vardenafil
Sources réglementaires consultées
Indications approuvées
- Traitement de la dysfonction érectile chez l’homme adulte ; une stimulation sexuelle est nécessaire.
Contre-indications
Absolues
- Utilisation de dérivés nitrés ou donneurs de monoxyde d’azote ; utilisation de stimulateurs de la guanylate cyclase tels que le riociguat ; hypersensibilité.
- Insuffisance hépatique sévère ou traitement par dialyse.
Mises en garde cliniques
- Mise en garde majeure · Ne pas utiliser si l’activité sexuelle est déconseillée en raison de l’état cardiovasculaire. Une érection durant plus de 4 heures nécessite une prise en charge urgente. — FDA/DailyMed, set_id 083a3282-254f-4042-b0eb-70f76a279f10
- Mise en garde majeure · Arrêter et consulter immédiatement en cas de perte soudaine de la vision ou de diminution/perte soudaine de l’audition. — FDA/DailyMed, set_id 083a3282-254f-4042-b0eb-70f76a279f10
- Mise en garde majeure · Éviter en cas de syndrome du QT long congénital et avec les antiarythmiques de classe IA ou III. — FDA/DailyMed, set_id 083a3282-254f-4042-b0eb-70f76a279f10
Interactions médicamenteuses
- SévèreDérivés nitrés, donneurs de monoxyde d’azote ou riociguat
Mécanisme: La vasodilatation additive peut provoquer une hypotension sévère.
Recommandation: Association contre-indiquée.
FDA/DailyMed, set_id 083a3282-254f-4042-b0eb-70f76a279f10https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=083a3282-254f-4042-b0eb-70f76a279f10
- ModéréeAlpha-bloquants ou antihypertenseurs
Mécanisme: Ils peuvent provoquer une hypotension symptomatique additive.
Recommandation: Stabiliser le traitement, commencer à faible dose et surveiller la pression artérielle et les symptômes.
FDA/DailyMed, set_id 083a3282-254f-4042-b0eb-70f76a279f10https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=083a3282-254f-4042-b0eb-70f76a279f10
- SévèreInhibiteurs puissants ou modérés du CYP3A4
Mécanisme: Ils augmentent fortement l’exposition et prolongent la demi-vie.
Recommandation: Appliquer strictement les doses maximales réduites propres à chaque inhibiteur ; avec le ritonavir ou le cobicistat, ne pas dépasser 2,5 mg en 72 heures.
FDA/DailyMed, set_id 083a3282-254f-4042-b0eb-70f76a279f10https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=083a3282-254f-4042-b0eb-70f76a279f10
Effets indésirables
Communs (≥1%)
Céphalées · Bouffées vasomotrices · Congestion nasale · Dyspepsie · Vertiges · Nausées
Rares mais graves
Priapisme · Neuropathie optique ischémique antérieure non artéritique · Perte auditive soudaine · Événement cardiovasculaire grave
Grossesse et allaitement
Non indiqué chez la femme.
Bibliographie récente (PubMed)
Lodenafil is a class of drugs called an inhibitor of PDE5 which also include a wide range of other erectile medicines, such as sildenafil, tadalafil and vardenafil. It is part of a new generation of PDE5 inhibitors that includes udenafil and avanafil. Lodenafil is a prodrug manufactured in the form of lodenafil carbonate, the carbonate dimer that divides in the body into two active drug lodenafil molecules. The oral bioavailability of this formulation is higher than that of the parent drug. This article discusses, by a critical comprehensive review of the literature on lodenafil in terms of its description, names, formulae, elemental composition, appearance, and therapeutic uses. The article also discusses the methods for preparation of lodenafil, its physical-chemical properties, analytical methods for its determination, pharmacological-toxicological properties, and dosing information.
The management of Alzheimer's disease (AD) poses considerable challenges, necessitating the pursuit of innovative therapeutic approaches. Recent research has spotlighted the promising role of phosphodiesterase type 5 inhibitors (PDE5Is) in reducing the prevalence of AD, utilizing their vasodilatory properties to suggest a potential neuroprotective effect. This meta-analysis and systematic review aims to assess the relationship between the use of PDE5Is and the risk of AD. A detailed examination was carried out across several electronic databases till March 2024, including PubMed, Web of Science, Scopus, CENTRAL, and Embase. The focus was on identifying studies that compare the occurrence of AD among PDE5I users vs non-users. Through a random-effects model, pooled hazard ratios (HRs) were calculated, in alignment with guidelines from the Cochrane Handbook for Systematic Reviews and Meta-Analysis and the PRISMA standards. This analysis included six studies, cumulating a participant count of 8,337,313, involving individuals treated with sildenafil, tadalafil, and vardenafil, against a control group undergoing other or no treatments. The cumulative HR for AD risk among PDE5I users versus the control group was 0.53 (95% CI: 0.32-0.86, p = 0.008), signaling a markedly reduced likelihood of AD development in the PDE5I group. Particularly, sildenafil usage showed a significant risk reduction (HR: 0.46, 95% CI: 0.31-0.70, p < 0.001), while findings for tadalafil and vardenafil were not significant. Test of subgroup differences found no difference between male and female participants in the risk of AD. Our findings suggest that the use of PDE5Is is associated with a reduced risk of AD, highlighting its potential as a protective agent against neurodegenerative diseases. Given the very low quality of evidence and the heterogeneity among the included studies, further high-quality research is warranted to confirm these findings and elucidate the underlying mechanisms. Register nu
Pulmonary hypertension (PH) is a serious condition characterized by elevated blood pressure in the pulmonary arteries. Current treatment approaches mainly focus on using vasodilator agents to reduce pulmonary blood pressure and improve blood flow. Inhalation treatments offer targeted delivery to the lungs, improving efficacy and reducing systemic side effects. Understanding the pharmacokinetics (PK) of the molecules used in the inhalation treatment is crucial for dose optimization and drug product development. This review examines the clinical PK characteristics of key inhaled PH drugs (approved and investigational agents), including epoprostenol, iloprost, treprostinil, vardenafil, imatinib, seralutinib, MK-5475, milrinone, and sodium nitrite. We provide detailed analyses of their PK parameters and explore how disease conditions, inter-subject variability, and inhaled formulations and devices impact clinical PK characteristics. Future research would focus on how disease-specific factors affect drug behavior and the prediction of pulmonary drug concentrations. This will support more precise drug delivery and personalized treatment strategies for PH.
Vardenafil hydrochloride tablet is an inhibitor of phosphodiesterase type 5, primarily for the treatment of erectile dysfunction. This postprandial study evaluated the pharmacokinetics and bioequivalence of the test and reference formulations of vardenafil hydrochloride tablets in healthy Chinese volunteers. An open, randomized, single-center, single-dose, 2-period, 2-sequence bioequivalence test was conducted on 66 healthy subjects under fed conditions. Subjects were randomly assigned to a 20-mg test or reference formulation with a 7-day washout period. Venous blood samples (4 mL) were collected from each subject 25 times spanning predose (0 hour) to 24 hours after dosing. The plasma concentration of vardenafil was determined by high-performance liquid chromatography-tandem mass spectrometry. Sixty-two volunteers completed the study. Under fed conditions, the maximum plasma concentration was 29.1 ng/mL, the area under the concentration-time curve (AUC) from time 0 to the time of the last measurable concentration was 85.3 ng•h/mL, and AUC from time 0 to infinity was 87.1 ng•h/mL. The 90% confidence intervals of the geometric mean ratio of AUC time 0 to the time of the last measurable concentration and AUC from time 0 to infinity were within the bioequivalence acceptance range of 0.80-1.25. The test formulation was a bioequivalent alternative to the reference formulation when taken under fed conditions in healthy Chinese subjects.
Inflammatory bowel disease is a recurrent chronic intestinal inflammatory disease with unknown etiology and no effective treatment. Phosphodiesterase (PDE) regulates a variety of physiological and pathophysiological processes by mediating the hydrolysis of intracellular second messengers cyclic adenosine monophosphate and cyclic guanosine monophosphate. In recent years, a series of researches suggest that PDE inhibitors such as several PDE4 inhibitors, PDE5 inhibitors (sildenafil, tadalafil and vardenafil), PDE3 inhibitors (cilostazol), PDE9 inhibitor (PF-04447943) and PDE3/PDE4 double inhibitor (pumafentrine) have ameliorating effect on experimental colitis in animals. In clinical trials, PDE4 inhibitor apremilast showed more therapeutic advantage than tetomilast. This article reviews the recent research progress of PDE inhibitors in treatment of inflammatory bowel disease. Inflammatory bowel disease is a recurrent chronic intestinal inflammatory disease with unknown etiology and no effective treatment. Phosphodiesterase (PDE) regulates a variety of physiological and pathophysiological processes by mediating the hydrolysis of intracellular second messengers cyclic adenosine monophosphate and cyclic guanosine monophosphate. In recent years, a series of researches suggest that PDE inhibitors such as several PDE4 inhibitors, PDE5 inhibitors (sildenafil, tadalafil and vardenafil), PDE3 inhibitors (cilostazol), PDE9 inhibitor (PF-04447943) and PDE3/PDE4 double inhibitor (pumafentrine) have ameliorating effect on experimental colitis in animals. In clinical trials, PDE4 inhibitor apremilast showed more therapeutic advantage than tetomilast. This article reviews the recent research progress of PDE inhibitors in treatment of inflammatory bowel disease.