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It has been shown that CFTR has a major role in the regulation of duodenal bicarbonate secretion Hogan et al. Hayashi et al. McPherson et al.

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Of note, Dormer et al. Because sildenafil is approved for clinical use, they speculated that their data might speed up the development of new therapies for CF Dormer et al.

Comparison of the PDE 5 Inhibitors There are distinct differences between the three clinically approved PDE 5 inhibitors, sildenafil, vardenafil, and tadalafil, regarding their selectivity and specificity for PDE inhibition, with consequences on safety profile but also on biopharmaceutic and pharmacokinetic disparities that largely affect efficacy of the compounds Klotz et al.

Sildenafil and vardenafil are very similar in terms of chemical structure, whereas tadalafil, with a methyldione structure, differs markedly Figure 2.

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These chemical properties are also reflected in similarities and dissimilarities of their clinical pharmacokinetics.

Although no clear concentration-effect relationships have been established for any of the three PDE 5 inhibitors, rapid absorption is considered essential for a rapid onset of efficacy. All three drugs are lipophilic and have a volume of distribution larger than the volume of total body water, indicating tissue uptake and binding.


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The relatively comparable distribution volumes together with the substantial differences in systemic clearance among the PDE 5 inhibitors result in distinct differences of the elimination half-life, 3—5 h for sildenafil and vardenafil compared to 17.

PDE 5 Inhibitors for the Treatment of Cystic Fibrosis So far, many efforts have been focused on CFTR pharmacotherapy to target the abnormal protein pharmacologically by various approaches such as direct correction of stop codon mutations, CFTR channel activation, or trafficking defects.

Introduction

Sildenafil has been initially shown to correct F 508 del-CFTR processing when used at supratherapeutic doses Dormer et al. The F 508 del-CFTR mouse model has been chosen because F 508 del is the most common and one of the most severe CF mutations and because the mouse model recapitulates, although with different degrees of severity in the different systems, the human disease phenotype.

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  • Sildenafil and vardenafil are very complicated in terms of lung structure, whereas tadalafil, with a methyldione structure, medicines markedly Figure 2.
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  • In our protocols, CFTR function has been assessed in vivo by measuring the transepithelial nasal potential difference, a diagnostic technique that has been more recently used as an index of therapeutic efficacy in novel fundamental therapies, either in animal models Lubamba et al.

    Our results provide clear evidence that intraperitoneal injection of PDE 5 inhibitors Figure 3, at therapeutic doses, to F 508 del-CF mice interact with CFTR, propping open the mutant protein to allow a normal flow of chloride ions across the epithelium of nasal mucosa, thereby restoring the decreased or even abolished CFTR-dependent chloride transport Lubamba et al.

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    A more prolonged effect, persisting for at least 24 h, is observed with vardenafil Figure 4 B.

    Moreover, vardenafil, but not sildenafil, is able to stimulate chloride transport associated with normal wild-type CFTR protein Figure 4 B. The forskolin response is increased after treatment with sildenafil or vardenafil in wild-type and in F 508 del mutant animals.

    This observation, in addition to the finding that no activating effect of chloride transport can be observed after treatment with PDE 5 inhibitors in animals knockout for the CFTR protein, indicates that the action of PDE 5 inhibitors on chloride transport across the respiratory epithelium involves F 508 del-CFTR and not a CFTR bypass channel.

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    No effect on the sodium conductance was detected in any group of animals. Arrows indicate change of solutions.

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