages. Notwithstanding potent bronchoconstrictor activity, cysLTs are also proinflammatory consequent to their autocrine and paracrine interactions with G-protein-coupled receptors expressed not only on the aforementioned cell types, but also on Th2 lymphocytes, as well as structural cells, and to a lesser extent neutrophils and CD8+cells. Recognition of the involvement of cysLTs in the immunopathogenesis of various types of acute and chronic inflammatory disorders, especially bronchial asthma, prompted the development of selective cysLT receptor-1 (cysLTR1) antagonists, specifically montelukast, pranlukast, and zafirlukast. More recently these agents have also been reported to possess secondary anti-inflammatory activities, distinct from cysLTR1 antagonism, which appear to be particularly effective in targeting neutrophils and monocytes/macrophages. Underlying mechanisms include interference with cyclic nucleotide phosphodiesterases, 5′-lipoxygenase, and the proinflammatory transcription factor, nuclear factor kappa B. These and other secondary anti-inflammatory mechanisms of the commonly used cysLTR1 antagonists are the major focus of the current review, which also includes a comparison of the anti-inflammatory effects of montelukast, pranlukast, and zafirlukast on human neutrophilsin vitro, as well as an overview of both the current clinical applications of these agents and potential future applications based on preclinical and early clinical studies.

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&NA;. "Pranlukast was found to be 'safe and well tolerated'". Reactions Weekly &NA;, n.º 667 (septiembre de 1997): 4. http://dx.doi.org/10.2165/00128415-199706670-00009.

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23

Matsuse, Hiroto y Shigeru Kohno. "Leukotriene receptor antagonists pranlukast and montelukast for treating asthma". Expert Opinion on Pharmacotherapy 15, n.º 3 (19 de diciembre de 2013): 353–63. http://dx.doi.org/10.1517/14656566.2014.872241.

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24

Schurman, Scott J., Janice M. Alderman, Marc Massanari, Atilano G. Lacson y Sharon A. Perlman. "Tubulointerstitial Nephritis Induced by the Leukotriene Receptor Antagonist Pranlukast". Chest 114, n.º 4 (octubre de 1998): 1220–23. http://dx.doi.org/10.1378/chest.114.4.1220.

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Kobayashi, Shigeto, Shyugo Ishizuka, Naoto Tamura, Makiyo Takaya, Kazuhiko Kaneda y Hiroshi Hashimoto. "Churg?Strauss syndrome (CSS) in a patient receiving pranlukast". Clinical Rheumatology 22, n.º 6 (1 de diciembre de 2003): 491–92. http://dx.doi.org/10.1007/s10067-003-0791-5.

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Shimbo, Junsuke, Osamu Onodera, Keiko Tanaka y Shoji Tsuji. "Churg-Strauss syndrome and the leukotriene receptor antagonist pranlukast". Clinical Rheumatology 24, n.º 6 (2 de diciembre de 2004): 661–62. http://dx.doi.org/10.1007/s10067-004-1035-z.

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27

Schierle, Simone, Jurema Schmidt, Astrid Kaiser y Daniel Merk. "Selective Optimization of Pranlukast to Farnesoid X Receptor Modulators". ChemMedChem 13, n.º 23 (20 de noviembre de 2018): 2530–45. http://dx.doi.org/10.1002/cmdc.201800549.

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28

Hao, Yanli, Lan Wang, Jun Li, Nan Liu, Jinfeng Feng, Mojiao Zhao y Xiaoning Zhang. "Enhancement of Solubility, Transport Across Madin-Darby Canine Kidney Monolayers and Oral Absorption of Pranlukast Through Preparation of a Pranlukast-Phospholipid Complex". Journal of Biomedical Nanotechnology 11, n.º 3 (1 de marzo de 2015): 469–77. http://dx.doi.org/10.1166/jbn.2015.1914.

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Yoshida, Ishizaki, Shoji, Onuma, Nakagawa, Nakabayashi, Akahori, Hasegawa y Amayasu. "Effect of pranlukast on bronchial inflammation in patients with asthma". Clinical & Experimental Allergy 30, n.º 7 (julio de 2000): 1008–14. http://dx.doi.org/10.1046/j.1365-2222.2000.00834.x.

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SAKAGUCHI, KAZUO, JUNKO KUWABARA, AKIYO SAITOU, EMIKO MIYASHITA, YOSHIAKI TAKAYAMA, MASAHIRO AIZAKI, HISAO KUMAKURA, SHOICHI TANGE y SHUICHI ICHIKAWA. "The Pharmacokinetic Interaction between Theophylline and Leukotriene Receptor Antagonist, Pranlukast." Japanese Journal of Hospital Pharmacy 23, n.º 6 (1997): 507–11. http://dx.doi.org/10.5649/jjphcs1975.23.507.

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Watanabe, Toru, Yasufumi Iinuma, Shin-ichi Naito y Koju Nitta. "Eosinophilic tumor in a patient with bronchial asthma receiving pranlukast". European Journal of Pediatrics 166, n.º 2 (17 de agosto de 2006): 183–84. http://dx.doi.org/10.1007/s00431-006-0226-9.

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32

Nakade, Susumu, Akinori Yamauchi, Junji Komaba, Tomoya Ohno, Junsaku Kitagawa, Naoki Honda, Chihiro Hasegawa et al. "Effect of Clarithromycin on the Pharmacokinetics of Pranlukast in Healthy Volunteers". Drug Metabolism and Pharmacokinetics 23, n.º 6 (2008): 428–33. http://dx.doi.org/10.2133/dmpk.23.428.

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33

Yoshifuku, Kousuke, Shoji Matsune y Yuichi Kurono. "The Efficacy of Pranlukast Hydrate for Chronic Sinusitis with Nasal Polyp". Practica Oto-Rhino-Laryngologica 101, n.º 9 (2008): 715–20. http://dx.doi.org/10.5631/jibirin.101.715.

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Kim, Hyeong-Eun, Jun-Seok Hwang, Sun-Hang Cho, Young-Jin Kim y Kang-Moo Huh. "Preparation and Characterization of Poly(ethylene glycol) Based Pranlukast Solid Dispersion". Polymer Korea 36, n.º 1 (25 de enero de 2012): 41–46. http://dx.doi.org/10.7317/pk.2012.36.1.041.

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UNDERWOOD, D., S. BOCHNOWICZ, R. OSBORN, S. NEWSHOLME, T. TORPHY y D. HAY. "426 The cysteinyl-leukotriene (CysLT) receptor antagonist, pranlukast, attenuates airway inflammation". Journal of Allergy and Clinical Immunology 97, n.º 1 (enero de 1996): 289. http://dx.doi.org/10.1016/s0091-6749(96)80644-0.

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Brocks, D. R., J. W. Upward, P. Georgiou, G. Stelman, E. Doyle, E. Allen, P. Wyld y M. J. Dennis. "The single and multiple dose pharmacokinetics of pranlukast in healthy volunteers". European Journal of Clinical Pharmacology 51, n.º 3-4 (12 de diciembre de 1996): 303–8. http://dx.doi.org/10.1007/s002280050202.

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Kanazawa, Hiroshi. "Effects of Pranlukast on Vascular Endothelial Growth Factor Levels in Asthma". Chest 127, n.º 4 (abril de 2005): 1461. http://dx.doi.org/10.1016/s0012-3692(15)34509-8.

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Sun, Tao, Zhihua Wu, Mengyao Luo, Donghai Lin y Chenyun Guo. "Pranlukast, a novel binding ligand of human Raf1 kinase inhibitory protein". Biotechnology Letters 38, n.º 8 (5 de mayo de 2016): 1375–80. http://dx.doi.org/10.1007/s10529-016-2117-0.

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Kanazawa, Hiroshi. "Effects of Pranlukast on Vascular Endothelial Growth Factor Levels in Asthma". CHEST Journal 127, n.º 4 (1 de abril de 2005): 1461. http://dx.doi.org/10.1378/chest.127.4.1461.

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Baek, In-hwan, Jung-Soo Kim, Eun-Sol Ha, Gwang-Ho Choo, Wonkyung Cho, Sung-Joo Hwang y Min-Soo Kim. "Dissolution and oral absorption of pranlukast nanosuspensions stabilized by hydroxypropylmethyl cellulose". International Journal of Biological Macromolecules 67 (junio de 2014): 53–57. http://dx.doi.org/10.1016/j.ijbiomac.2014.03.006.

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Takahashi, Yukitoshi, Katsumi Imai, Hitoshi Ikeda, Yuko Kubota, Etsuko Yamazaki y Fuminobu Susa. "Open study of pranlukast add-on therapy in intractable partial epilepsy". Brain and Development 35, n.º 3 (marzo de 2013): 236–44. http://dx.doi.org/10.1016/j.braindev.2012.04.001.

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TAKAHASHI, Naotsugu, Tomoaki IWANAGA, Hisamichi AIZAWA, Hiroshi KOTO, Kentaroh WATANABE, Reiko KISHIKAWA, Togo IKEDA, Shunsuke SHOJI, Sankei NISHIMA y Nobuyuki KARA. "Acute Interstitial Pneumonia Induced by ONO-1078 (pranlukast), a Leukotriene Receptor Antagonist." Internal Medicine 40, n.º 8 (2001): 791–94. http://dx.doi.org/10.2169/internalmedicine.40.791.

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Lee, Sin Hyung, Jae Jeong Shim, Kyung Kyu Kim, Hye Cheol Jeong, Young Hwan Kwon, Je Hyeong Kim, Sung Yong Lee et al. "Effects of pranlukast on ovalbumin induced early-phase bronchoconstriction in guinea pigs". Tuberculosis and Respiratory Diseases 46, n.º 5 (1999): 697. http://dx.doi.org/10.4046/trd.1999.46.5.697.

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KOBAYASHI, Maiko, Takako MASUDA, Yusuke KINOSHITA y Hiroyuki HARA. "Churg-Strauss Syndrome in a Patient Receiving Pranlukast as Treatment for Asthma". Nishi Nihon Hifuka 67, n.º 4 (2005): 319–22. http://dx.doi.org/10.2336/nishinihonhifu.67.319.

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Endo, Shuichiro, Minoru Gotoh, Kimihiro Okubo, Kazuhiro Hashiguchi, Hidenori Suzuki y Keisuke Masuyama. "Trial of pranlukast inhibitory effect for cedar exposure using an OHIO chamber". Journal of Drug Assessment 1, n.º 1 (22 de febrero de 2012): 48–54. http://dx.doi.org/10.3109/21556660.2012.703630.

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Velázquez-Quesada, Inés, Angel J. Ruiz-Moreno, Diana Casique-Aguirre, Charmina Aguirre-Alvarado, Fabiola Cortés-Mendoza, Marisol de la Fuente-Granada, Carlos García-Pérez et al. "Pranlukast Antagonizes CD49f and Reduces Stemness in Triple-Negative Breast Cancer Cells". Drug Design, Development and Therapy Volume 14 (mayo de 2020): 1799–811. http://dx.doi.org/10.2147/dddt.s247730.

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Ichiyama, T., S. Hasegawa, M. Umeda, K. Terai, T. Matsubara y S. Furukawa. "Pranlukast inhibits NF-κB activation in human monocytes/macrophages and T cells". Clinical & Experimental Allergy 33, n.º 6 (junio de 2003): 802–7. http://dx.doi.org/10.1046/j.1365-2222.2003.01673.x.

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48

Inoue, Ryosuke, Takahide Teramoto, Susumu Nakade, Hiroyuki Okamoto, Eiji Yukawa, Shun Higuchi, Naomi Kondo y Haruki Mikawa. "Population pharmacokinetics of pranlukast hydrate dry syrup in children with bronchial asthma". Allergology International 52, n.º 4 (2003): 213–18. http://dx.doi.org/10.1046/j.1323-8930.2003.00304.x.

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Horiguchi, Takahiko, Soichi Tachikawa, Rieko Kondo, Junichi Miyazaki, Yasushi Sasaki, Kengo Banno y Misuzu Handa. "Evaluation of the Combined Effect of Pranlukast during High-dose Steroid Inhalation". Arzneimittelforschung 52, n.º 11 (26 de diciembre de 2011): 813–16. http://dx.doi.org/10.1055/s-0031-1299972.

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Nagata, Makoto, Keiko Saito, Izumi Kikuchi, Koichi Hagiwara y Minoru Kanazawa. "Effect of the Cysteinyl Leukotriene Antagonist Pranlukast on Transendothelial Migration of Eosinophils". International Archives of Allergy and Immunology 137, n.º 1 (2005): 2–6. http://dx.doi.org/10.1159/000085424.

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