Relevant bibliographies by topics / Phosphodiesterase 4 (PDE -4) inhibitors

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Phosphodiesterase 4 (PDE -4) inhibitors'

Author: Grafiati
Published: 5 June 2025
Last updated: 2 August 2025

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Journal articles on the topic "Phosphodiesterase 4 (PDE -4) inhibitors"

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Germain, Nöella, Elisabeth Boichot, Jean-Michel Planquois, and Vincent Lagente. "Reduced Airway Hyperresponsiveness by Phosphodiesterase 3 and 4 Inhibitors in Guinea-Pigs." Mediators of Inflammation 8, no. 3 (1999): 153–57. http://dx.doi.org/10.1080/09629359990487.

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The aim of the present study was to compare the effects of selective phosphodiesterase (PDE) 3, 4 and 5 inhibitors on antigen-induced airway hyperresponsiveness in sensitized guinea-pigs. When the sensitized guinea-pigs were orally pre-treated with the selective PDE4 inhibitor, Ro 20-1724 (30 mg/kg), and studied 48 h after OA, a significant reduction (p<0.01) of the leftward shift of the dose-response curve to ACh was noted, whereas it was ineffective at the lower dose (10 mg/kg). Administration of the selective PDE3 inhibitor, milrinone (30 mg/kg) also elicited a significant reduction (p&l
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Ghavami, Afshin, Warren D. Hirst, and Thomas J. Novak. "Selective Phosphodiesterase (PDE)-4 Inhibitors." Drugs in R & D 7, no. 2 (2006): 63–71. http://dx.doi.org/10.2165/00126839-200607020-00001.

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Sarfati, Marika, Véronique Mateo, Sylvie Baudet, et al. "Sildenafil and vardenafil, types 5 and 6 phosphodiesterase inhibitors, induce caspase-dependent apoptosis of B-chronic lymphocytic leukemia cells." Blood 101, no. 1 (2003): 265–69. http://dx.doi.org/10.1182/blood-2002-01-0075.

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Abstract Type 4 phosphodiesterase (PDE4) inhibitors reportedly induce apoptosis in chronic lymphocytic leukemia (CLL) cells. Following clinical improvement of one previously untreated CLL patient with sildenafil therapy, we evaluated the in vitro induction of apoptosis in CLL cells by 4 PDE5/6 inhibitors, including sildenafil, vardenafil, zaprinast, and methoxyquinazoline (MQZ). After 24 hours of culture, the various PDE inhibitors differed in their ability to induce apoptosis, with zaprinast displaying no killing effect. Normal B cells isolated from control donors were totally resistant to PD
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Phillips, Peter G., Lu Long, Martin R. Wilkins, and Nicholas W. Morrell. "cAMP phosphodiesterase inhibitors potentiate effects of prostacyclin analogs in hypoxic pulmonary vascular remodeling." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 1 (2005): L103—L115. http://dx.doi.org/10.1152/ajplung.00095.2004.

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We investigated the effects of prostacyclin analogs and isoform-selective phosphodiesterase (PDE) inhibitors, alone and in combination, on pulmonary vascular remodeling in vitro and in vivo. Vascular smooth muscle cells (VSMC) isolated from pulmonary (proximal and distal) and systemic circulations demonstrated subtle variations in expression of PDE isoform mRNA. However, using biochemical assays, we found PDE3 and PDE4 isoforms to be responsible for the majority of cAMP hydrolysis in all VSMC. In growth assays, the prostacyclin analogs cicaprost and iloprost inhibited mitogen-induced prolifera
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Schick, Martin Alexander, and Nicolas Schlegel. "Clinical Implication of Phosphodiesterase-4-Inhibition." International Journal of Molecular Sciences 23, no. 3 (2022): 1209. http://dx.doi.org/10.3390/ijms23031209.

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The pleiotropic function of 3′,5′-cyclic adenosine monophosphate (cAMP)-dependent pathways in health and disease led to the development of pharmacological phosphodiesterase inhibitors (PDE-I) to attenuate cAMP degradation. While there are many isotypes of PDE, a predominant role of PDE4 is to regulate fundamental functions, including endothelial and epithelial barrier stability, modulation of inflammatory responses and cognitive and/or mood functions. This makes the use of PDE4-I an interesting tool for various therapeutic approaches. However, due to the presence of PDE4 in many tissues, there
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Cheng, Jingfei, Michael A. Thompson, Henry J. Walker, et al. "Differential regulation of mesangial cell mitogenesis by cAMP phosphodiesterase isozymes 3 and 4." American Journal of Physiology-Renal Physiology 287, no. 5 (2004): F940—F953. http://dx.doi.org/10.1152/ajprenal.00079.2004.

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Mesangial cell (MC) mitogenesis is regulated through “negative cross talk” between cAMP-PKA and ERK signaling. Although it is widely accepted that cAMP inhibits mitogenesis through PKA-mediated phosphorylation of Raf-1, recent studies have indicated that cAMP-mediated inhibition of mitogenesis may occur independently of Raf-1 phosphorylation or without inhibiting ERK activity. We previously showed that MCs possess functionally compartmentalized intracellular pools of cAMP that are differentially regulated by cAMP phosphodiesterases (PDE); an intracellular pool directed by PDE3 but not by PDE4
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Kopanitsa, Liliya, Maksym V. Kopanitsa, Dewi Safitri, Graham Ladds, and David S. Bailey. "Suppression of Proliferation of Human Glioblastoma Cells by Combined Phosphodiesterase and Multidrug Resistance-Associated Protein 1 Inhibition." International Journal of Molecular Sciences 22, no. 18 (2021): 9665. http://dx.doi.org/10.3390/ijms22189665.

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The paucity of currently available therapies for glioblastoma multiforme requires novel approaches to the treatment of this brain tumour. Disrupting cyclic nucleotide-signalling through phosphodiesterase (PDE) inhibition may be a promising way of suppressing glioblastoma growth. Here, we examined the effects of 28 PDE inhibitors, covering all the major PDE classes, on the proliferation of the human U87MG, A172 and T98G glioblastoma cells. The PDE10A inhibitors PF-2545920, PQ10 and papaverine, the PDE3/4 inhibitor trequinsin and the putative PDE5 inhibitor MY-5445 potently decreased glioblastom
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Sherpa, Rinzhin T., Cynthia J. Koziol-White, and Reynold A. Panettieri. "Advancing Obstructive Airway Disease Treatment: Dual PDE3/4 Inhibition as a Therapeutic Strategy." Cells 14, no. 9 (2025): 659. https://doi.org/10.3390/cells14090659.

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Obstructive airway diseases, including asthma and chronic obstructive pulmonary disease (COPD), evoke significant global health concerns manifested by airway inflammation and obstruction. Despite their differing origins, shared pathophysiological features and responses to therapeutic interventions highlight common molecular mechanisms. Standard treatments include inhaled bronchodilators, with combination therapies offering enhanced symptom control. Cyclic AMP (cAMP) plays a crucial role in airway relaxation. Phosphodiesterase (PDE) decreases cAMP levels, thereby attenuating the relaxation of a
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Organtzis, John, Sofia Lampaki, Paul Zarogoulidis, et al. "Phosphodiesterase (PDE)-4 Inhibitors and COPD Correlation with Cancer." Journal of Cancer 5, no. 8 (2014): 625–27. http://dx.doi.org/10.7150/jca.9730.

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Neumann, Joachim, Rafaela Voss, Ulrich Laufs, Christian Werner, and Ulrich Gergs. "Phosphodiesterases 2, 3 and 4 can decrease cardiac effects of H2-histamine-receptor activation in isolated atria of transgenic mice." Naunyn-Schmiedeberg's Archives of Pharmacology 394, no. 6 (2021): 1215–29. http://dx.doi.org/10.1007/s00210-021-02052-y.

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AbstractHistamine exerts cAMP-dependent positive inotropic effects (PIE) and positive chronotropic effects (PCE) on isolated left and right atria, respectively, of transgenic mice which overexpress the human H2-receptor in the heart (=H2-TG). To determine whether these effects are antagonized by phosphodiesterases (PDEs), contractile studies were done in isolated left and right atrial preparations of H2-TG. The contractile effects of histamine were tested in the additional presence of the PDE-inhibitorserythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride (EHNA, 1 μM, PDE2-inhibitor) or cilostami
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Dissertations / Theses on the topic "Phosphodiesterase 4 (PDE -4) inhibitors"

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Cooper, Nicola. "Phosphodiesterase 4 inhibitors for the treatment of inflammation associated with respiratory disease." Thesis, University of Greenwich, 2010. http://gala.gre.ac.uk/6364/.

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This submission for a PhD, by publication, which is based upon a series of original research studies published between 1998 and 2002 focuses on the selection of novel phosphodiesterase 4 (PDE4) inhibitors for the treatment of inflammation associated with respiratory diseases such as asthma and chronic obstructive pulmonary disease. A number of issues, relevant at the time, have been considered including: a) in vitro methods predictive of in vivo therapeutic index of anti-inflammatory efficacy over emetic side effects, b) in vivo methods for confirming therapeutic index and c) early confirmatio
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Irvine, Mark William. "The design and synthesis of novel phosphodiesterase 4 inhibitors for the treatment of asthma." Thesis, University of the West of Scotland, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441083.

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Mulubwe, Ngosa. "A comparative study of the Phosphodiesterase 4 inhibitory activity of Artemisia Afra, Leonotis Leonorus and mentha longifolia plant medicines. /." Thesis, Online Access, 2007. http://etd.uwc.ac.za/usrfiles/modules/etd/docs/etd_gen8Srv25Nme4_7163_1257926263.pdf.

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Ebling, Annette. "Die funktionelle Modifikation der proinflammatorischen M-DC8+ dendritischen Zellen durch zyklisches Adenosin-Monophosphat." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2005. http://nbn-resolving.de/urn:nbn:de:swb:14-1121945852623-20616.

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In this work, the influence of the second messenger cAMP on the functional plasticity of M-DC8+ dendritic cells (DC) was examined. The marker M-DC8 defines a population of native DC first described in blood. After their isolation, M-DC8+ DC acquire a mature CD83+ phenotype during a short culture ex vivo. After a challenge with LPS and IFN-g, M-DC8+ DC secrete large amounts of the proinflammatory cytokines IL-12(p70) and TNF-a surpassing by far other DC populations and monocytes. Due to their preferential induction of TH1-dominated T cell responses, M-DC8+ DC might play a role in the pathogenes
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Moniot, Aurélie. "Etude des effets anti-inflammatoires et anti-cancéreux de nouvelles molécules agrosourcées à motif pyridazinone Synthesis and biological evaluation of pyridazinone derivatives as potential antiinflammatory agents Osteoinductive Material to Fine-Tune Paracrine Crosstalk of Mesenchymal Stem Cells With Endothelial Cells and Osteoblasts." Thesis, Reims, 2020. http://www.theses.fr/2020REIMS022.

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L’ostéosarcome est un cancer primitif rare de l’os dont les approches thérapeutiques actuelles sont encore malheureusement insuffisantes pour espérer une totale guérison, et pour lequel la recherche de nouvelles molécules efficaces est constante. De plus, après exérèse de la tumeur, le défaut généré peut nécessiter de recourir à des matériaux aidant la reconstruction osseuse. Or le potentiel inflammatoire de ces matériaux est bien documenté. Les inhibiteurs de phosphodiestérase de type 4, parmi lesquels des molécules à motif pyridazinone, ont d’ores et déjà fait leurs preuves en tant qu’agents
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Chang, Tsu-Ya, and 張慈雅. "Anti-asthmatic effects of hesperetin, a selective phosphodiesterase (PDE)4 inhibitor, potentiated by daidzein, a selective PDE3 inhibitor." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/88830513624619954883.

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碩士<br>臺北醫學大學<br>藥理學研究所<br>94<br>Selective PDE4 inhibitors increase cAMP level, therefore have bronchodilatory and anti-inflammatory effects, and is worth to develop for ameliorating asthma in the future. Selective PDE3 inhibitors also increase cAMP level. Whether addition or potentiation will be observed when they combine each other is the aim of the present study. Hesperetin (PDE4 inhibitor) at 100 μM dilated baseline tension of ovalbumin (OVA)-sensitized guinea pig trachealis. When combined with 100 μM of diadzein (PDE3 inhibitor), addition was observed. In addition, the relaxant effect of
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Books on the topic "Phosphodiesterase 4 (PDE -4) inhibitors"

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Mease, Philip. Biologic treatments for psoriatic arthritis apart from TNF inhibition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0030.

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Psoriatic arthritis (PsA) is an immunologically mediated inflammatory disease characterized by arthritis, enthesitis, dactylitis, spondylitis, and psoriasis. Prior to the introduction of targeted biologic medications, such as TNF inhibitors, the ability to control disease activity was limited, with only modest effects noted with traditional oral medications such as methotrexate and sulfasalazine. The introduction of TNF inhibitors substantially changed the outlook of PsA patients, yielding significant response in all relevant clinical domains and demonstrating the ability to inhibit progressiv
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Book chapters on the topic "Phosphodiesterase 4 (PDE -4) inhibitors"

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Barnette, Mary S. "Phosphodiesterase 4 (PDE4) inhibitors in asthma and chronic obstructive pulmonary disease (COPD)." In Progress in Drug Research. Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8735-9_5.

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Torphy, Theodore J., Christopher H. Compton, Meretta J. Marks, and Graham Sturton. "Phosphodiesterase 4 Inhibitors." In New Drugs for Asthma, Allergy and COPD. KARGER, 2001. http://dx.doi.org/10.1159/000062165.

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Bischoff, Erwin. "Pharmacology of Phosphodiesterase Inhibitors." In Oral Pharmacotherapy for Male Sexual Dysfunction. Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-871-4:043.

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Graham, Garry G., and Kevin D. Pile. "Phosphodiesterase 4 Inhibitors: Apremilast and Roflumilast." In Compendium of Inflammatory Diseases. Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_56.

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Graham, Garry G., and Kevin D. Pile. "Phosphodiesterase 4 Inhibitors: Apremilast and Roflumilast." In Encyclopedia of Inflammatory Diseases. Springer Basel, 2015. http://dx.doi.org/10.1007/978-3-0348-0620-6_56-1.

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Giembycz, Mark A. "Alkylxanthines and Phosphodiesterase 4 Inhibitors for Allergic Diseases." In Allergy Frontiers: Therapy and Prevention. Springer Japan, 2009. http://dx.doi.org/10.1007/978-4-431-99362-9_7.

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Polymeropoulos, E. E., and N. Höfgen. "A Peptidic Binding Site Model for PDE 4 Inhibitors." In Molecular Modeling and Prediction of Bioactivity. Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4141-7_93.

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Giembycz, Mark A., and Robert Newton. "Harnessing the Clinical Efficacy of Phosphodiesterase 4 Inhibitors in Inflammatory Lung Diseases: Dual-Selective Phosphodiesterase Inhibitors and Novel Combination Therapies." In Phosphodiesterases as Drug Targets. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-17969-3_18.

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McCullough, Andrew R. "Sexual Dysfunction After Radical Prostatectomy and the Use of PDE-5 Inhibitors." In Oral Pharmacotherapy for Male Sexual Dysfunction. Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-871-4:409.

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Tenor, Hermann, Armin Hatzelmann, Rolf Beume, Gezim Lahu, Karl Zech, and Thomas D. Bethke. "Pharmacology, Clinical Efficacy, and Tolerability of Phosphodiesterase-4 Inhibitors: Impact of Human Pharmacokinetics." In Phosphodiesterases as Drug Targets. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-17969-3_3.

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Conference papers on the topic "Phosphodiesterase 4 (PDE -4) inhibitors"

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Rheault, Tara, Joseph A. Boscia, Brian Maurer, and Kathleen Rickard. "Ensifentrine, a novel dual phosphodiesterase (PDE) 3 and 4 inhibitor, provides effective bronchodilation when administered by dry powder inhaler in COPD." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.oa265.

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Gray, S. J., and S. Heptinstall. "INTERACTIONS BETWEEn PGE2 AND INHIBITORS OF PLATELET AGGREGATION THAT ACT THROUGH cAMP." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643582.

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PGE2 has a biphasic effect on platelet aggregation with low concentrations of the prostaglandin potentiating aggregation and high concentrations inhibiting it. In this investigation we have studied the interaction of PGE2 with agents that inhibit platelet aggregation through an effect on cAMP. The agents chosen raise the level of cAMP in platelets by different mechanisms: PGI2, PGD9 and adenosine combine with specific surface-located receptors and stimulate adenylate cyclase (AC) via a guanine nucleotide-binding protein (GNBP), forskolin stimulates AC directly, and AH-P 719 and DN 9693 inhibit
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Anzueto, A., I. Barjaktarevic, T. Rheault, T. Bengtsson, and K. Rickard. "Ensifentrine, a Novel Dual Phosphodiesterase (PDE) 3 and 4 Inhibitor, Improves Lung Function and Reduces Exacerbation Rate and Risk in Phase 3 Enhance-2 Trial." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a4494.

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Sciurba, F. C., T. Rheault, T. Bengtsson, and K. Rickard. "Ensifentrine, a Novel Dual Phosphodiesterase (PDE) 3 and 4 Inhibitor, Significantly Improves COPD Symptoms and Quality of Life in the Phase 3 Enhance-1 Trial." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5007.

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Rheault, T., K. Rickard, J. A. Boscia, and T. Bengtsson. "Ensifentrine, A Novel Dual Phosphodiesterase (PDE) 3 and 4 Inhibitor, Provides Effective Bronchodilation in COPD When Administered Twice Daily Over 7 Days Via a Dry Powder Inhaler." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4296.

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Rheault, T., T. Bengtsson, and K. Rickard. "Ensifentrine, a Novel Dual Phosphodiesterase (PDE) 3 and 4 Inhibitor, in Moderate and Severe COPD: Symptoms, Quality of Life and Health Status From the Phase 3 Trial Enhance-2." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5000.

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Sciurba, F. C., A. Anzueto, T. Rheault, T. Bengtsson, and K. Rickard. "Ensifentrine, a Novel Dual Phosphodiesterase (PDE) 3 and 4 Inhibitor, Improves Lung Function, Symptoms, Quality of Life and Reduces Exacerbation Rate and Risk in Patients With COPD: Results From Replicate Phase 3 Trials." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5005.

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Chen, W., Z. Xu, H. Wee, et al. "THU0097 Phosphodiesterases 4 (PDE4) inhibitor ameliorates experimental arthritis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4989.

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Sciurba, F. C., R. A. A. Wise, T. Rheault, T. Bengtsson, and K. Rickard. "Ensifentrine, a Novel Dual Phosphodiesterase (PDE) 3 and 4 Inhibitor, Improves Lung Function, Symptoms, Quality of Life and Reduces Exacerbation Rate and Risk in the Enhance-1 Phase 3 Trial of Ensifentrine in COPD." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5006.

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Barjaktarevic, I., T. Rheault, T. Bengtsson, and K. Rickard. "Ensifentrine, a Novel Dual Phosphodiesterase (PDE) 3 and 4 Inhibitor, Significantly Reduces Annualized Exacerbations and Delays the Time to First Exacerbation in COPD: Pooled Sub-Group Analyses of Enhance-1 and Enhance-2 Phase 3 Trials." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5008.

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Reports on the topic "Phosphodiesterase 4 (PDE -4) inhibitors"

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Wang, Long, Le-qu Zeng, Yuyu Wu, Min Zhong, Lizhen Zhang, and Chen Li. Effectiveness and safety of topical phosphodiesterase 4 inhibitors in children with Mild to Moderate Atopic Dermatitis: systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2025. https://doi.org/10.37766/inplasy2025.2.0121.

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