PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 28196856-0 2017 Vardenafil reduces macrophage pro-inflammatory overresponses in cystic fibrosis through PDE5- and CFTR-dependent mechanisms. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A, cGMP-specific Mus musculus 88-92 28486684-10 2017 Vardenafil appears to be the most potent of the PDE-5 inhibitors tested. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 48-53 28626017-4 2017 We demonstrate that the increase of cGMP levels by the phosphodiesterase-5 inhibitors sildenafil and vardenafil induces a parallel release of Abeta due to a change in the approximation of amyloid precursor protein (APP) and the beta-site APP cleaving enzyme 1. Vardenafil Dihydrochloride 101-111 amyloid beta (A4) precursor protein Mus musculus 142-147 28626017-4 2017 We demonstrate that the increase of cGMP levels by the phosphodiesterase-5 inhibitors sildenafil and vardenafil induces a parallel release of Abeta due to a change in the approximation of amyloid precursor protein (APP) and the beta-site APP cleaving enzyme 1. Vardenafil Dihydrochloride 101-111 amyloid beta (A4) precursor protein Mus musculus 188-213 28626017-4 2017 We demonstrate that the increase of cGMP levels by the phosphodiesterase-5 inhibitors sildenafil and vardenafil induces a parallel release of Abeta due to a change in the approximation of amyloid precursor protein (APP) and the beta-site APP cleaving enzyme 1. Vardenafil Dihydrochloride 101-111 beta-site APP cleaving enzyme 1 Mus musculus 228-259 28196856-6 2017 We confirmed that macrophages from different body compartments express CF transmembrane conductance regulator (CFTR) and showed that vardenafil targets the cells through PDE5- and CFTR-dependent mechanisms. Vardenafil Dihydrochloride 133-143 cystic fibrosis transmembrane conductance regulator Mus musculus 111-115 28196856-6 2017 We confirmed that macrophages from different body compartments express CF transmembrane conductance regulator (CFTR) and showed that vardenafil targets the cells through PDE5- and CFTR-dependent mechanisms. Vardenafil Dihydrochloride 133-143 phosphodiesterase 5A, cGMP-specific Mus musculus 170-174 28196856-6 2017 We confirmed that macrophages from different body compartments express CF transmembrane conductance regulator (CFTR) and showed that vardenafil targets the cells through PDE5- and CFTR-dependent mechanisms. Vardenafil Dihydrochloride 133-143 cystic fibrosis transmembrane conductance regulator Mus musculus 180-184 28196856-0 2017 Vardenafil reduces macrophage pro-inflammatory overresponses in cystic fibrosis through PDE5- and CFTR-dependent mechanisms. Vardenafil Dihydrochloride 0-10 cystic fibrosis transmembrane conductance regulator Mus musculus 98-102 28196856-7 2017 In the presence of the F508del mutation, vardenafil down-regulated overresponses of the M1 markers, tumour necrosis factor (TNF)-alpha and inducible nitric oxide synthase (NOS)-2. Vardenafil Dihydrochloride 41-51 tumor necrosis factor Mus musculus 100-134 28196856-2 2017 In mice, vardenafil, an inhibitor of phosphodiesterase type 5 (PDE5), restores transepithelial ion transport and corrects mislocalization of the most common CF mutation, F508del-CFTR. Vardenafil Dihydrochloride 9-19 phosphodiesterase 5A, cGMP-specific Mus musculus 37-61 28196856-7 2017 In the presence of the F508del mutation, vardenafil down-regulated overresponses of the M1 markers, tumour necrosis factor (TNF)-alpha and inducible nitric oxide synthase (NOS)-2. Vardenafil Dihydrochloride 41-51 nitric oxide synthase 2, inducible Mus musculus 149-178 28196856-2 2017 In mice, vardenafil, an inhibitor of phosphodiesterase type 5 (PDE5), restores transepithelial ion transport and corrects mislocalization of the most common CF mutation, F508del-CFTR. Vardenafil Dihydrochloride 9-19 phosphodiesterase 5A, cGMP-specific Mus musculus 63-67 28196856-8 2017 Our study identifies lung macrophages as target cells of the anti-inflammatory effect of vardenafil in CF and supports the view that the drug is potentially beneficial for treating CF as it combines rescue of CFTR protein and anti-inflammatory properties. Vardenafil Dihydrochloride 89-99 cystic fibrosis transmembrane conductance regulator Mus musculus 209-213 28196856-2 2017 In mice, vardenafil, an inhibitor of phosphodiesterase type 5 (PDE5), restores transepithelial ion transport and corrects mislocalization of the most common CF mutation, F508del-CFTR. Vardenafil Dihydrochloride 9-19 cystic fibrosis transmembrane conductance regulator Mus musculus 178-182 27904146-0 2017 The correlation between high sensitivity C-reactive protein and erectile dysfunction patients with hypertension treated with vardenafil. Vardenafil Dihydrochloride 125-135 C-reactive protein Homo sapiens 41-59 27995696-0 2017 Prevention of the development of heart failure with preserved ejection fraction by the phosphodiesterase-5A inhibitor vardenafil in rats with type 2 diabetes. Vardenafil Dihydrochloride 118-128 phosphodiesterase 5A Rattus norvegicus 87-107 27995696-4 2017 We investigated the effect of long-term preventive application of the phosphodiesterase-5A (PDE5A) inhibitor vardenafil in diabetic cardiomyopathy-associated HFpEF. Vardenafil Dihydrochloride 109-119 phosphodiesterase 5A Rattus norvegicus 70-90 27995696-4 2017 We investigated the effect of long-term preventive application of the phosphodiesterase-5A (PDE5A) inhibitor vardenafil in diabetic cardiomyopathy-associated HFpEF. Vardenafil Dihydrochloride 109-119 phosphodiesterase 5A Rattus norvegicus 92-97 27904146-1 2017 We evaluate the correlation between the plasma level of C-reactive protein (CRP) in patients with erectile dysfunction (ED) and hypertension and to set up whether the CRP level affected by the treatment of vardenafil 10 mg orally once daily. Vardenafil Dihydrochloride 206-216 C-reactive protein Homo sapiens 167-170 27998725-7 2017 Treatment of mice with the phosphodiesterase-5 inhibitor vardenafil (Levitra) mobilized FoxO3a to the nucleus of luminal epithelial cells, which corresponded to increased FoxO target gene expression, reduced redox stress, and increased epithelial barrier integrity. Vardenafil Dihydrochloride 57-67 forkhead box O3 Mus musculus 88-94 27762466-7 2017 Vardenafil pretreatment significantly alleviated the expression of nuclear factor kappa-B and inducible nitric oxide synthase in the hepatic tissue. Vardenafil Dihydrochloride 0-10 nitric oxide synthase 2, inducible Mus musculus 94-125 27998725-7 2017 Treatment of mice with the phosphodiesterase-5 inhibitor vardenafil (Levitra) mobilized FoxO3a to the nucleus of luminal epithelial cells, which corresponded to increased FoxO target gene expression, reduced redox stress, and increased epithelial barrier integrity. Vardenafil Dihydrochloride 69-76 forkhead box O3 Mus musculus 88-94 27800121-8 2016 In addition, low doses of tadalafil and vardenafil induced the protein expression of CYP2E1. Vardenafil Dihydrochloride 40-50 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 85-91 27871960-2 2016 Oral PDE-5 inhibitors such as sildenafil, vardenafil, tadalafil, and avanafil have provided noninvasive, effective, well-tolerated treatment for erectile dysfunction (ED) patients and, at the same time, stimulated both academic and clinical interests. Vardenafil Dihydrochloride 42-52 phosphodiesterase 5A Homo sapiens 5-10 26887831-11 2016 Vardenafil (25 nM), a PDE5 inhibitor, restored NO"s ability to inhibit NKCC2 activity in THALs from ANG II-hypertensive rats (Delta: -60 +- 9%, P < 0.003). Vardenafil Dihydrochloride 0-10 solute carrier family 12 member 1 Rattus norvegicus 71-76 27800121-10 2016 Moreover, low doses of both vardenafil and sildenafil markedly increased AHH activity by 162 and 247%, respectively, whereas high doses of tadalafil, vardenafil, and sildenafil inhibited such activity by 36, 49, and 57% and inhibited the EROD activity by 39, 49, and 33%, respectively. Vardenafil Dihydrochloride 28-38 cytochrome P450, family 1, subfamily a, polypeptide 1 Rattus norvegicus 73-76 26328208-4 2015 Today, the American Urological Association recommends the use of three PDE5 inhibitors (sildenafil, tadalafil, and vardenafil) as a first-line therapy for the treatment of ED. Vardenafil Dihydrochloride 115-125 phosphodiesterase 5A Homo sapiens 71-75 28962432-7 2015 The present study showed that sildenafil, vardenafil, and tadalafil treatments significantly decreased the levels of glutathione, MDA and the activity of glutathione reductase. Vardenafil Dihydrochloride 42-52 glutathione-disulfide reductase Rattus norvegicus 154-175 28962432-8 2015 In addition, vardenafil and sildenafil increased the activity of superoxide dismutase and catalase. Vardenafil Dihydrochloride 13-23 catalase Rattus norvegicus 90-98 26664380-8 2015 Our results suggest that phosphodiesterase type-5 inhibitor vardenafil may offer a new therapeutic tool to treat pain. Vardenafil Dihydrochloride 60-70 phosphodiesterase 5A Rattus norvegicus 25-49 25736325-0 2015 Drug Repositioning for Preeclampsia Therapeutics by In Vitro Screening: Phosphodiesterase-5 Inhibitor Vardenafil Restores Endothelial Dysfunction via Induction of Placental Growth Factor. Vardenafil Dihydrochloride 102-112 placental growth factor Homo sapiens 163-186 25736325-6 2015 Of the drugs that induced PlGF, vardenafil was the only compound that significantly facilitated tube formation in comparison with the control cells (P < .01). Vardenafil Dihydrochloride 32-42 placental growth factor Homo sapiens 26-30 25736325-7 2015 Treatment with vardenafil at concentrations of 50, 100, and 250 micromol/L increased expression of PlGF in a dose-dependent manner. Vardenafil Dihydrochloride 15-25 placental growth factor Homo sapiens 99-103 25736325-9 2015 Production of PlGF from HUVECs in the presence of sera derived from patients with preeclampsia was significantly elevated by administration of vardenafil (250 micromol/L). Vardenafil Dihydrochloride 143-153 placental growth factor Homo sapiens 14-18 26047999-6 2015 Sildenafil, tadalafil and vardenafil are 3 specific PDE-5 inhibitors in current clinical use, which share similar mechanisms of action but present some significant differences regarding potency, selectivity for PDE-5 and pharmacokinetic properties. Vardenafil Dihydrochloride 26-36 phosphodiesterase 5A Homo sapiens 52-57 26047999-6 2015 Sildenafil, tadalafil and vardenafil are 3 specific PDE-5 inhibitors in current clinical use, which share similar mechanisms of action but present some significant differences regarding potency, selectivity for PDE-5 and pharmacokinetic properties. Vardenafil Dihydrochloride 26-36 phosphodiesterase 5A Homo sapiens 211-216 26103029-5 2015 EXPOSURES: Number of filled prescriptions for the PDE5 inhibitors sildenafil and vardenafil or tadalafil. Vardenafil Dihydrochloride 81-91 phosphodiesterase 5A Homo sapiens 50-54 25801159-2 2015 Sildenafil, vardenafil, tadalafil and avanafil are FDA approved drugs in market as PDE5 inhibitors for treating erectile dysfunction. Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 83-87 24887326-7 2014 Inhibition of ABCB1 using vardenafil or verapamil resulted in a significant increase in sensitivity to etoposide in ABCB1-expressing MB cell lines. Vardenafil Dihydrochloride 26-36 ATP binding cassette subfamily B member 1 Homo sapiens 14-19 25420893-7 2015 The relative expressions of COX-1 and COX-2 genes to GAPDH revealed that the maximum increase was obtained in the group treated with CyA and vardenafil for both COX-1 and COX-2 genes. Vardenafil Dihydrochloride 141-151 cytochrome c oxidase I, mitochondrial Mus musculus 28-33 25420893-7 2015 The relative expressions of COX-1 and COX-2 genes to GAPDH revealed that the maximum increase was obtained in the group treated with CyA and vardenafil for both COX-1 and COX-2 genes. Vardenafil Dihydrochloride 141-151 cytochrome c oxidase II, mitochondrial Mus musculus 38-43 25420893-7 2015 The relative expressions of COX-1 and COX-2 genes to GAPDH revealed that the maximum increase was obtained in the group treated with CyA and vardenafil for both COX-1 and COX-2 genes. Vardenafil Dihydrochloride 141-151 glyceraldehyde-3-phosphate dehydrogenase Mus musculus 53-58 25420893-7 2015 The relative expressions of COX-1 and COX-2 genes to GAPDH revealed that the maximum increase was obtained in the group treated with CyA and vardenafil for both COX-1 and COX-2 genes. Vardenafil Dihydrochloride 141-151 cytochrome c oxidase I, mitochondrial Mus musculus 161-166 25420893-7 2015 The relative expressions of COX-1 and COX-2 genes to GAPDH revealed that the maximum increase was obtained in the group treated with CyA and vardenafil for both COX-1 and COX-2 genes. Vardenafil Dihydrochloride 141-151 cytochrome c oxidase II, mitochondrial Mus musculus 171-176 25444755-1 2015 The phosphodiesterase 5 (PDE5) inhibitors, including sildenafil (Viagra ), vardenafil (Levitra ), and tadalafil (Cialis ) have been developed for treatment of erectile dysfunction. Vardenafil Dihydrochloride 75-85 phosphodiesterase 5A Homo sapiens 4-23 25444755-1 2015 The phosphodiesterase 5 (PDE5) inhibitors, including sildenafil (Viagra ), vardenafil (Levitra ), and tadalafil (Cialis ) have been developed for treatment of erectile dysfunction. Vardenafil Dihydrochloride 75-85 phosphodiesterase 5A Homo sapiens 25-29 25444755-1 2015 The phosphodiesterase 5 (PDE5) inhibitors, including sildenafil (Viagra ), vardenafil (Levitra ), and tadalafil (Cialis ) have been developed for treatment of erectile dysfunction. Vardenafil Dihydrochloride 87-94 phosphodiesterase 5A Homo sapiens 4-23 25444755-1 2015 The phosphodiesterase 5 (PDE5) inhibitors, including sildenafil (Viagra ), vardenafil (Levitra ), and tadalafil (Cialis ) have been developed for treatment of erectile dysfunction. Vardenafil Dihydrochloride 87-94 phosphodiesterase 5A Homo sapiens 25-29 25848165-8 2015 The obtained binding mode was as same as that of vardenafil, X-ray ligand with different orientation with varied PDE5 inhibitors scaffold. Vardenafil Dihydrochloride 49-59 phosphodiesterase 5A Homo sapiens 113-117 25445042-5 2014 The present study aimed to determine Ki-values for specific or relative specific PDE5 inhibitors (vardenafil, tadalafil, zaprinast and dipyridamole) and the non-specific PDE inhibitors (IBMX, caffeine and theophylline) for ABCC5 and ABCC4 transport. Vardenafil Dihydrochloride 98-108 phosphodiesterase 5A Homo sapiens 81-85 25372140-3 2014 In the present study, we examined the acute cognition enhancing effects of vardenafil, a PDE5 inhibitor, which stimulates protein kinase G/CREB signaling in cells, in three different groups of male Wistar rats tested in an object recognition task (ORT). Vardenafil Dihydrochloride 75-85 phosphodiesterase 5A Homo sapiens 89-93 25372140-3 2014 In the present study, we examined the acute cognition enhancing effects of vardenafil, a PDE5 inhibitor, which stimulates protein kinase G/CREB signaling in cells, in three different groups of male Wistar rats tested in an object recognition task (ORT). Vardenafil Dihydrochloride 75-85 cAMP responsive element binding protein 1 Rattus norvegicus 139-143 25202655-3 2014 Augmenting the effect of NO in the renal medulla by the use of selective inhibitors of cyclic guanosine monophosphate (cGMP)-specific phosphadiesterase type 5 (PDE 5) such as sildenafil (Viagra ), vardenafil (Levitra ) or tadalafil (Cialis ) could reduce the severity of the hypoxic insult induced by the contrast medium and reduce the risk of CIN. Vardenafil Dihydrochloride 197-207 phosphodiesterase 5A Homo sapiens 160-165 25202655-3 2014 Augmenting the effect of NO in the renal medulla by the use of selective inhibitors of cyclic guanosine monophosphate (cGMP)-specific phosphadiesterase type 5 (PDE 5) such as sildenafil (Viagra ), vardenafil (Levitra ) or tadalafil (Cialis ) could reduce the severity of the hypoxic insult induced by the contrast medium and reduce the risk of CIN. Vardenafil Dihydrochloride 209-216 phosphodiesterase 5A Homo sapiens 160-165 24887326-10 2014 CONCLUSIONS: ABCB1 is associated with high-risk MB; hence, inhibition of ABCB1 by vardenafil may represent a valid approach in these patients. Vardenafil Dihydrochloride 82-92 ATP binding cassette subfamily B member 1 Homo sapiens 13-18 24887326-10 2014 CONCLUSIONS: ABCB1 is associated with high-risk MB; hence, inhibition of ABCB1 by vardenafil may represent a valid approach in these patients. Vardenafil Dihydrochloride 82-92 ATP binding cassette subfamily B member 1 Homo sapiens 73-78 24887326-7 2014 Inhibition of ABCB1 using vardenafil or verapamil resulted in a significant increase in sensitivity to etoposide in ABCB1-expressing MB cell lines. Vardenafil Dihydrochloride 26-36 ATP binding cassette subfamily B member 1 Homo sapiens 116-121 24940471-5 2014 To our knowledge, no study has reported cluster headaches triggered by the less commonly used PDE-5 inhibitors, namely vardenafil and tadalafil. Vardenafil Dihydrochloride 119-129 phosphodiesterase 5A Homo sapiens 94-99 24290227-8 2014 CONCLUSION: Among the different radiolabeled PDE5 inhibitors evaluated in this study, the vardenafil derivatives [(11)C]-7 and [(18)F]-11 are found to be promising tracers for in vivo visualization of PDE5. Vardenafil Dihydrochloride 90-100 phosphodiesterase 5A, cGMP-specific Mus musculus 45-49 24103790-5 2014 In recent years, ABCC10 inhibitors, including cepharanthine, lapatinib, erlotinib, nilotinib, imatinib, sildenafil, and vardenafil, have been reported to overcome ABCC10-mediated MDR. Vardenafil Dihydrochloride 120-130 ATP binding cassette subfamily C member 10 Homo sapiens 17-23 24103790-5 2014 In recent years, ABCC10 inhibitors, including cepharanthine, lapatinib, erlotinib, nilotinib, imatinib, sildenafil, and vardenafil, have been reported to overcome ABCC10-mediated MDR. Vardenafil Dihydrochloride 120-130 ATP binding cassette subfamily C member 10 Homo sapiens 163-169 24486698-11 2014 Also neutralization of TNFalpha with infliximab treatment fully normalized HFD-induced hypo-responsiveness to Ach, as well as responsiveness to vardenafil, a phosphodiesterase type 5 inhibitor. Vardenafil Dihydrochloride 144-154 tumor necrosis factor Oryctolagus cuniculus 23-31 24593781-3 2014 The protective efficacy of the selective PDE5 inhibitor vardenafil against mast-cell-mediated allergic reactions in murine models has been investigated. Vardenafil Dihydrochloride 56-66 phosphodiesterase 5A, cGMP-specific Mus musculus 41-45 24593781-9 2014 In conclusion, inhibition of PDE5 by vardenafil ameliorated immunologic and non-immunologic mast-cell-mediated allergic reactions and reduced histamine release, providing evidence for the potential anti-allergic properties of vardenafil. Vardenafil Dihydrochloride 37-47 phosphodiesterase 5A, cGMP-specific Mus musculus 29-33 24593781-9 2014 In conclusion, inhibition of PDE5 by vardenafil ameliorated immunologic and non-immunologic mast-cell-mediated allergic reactions and reduced histamine release, providing evidence for the potential anti-allergic properties of vardenafil. Vardenafil Dihydrochloride 226-236 phosphodiesterase 5A, cGMP-specific Mus musculus 29-33 24877179-9 2014 RESULTS: Treatment with nebivolol (1 muM) significantly potentiated sildenafil-, tadalafil- and vardenafil-induced relaxations of HCC and vasodilations of HPRA from both NEND and DMED. Vardenafil Dihydrochloride 96-106 latexin Homo sapiens 37-40 24270408-3 2014 We increased cGMP in the gut of Prkg2(+/+) and Prkg2(-/-) mice by treating with the PDE5 inhibitor Vardenafil (IP). Vardenafil Dihydrochloride 99-109 protein kinase, cGMP-dependent, type II Mus musculus 32-37 24270408-3 2014 We increased cGMP in the gut of Prkg2(+/+) and Prkg2(-/-) mice by treating with the PDE5 inhibitor Vardenafil (IP). Vardenafil Dihydrochloride 99-109 protein kinase, cGMP-dependent, type II Mus musculus 47-52 24270408-3 2014 We increased cGMP in the gut of Prkg2(+/+) and Prkg2(-/-) mice by treating with the PDE5 inhibitor Vardenafil (IP). Vardenafil Dihydrochloride 99-109 phosphodiesterase 5A, cGMP-specific Mus musculus 84-88 24270408-5 2014 Vardenafil (Vard) treatment increased cGMP in colon mucosa of all mice, but reduced proliferation and apoptosis, and increased differentiation only in Prkg2(+/+) mice. Vardenafil Dihydrochloride 0-10 protein kinase, cGMP-dependent, type II Mus musculus 151-156 24290227-8 2014 CONCLUSION: Among the different radiolabeled PDE5 inhibitors evaluated in this study, the vardenafil derivatives [(11)C]-7 and [(18)F]-11 are found to be promising tracers for in vivo visualization of PDE5. Vardenafil Dihydrochloride 90-100 phosphodiesterase 5A, cGMP-specific Mus musculus 201-205 24204804-0 2013 Correction of chloride transport and mislocalization of CFTR protein by vardenafil in the gastrointestinal tract of cystic fibrosis mice. Vardenafil Dihydrochloride 72-82 cystic fibrosis transmembrane conductance regulator Mus musculus 56-60 23721687-2 2014 PDE-5 inhibitors, namely sildenafil, tadalafil and vardenafil, and their unapproved designer analogues are being increasingly used as adulterants in the herbal products and health supplements marketed for sexual performance enhancement. Vardenafil Dihydrochloride 51-61 phosphodiesterase 5A Homo sapiens 0-5 24180640-1 2013 Great attention has been paid to the clinical significance of phosphodiesterase 5 (PDE5) inhibitors, such as sildenafil, tadalafil, and vardenafil widely used for erectile dysfunction. Vardenafil Dihydrochloride 136-146 phosphodiesterase 5A Homo sapiens 83-87 24180640-1 2013 Great attention has been paid to the clinical significance of phosphodiesterase 5 (PDE5) inhibitors, such as sildenafil, tadalafil, and vardenafil widely used for erectile dysfunction. Vardenafil Dihydrochloride 136-146 phosphodiesterase 5A Homo sapiens 62-81 24204804-3 2013 Using F508del-CF mice, we examined the transrectal potential difference 1 hour after intraperitoneal injection of the PDE5 inhibitor vardenafil or saline to assess the amiloride-sensitive sodium transport and the chloride gradient and forskolin-dependent chloride transport across the GI tract. Vardenafil Dihydrochloride 133-143 phosphodiesterase 5A, cGMP-specific Mus musculus 118-122 24204804-10 2013 Vardenafil increased the peak of intensity of the fluorescence CFTR signal in F508del-CF mice and displaced it towards the apical cell compartment. Vardenafil Dihydrochloride 0-10 cystic fibrosis transmembrane conductance regulator Mus musculus 63-67 24204804-12 2013 From our data we conclude that vardenafil mediates potentiation of the CFTR chloride channel and corrects mislocalization of the mutant protein. Vardenafil Dihydrochloride 31-41 cystic fibrosis transmembrane conductance regulator Mus musculus 71-75 23917809-6 2013 Subsequently, two more PDE 5 inhibitors (vardenafil and tadalafil) were developed and approved by the Food and Drug Administration (FDA) for the treatment of ED. Vardenafil Dihydrochloride 41-51 phosphodiesterase 5A Homo sapiens 23-28 23850358-4 2013 To this aim, the effects of Sildenafil (10mg/kg) or Vardenafil (2mg/kg) (t.i.w., for 5 weeks) were observed in CD1 subordinate male mice in a low aggression and social subordination context. Vardenafil Dihydrochloride 52-62 CD1 antigen complex Mus musculus 111-114 23765639-6 2013 METHODS: Evaluation of the effect of tadalafil and vardenafil on secretion of interleukin 8 (IL-8, a surrogate marker of prostate inflammation) by human myofibroblast prostatic cells (hBPH) exposed to different inflammatory stimuli. Vardenafil Dihydrochloride 51-61 C-X-C motif chemokine ligand 8 Homo sapiens 78-91 26558086-2 2013 Currently, three PDE5 inhibitors are widely available clinically, i.e., sildenafil, vardenafil and tadalafil. Vardenafil Dihydrochloride 84-94 phosphodiesterase 5A Homo sapiens 17-21 23765639-8 2013 RESULTS: In vitro treatment with tadalafil or vardenafil on hBPH reduced IL-8 secretion induced by either TNFalpha or metabolic factors, including oxidized low-density lipoprotein, oxLDL, to the same extent as a PDE5-insensitive PKG agonist Sp-8-Br-PET-cGMP. Vardenafil Dihydrochloride 46-56 C-X-C motif chemokine ligand 8 Homo sapiens 73-77 23765639-8 2013 RESULTS: In vitro treatment with tadalafil or vardenafil on hBPH reduced IL-8 secretion induced by either TNFalpha or metabolic factors, including oxidized low-density lipoprotein, oxLDL, to the same extent as a PDE5-insensitive PKG agonist Sp-8-Br-PET-cGMP. Vardenafil Dihydrochloride 46-56 tumor necrosis factor Homo sapiens 106-114 23765639-8 2013 RESULTS: In vitro treatment with tadalafil or vardenafil on hBPH reduced IL-8 secretion induced by either TNFalpha or metabolic factors, including oxidized low-density lipoprotein, oxLDL, to the same extent as a PDE5-insensitive PKG agonist Sp-8-Br-PET-cGMP. Vardenafil Dihydrochloride 46-56 phosphodiesterase 5A Homo sapiens 212-216 23765639-8 2013 RESULTS: In vitro treatment with tadalafil or vardenafil on hBPH reduced IL-8 secretion induced by either TNFalpha or metabolic factors, including oxidized low-density lipoprotein, oxLDL, to the same extent as a PDE5-insensitive PKG agonist Sp-8-Br-PET-cGMP. Vardenafil Dihydrochloride 46-56 protein kinase cGMP-dependent 1 Homo sapiens 229-232 23765639-10 2013 Treatment with tadalafil or vardenafil significantly suppressed oxLDL receptor (LOX-1) expression. Vardenafil Dihydrochloride 28-38 oxidized low density lipoprotein receptor 1 Homo sapiens 80-85 23765639-13 2013 In the MetS cohort there was a significant lower CD45 score in the vardenafil-arm versus the placebo-one. Vardenafil Dihydrochloride 67-77 protein tyrosine phosphatase receptor type C Homo sapiens 49-53 23623933-11 2013 In the hypochlorite groups immunohistochemical analysis showed enhanced poly(ADP-ribose)-formation and nuclear translocation of AIF, which were prevented by vardenafil-pretreatment. Vardenafil Dihydrochloride 157-167 apoptosis inducing factor, mitochondria associated 1 Rattus norvegicus 128-131 23203993-9 2013 Vardenafil treatment resulted in preserved podocyte cGMP levels, less proteinuria, reduced renal TGF-beta1 expression, desmin immunostaining in podocytes and restored both nephrin and podocin mRNA expression. Vardenafil Dihydrochloride 0-10 transforming growth factor, beta 1 Rattus norvegicus 97-106 23203993-9 2013 Vardenafil treatment resulted in preserved podocyte cGMP levels, less proteinuria, reduced renal TGF-beta1 expression, desmin immunostaining in podocytes and restored both nephrin and podocin mRNA expression. Vardenafil Dihydrochloride 0-10 NPHS1 adhesion molecule, nephrin Rattus norvegicus 172-179 23203993-9 2013 Vardenafil treatment resulted in preserved podocyte cGMP levels, less proteinuria, reduced renal TGF-beta1 expression, desmin immunostaining in podocytes and restored both nephrin and podocin mRNA expression. Vardenafil Dihydrochloride 0-10 NPHS2 stomatin family member, podocin Rattus norvegicus 184-191 23372609-1 2013 Orally active, selective inhibitors of phosphodiesterase type 5 (PDE 5, cyclic GMP PDE), such as sildenafil, tadalafil and vardenafil, are currently the first-choice treatment options for the clinical management of erectile dysfunction (ED) of various etiologies and severities. Vardenafil Dihydrochloride 123-133 phosphodiesterase 5A Homo sapiens 39-63 23421435-14 2013 BAY 60-4552 and vardenafil have synergistic effects on relaxation of HCC of PDE5-i nonresponders. Vardenafil Dihydrochloride 16-26 phosphodiesterase 5A Homo sapiens 76-80 23421435-16 2013 CONCLUSION: Despite downregulation of the NO/cGMP/PKG pathway, combining BAY 60-4552 with vardenafil significantly enhanced relaxation HCC strips of PDE5-i nonresponders. Vardenafil Dihydrochloride 90-100 phosphodiesterase 5A Homo sapiens 149-153 23369145-5 2013 On the other hand, growing evidence suggests that PDE 5 inhibitors (vardenafil, tadalafil and sildenafil) seem to better satisfy the needs of NYHA HF I- II class men suffering from ED. Vardenafil Dihydrochloride 68-78 phosphodiesterase 5A Homo sapiens 50-55 23386068-9 2013 The available PDE-5 inhibitors (sildenafil, tadalafil, and vardenafil) have shown efficacy in the treatment of LUTS in several randomized controlled trials in men with and without concomitant ED. Vardenafil Dihydrochloride 59-69 phosphodiesterase 5A Homo sapiens 14-19 23656343-3 2013 PDE inhibitors, in particular the PDE5 (cyclic GMP PDE) inhibitors avanafil, lodenafil, sildenafil, tadalafil, udenafil and vardenafil, are regarded as efficacious, having a fast onset of drug action and an improved effect-to-adverse event ratio, combining a high response rate with the advantage of an on-demand intake. Vardenafil Dihydrochloride 124-134 phosphodiesterase 5A Homo sapiens 34-38 23372609-1 2013 Orally active, selective inhibitors of phosphodiesterase type 5 (PDE 5, cyclic GMP PDE), such as sildenafil, tadalafil and vardenafil, are currently the first-choice treatment options for the clinical management of erectile dysfunction (ED) of various etiologies and severities. Vardenafil Dihydrochloride 123-133 phosphodiesterase 5A Homo sapiens 65-70 22855271-0 2013 The PDE5 inhibitor vardenafil does not affect auditory sensory gating in rats and humans. Vardenafil Dihydrochloride 19-29 phosphodiesterase 5A Homo sapiens 4-8 23348740-7 2013 Vardenafil, a PDE5 inhibitor that is used to treat erectile dysfunction, significantly potentiated the EGCG-activated 67LR-dependent apoptosis without affecting normal cells and prolonged the survival time in a mouse xenograft model. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A, cGMP-specific Mus musculus 14-18 23348740-7 2013 Vardenafil, a PDE5 inhibitor that is used to treat erectile dysfunction, significantly potentiated the EGCG-activated 67LR-dependent apoptosis without affecting normal cells and prolonged the survival time in a mouse xenograft model. Vardenafil Dihydrochloride 0-10 ribosomal protein SA Mus musculus 118-122 23417046-1 2013 Phosphodiesterase-5 (PDE5) inhibitors, such as sildenafil, tadalafil and vardenafil are first line treatment for erectile dysfunction (ED). Vardenafil Dihydrochloride 73-83 phosphodiesterase 5A Homo sapiens 0-19 23417046-1 2013 Phosphodiesterase-5 (PDE5) inhibitors, such as sildenafil, tadalafil and vardenafil are first line treatment for erectile dysfunction (ED). Vardenafil Dihydrochloride 73-83 phosphodiesterase 5A Homo sapiens 21-25 22855271-6 2013 METHODS: In the rat study, vehicle or 0.3-3 mg/kg of the PDE5-I vardenafil was given orally 30 min before testing and electrode locations were the vertex, hippocampus and the striatum. Vardenafil Dihydrochloride 64-74 phosphodiesterase 5A Homo sapiens 57-61 22515706-7 2012 There was a correlation between the plasma concentrations of vardenafil and change in mPAP (r = -0.579, P = 0.019) and between vardenafil concentrations and change in PVR (r = -0.662, P = 0.005). Vardenafil Dihydrochloride 61-71 phospholipid phosphatase 1 Mus musculus 86-90 22515706-8 2012 CONCLUSIONS: Vardenafil causes rapid changes in cardiopulmonary haemodynamics and there is a correlation between plasma vardenafil drug concentration and the acute changes in mPAP as well as PVR in patients with PH. Vardenafil Dihydrochloride 13-23 phospholipid phosphatase 1 Mus musculus 175-179 22515706-8 2012 CONCLUSIONS: Vardenafil causes rapid changes in cardiopulmonary haemodynamics and there is a correlation between plasma vardenafil drug concentration and the acute changes in mPAP as well as PVR in patients with PH. Vardenafil Dihydrochloride 13-23 PVR cell adhesion molecule Homo sapiens 191-194 22515706-8 2012 CONCLUSIONS: Vardenafil causes rapid changes in cardiopulmonary haemodynamics and there is a correlation between plasma vardenafil drug concentration and the acute changes in mPAP as well as PVR in patients with PH. Vardenafil Dihydrochloride 120-130 phospholipid phosphatase 1 Mus musculus 175-179 22515706-8 2012 CONCLUSIONS: Vardenafil causes rapid changes in cardiopulmonary haemodynamics and there is a correlation between plasma vardenafil drug concentration and the acute changes in mPAP as well as PVR in patients with PH. Vardenafil Dihydrochloride 120-130 PVR cell adhesion molecule Homo sapiens 191-194 22948216-6 2012 Enhancement of nitric oxide/cyclic guanosine monophosphate signaling by vardenafil, sodium nitroprusside, or PDE5 knockdown reduced smooth muscle cell actin and IGF binding protein 3 mRNA and protein levels and restored fibroblast-like morphology in trans-differentiated myofibroblast. Vardenafil Dihydrochloride 72-82 insulin like growth factor binding protein 3 Homo sapiens 161-182 22948216-2 2012 Because BPH is primarily driven by fibroblast-to-myofibroblast trans-differentiation, this study aimed to evaluate the potential of the PDE5 inhibitor vardenafil to inhibit and reverse trans-differentiation of primary human prostatic stromal cells (PrSC). Vardenafil Dihydrochloride 151-161 phosphodiesterase 5A Homo sapiens 136-140 22948216-7 2012 This reversal of trans-differentiation was not affected by MAPK kinase, protein kinase G, RhoA, or RhoA/Rho kinase inhibition, but vardenafil attenuated phospho-AKT levels in myofibroblasts. Vardenafil Dihydrochloride 131-141 AKT serine/threonine kinase 1 Homo sapiens 161-164 22948216-5 2012 Vardenafil significantly attenuated TGFbeta1-induced PrSC trans-differentiation in vitro and in chorioallantoic membrane xenografts. Vardenafil Dihydrochloride 0-10 transforming growth factor beta 1 Homo sapiens 36-44 22948216-10 2012 Thus, enhancement of the nitric oxide/cyclic guanosine monophosphate signaling pathway by vardenafil attenuates and reverts fibroblast-to-myofibroblast trans-differentiation, hypothesizing that BPH patients might benefit from long-term therapy with PDE5 inhibitors. Vardenafil Dihydrochloride 90-100 phosphodiesterase 5A Homo sapiens 249-253 21546099-6 2012 RESULTS: Patients who took daily vardenafil (vs. on-demand) reported significant (P<0.01) improvements in arterial stiffness as evaluated by AI and reduction of plasma ADM levels (p<0.05) but no improvement in average RH. Vardenafil Dihydrochloride 33-43 adrenomedullin Homo sapiens 171-174 23024633-4 2012 We demonstrated, by measuring transepithelial nasal potential difference in F508del mice following intraperitoneal injection of sildenafil, vardenafil, or taladafil at clinical doses are able to restore the decreased CFTR-dependent chloride transport across the nasal mucosa. Vardenafil Dihydrochloride 140-150 cystic fibrosis transmembrane conductance regulator Mus musculus 217-221 23024633-5 2012 Moreover, vardenafil, but not sildenafil, stimulates chloride transport through the normal CFTR protein. Vardenafil Dihydrochloride 10-20 cystic fibrosis transmembrane conductance regulator Mus musculus 91-95 23024633-8 2012 More recently, we analyzed the bronchoalveolar lavage of CF and wild-type mice for cell infiltrates and expression of pro-inflammatory cytokines and chemokines; we found that the CFTR activating effect of vardenafil, selected as a representative long-lasting PDE5 inhibitor, breaks the vicious circle of lung inflammation which plays a major role in morbi-mortality in CF. Vardenafil Dihydrochloride 205-215 cystic fibrosis transmembrane conductance regulator Mus musculus 179-183 23024633-8 2012 More recently, we analyzed the bronchoalveolar lavage of CF and wild-type mice for cell infiltrates and expression of pro-inflammatory cytokines and chemokines; we found that the CFTR activating effect of vardenafil, selected as a representative long-lasting PDE5 inhibitor, breaks the vicious circle of lung inflammation which plays a major role in morbi-mortality in CF. Vardenafil Dihydrochloride 205-215 phosphodiesterase 5A, cGMP-specific Mus musculus 259-263 22775210-1 2012 OBJECTIVES: We aimed to characterize the efflux transport properties of vardenafil and sildenafil, and to compare the kinetics of these compounds via efflux transporters such as P-gp, BCRP and MRP2. Vardenafil Dihydrochloride 72-82 phosphoglycolate phosphatase Homo sapiens 178-182 22578167-0 2012 PDE5 inhibitors, sildenafil and vardenafil, reverse multidrug resistance by inhibiting the efflux function of multidrug resistance protein 7 (ATP-binding Cassette C10) transporter. Vardenafil Dihydrochloride 32-42 ATP binding cassette subfamily C member 10 Homo sapiens 110-140 22578167-0 2012 PDE5 inhibitors, sildenafil and vardenafil, reverse multidrug resistance by inhibiting the efflux function of multidrug resistance protein 7 (ATP-binding Cassette C10) transporter. Vardenafil Dihydrochloride 32-42 homeobox C10 Homo sapiens 163-166 22578167-3 2012 Previously, we had shown that sildenafil, vardenafil and tadalafil could reverse P-glycoprotein (ATP-binding cassette B1)-mediated MDR. Vardenafil Dihydrochloride 42-52 ATP binding cassette subfamily B member 1 Homo sapiens 81-95 22578167-5 2012 We found that sildenafil and vardenafil dose-dependently enhanced the sensitivity of MRP7-transfected HEK293 cells to paclitaxel, docetaxel and vinblastine, while tadalafil had only a minimal effect. Vardenafil Dihydrochloride 29-39 ATP binding cassette subfamily C member 10 Homo sapiens 85-89 22578167-6 2012 Accumulation and efflux experiments demonstrated that sildenafil and vardenafil increased the intracellular accumulation of [(3)H]-paclitaxel by inhibiting the efflux of [(3 H]-paclitaxel in HEK/MRP7 cells. Vardenafil Dihydrochloride 69-79 ATP binding cassette subfamily C member 10 Homo sapiens 195-199 22578167-8 2012 These results demonstrate that sildenafil and vardenafil reverse MRP7-mediated a MDR through inhibition of the drug efflux function of MRP7. Vardenafil Dihydrochloride 46-56 ATP binding cassette subfamily C member 10 Homo sapiens 65-69 22578167-8 2012 These results demonstrate that sildenafil and vardenafil reverse MRP7-mediated a MDR through inhibition of the drug efflux function of MRP7. Vardenafil Dihydrochloride 46-56 ATP binding cassette subfamily C member 10 Homo sapiens 135-139 22441938-3 2012 We found that PDE5 inhibitor (sildenafil or vardenafil) and the cGMP analog 8-CPT-cGMP stimulated CREB phosphorylation, leading to increased tyrosinase expression and melanin synthesis, which was counteracted by KT5823, a selective cGMP-dependent protein kinase (PKG) inhibitor. Vardenafil Dihydrochloride 44-54 phosphodiesterase 5A, cGMP-specific Mus musculus 14-18 22441938-3 2012 We found that PDE5 inhibitor (sildenafil or vardenafil) and the cGMP analog 8-CPT-cGMP stimulated CREB phosphorylation, leading to increased tyrosinase expression and melanin synthesis, which was counteracted by KT5823, a selective cGMP-dependent protein kinase (PKG) inhibitor. Vardenafil Dihydrochloride 44-54 cAMP responsive element binding protein 1 Mus musculus 98-102 22441938-3 2012 We found that PDE5 inhibitor (sildenafil or vardenafil) and the cGMP analog 8-CPT-cGMP stimulated CREB phosphorylation, leading to increased tyrosinase expression and melanin synthesis, which was counteracted by KT5823, a selective cGMP-dependent protein kinase (PKG) inhibitor. Vardenafil Dihydrochloride 44-54 tyrosinase Mus musculus 141-151 22947364-6 2012 Two more PDE-5 inhibitors are now US Food and Drug Administration-approved (vardenafil and tadalafil) for the treatment of erectile dysfunction. Vardenafil Dihydrochloride 76-86 phosphodiesterase 5A Homo sapiens 9-14 22775210-1 2012 OBJECTIVES: We aimed to characterize the efflux transport properties of vardenafil and sildenafil, and to compare the kinetics of these compounds via efflux transporters such as P-gp, BCRP and MRP2. Vardenafil Dihydrochloride 72-82 BCR pseudogene 1 Homo sapiens 184-188 22775210-1 2012 OBJECTIVES: We aimed to characterize the efflux transport properties of vardenafil and sildenafil, and to compare the kinetics of these compounds via efflux transporters such as P-gp, BCRP and MRP2. Vardenafil Dihydrochloride 72-82 ATP binding cassette subfamily C member 2 Homo sapiens 193-197 22775210-3 2012 KEY FINDINGS: Vardenafil had a much greater basal-to-apical than apical-to-basal transport rate in MDCKII cells overexpressing P-gp, BCRP and MRP2. Vardenafil Dihydrochloride 14-24 PGP Canis lupus familiaris 127-131 22775210-3 2012 KEY FINDINGS: Vardenafil had a much greater basal-to-apical than apical-to-basal transport rate in MDCKII cells overexpressing P-gp, BCRP and MRP2. Vardenafil Dihydrochloride 14-24 ATP binding cassette subfamily G member 2 Canis lupus familiaris 133-137 22775210-3 2012 KEY FINDINGS: Vardenafil had a much greater basal-to-apical than apical-to-basal transport rate in MDCKII cells overexpressing P-gp, BCRP and MRP2. Vardenafil Dihydrochloride 14-24 ATP binding cassette subfamily C member 2 Canis lupus familiaris 142-146 22775210-5 2012 Consequently, the absorptive transport of vardenafil and sildenafil in Caco-2 cells increased linearly over the concentration range of 1-100 microm, whereas the secretory transport of these drugs was saturable and inhibited by the presence of specific inhibitors of P-gp and BCRP. Vardenafil Dihydrochloride 42-52 phosphoglycolate phosphatase Homo sapiens 266-270 22775210-5 2012 Consequently, the absorptive transport of vardenafil and sildenafil in Caco-2 cells increased linearly over the concentration range of 1-100 microm, whereas the secretory transport of these drugs was saturable and inhibited by the presence of specific inhibitors of P-gp and BCRP. Vardenafil Dihydrochloride 42-52 BCR pseudogene 1 Homo sapiens 275-279 22775210-6 2012 MK571, a representative MRP2 inhibitor, inhibited the basal-to-apical transport of vardenafil, but not of sildenafil. Vardenafil Dihydrochloride 83-93 ATP binding cassette subfamily C member 2 Homo sapiens 24-28 22775210-7 2012 CONCLUSION: The involvement of P-gp, BCRP and MRP2 for vardenafil and the involvement of P-gp and BCRP for sildenafil in the secretory transport with linear absorptive transport may contribute to the limited intestinal absorption of these drugs. Vardenafil Dihydrochloride 55-65 phosphoglycolate phosphatase Homo sapiens 31-35 22775210-7 2012 CONCLUSION: The involvement of P-gp, BCRP and MRP2 for vardenafil and the involvement of P-gp and BCRP for sildenafil in the secretory transport with linear absorptive transport may contribute to the limited intestinal absorption of these drugs. Vardenafil Dihydrochloride 55-65 BCR pseudogene 1 Homo sapiens 37-41 22775210-7 2012 CONCLUSION: The involvement of P-gp, BCRP and MRP2 for vardenafil and the involvement of P-gp and BCRP for sildenafil in the secretory transport with linear absorptive transport may contribute to the limited intestinal absorption of these drugs. Vardenafil Dihydrochloride 55-65 ATP binding cassette subfamily C member 2 Homo sapiens 46-50 22503062-6 2012 Vardenafil globally attenuated inflammatory responses in both genotypes however reduction of macrophage infiltration, macrophage chemoattractant chemokine and interleukin-1beta was observed in the CF group only. Vardenafil Dihydrochloride 0-10 interleukin 1 beta Mus musculus 159-176 21890489-7 2012 Phosphodiesterase 5 inhibitors (sildenafil, vardenafil, and tadalafil) require at least a residual nNOS activity for their action. Vardenafil Dihydrochloride 44-54 nitric oxide synthase 1 Homo sapiens 99-103 22707162-1 2012 Recent publications on pharmaceutical monitoring are increasingly covering the field of illicit drugs and lately the forensic evaluation of designing illegal analogs of lifestyle drugs like the phosphodiesterase type 5 (PDE-5) inhibitors Viagra (sildenafil), Levitra (vardenafil) and Cialis (tadalafil). Vardenafil Dihydrochloride 268-278 phosphodiesterase 5A Homo sapiens 220-225 21793866-1 2012 We evaluated the effects of vardenafil on testicular androgen-binding protein secretion (ABP). Vardenafil Dihydrochloride 28-38 sex hormone binding globulin Homo sapiens 53-87 21793866-7 2012 Men of groups A1, B1 and B2 were treated with vardenafil, vardenafil and L-carnitine respectively. Vardenafil Dihydrochloride 46-56 BCL2 related protein A1 Homo sapiens 14-27 21793866-9 2012 Within the group A1 and within the group B1, ABP secretion rate was significantly larger after vardenafil treatment than prior to vardenafil treatment. Vardenafil Dihydrochloride 95-105 sex hormone binding globulin Homo sapiens 45-48 21793866-9 2012 Within the group A1 and within the group B1, ABP secretion rate was significantly larger after vardenafil treatment than prior to vardenafil treatment. Vardenafil Dihydrochloride 130-140 sex hormone binding globulin Homo sapiens 45-48 21793866-11 2012 Vardenafil administration in NOA-men increased ABP secretion and did not affect detrimentally the presence of testicular foci of advanced spermatogenesis. Vardenafil Dihydrochloride 0-10 sex hormone binding globulin Homo sapiens 47-50 21950284-1 2012 Vardenafil hydrochloride (HCl) is a potent and selective phosphodiesterase type-5 (PDE-5) inhibitor that enhances nitric oxide (NO)-mediated relaxation of human corpus cavernosum and NO-induced rabbit penile erection, and enhances erectile function in patients. Vardenafil Dihydrochloride 0-24 phosphodiesterase 5A Homo sapiens 57-81 21950284-1 2012 Vardenafil hydrochloride (HCl) is a potent and selective phosphodiesterase type-5 (PDE-5) inhibitor that enhances nitric oxide (NO)-mediated relaxation of human corpus cavernosum and NO-induced rabbit penile erection, and enhances erectile function in patients. Vardenafil Dihydrochloride 0-24 phosphodiesterase 5A Homo sapiens 83-88 22707162-1 2012 Recent publications on pharmaceutical monitoring are increasingly covering the field of illicit drugs and lately the forensic evaluation of designing illegal analogs of lifestyle drugs like the phosphodiesterase type 5 (PDE-5) inhibitors Viagra (sildenafil), Levitra (vardenafil) and Cialis (tadalafil). Vardenafil Dihydrochloride 268-278 phosphodiesterase 5A Homo sapiens 194-218 21950284-2 2012 In the present study, the effect of vardenafil on nitric oxide synthase (NOS) and neuronal NOS expressions in the paraventricular nucleus (PVN) of rats without sexual stimulation was investigated using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry and neuronal NOS (nNOS) immunohistochemistry and western blot analysis. Vardenafil Dihydrochloride 36-46 nitric oxide synthase 1 Rattus norvegicus 82-94 21950284-3 2012 The present results showed that NOS and nNOS expression in the PVN was increased by vardenafil treatment as the dose- and duration-dependently without sexual stimulation. Vardenafil Dihydrochloride 84-94 nitric oxide synthase 1 Rattus norvegicus 40-44 21950284-4 2012 The phosphodiesterase type-5 inhibitor, vardenafil, augmented NOS expression in the brain without sexual stimulation. Vardenafil Dihydrochloride 40-50 phosphodiesterase 5A Rattus norvegicus 4-28 22462626-3 2012 AIM: To evaluate the effect of vardenafil, a PDE5 inhibitor, dose escalation on recovery of EF after unilateral nsRP. Vardenafil Dihydrochloride 31-41 phosphodiesterase 5A Homo sapiens 45-49 22649315-2 2012 Therefore, we aimed to examine effects of vardenafil, a PDE-5 inhibitor, on the pulmonary arteries isolated from rats with monocrotaline- (MCT-) induced pulmonary hypertension. Vardenafil Dihydrochloride 42-52 phosphodiesterase 5A Rattus norvegicus 56-61 22270721-5 2012 Treatment of rats and wild-type mice with the Pde5 inhibitor vardenafil almost completely prevented NIHL and caused a Prkg1-dependent upregulation of poly (ADP-ribose) in hair cells and the spiral ganglion, suggesting an endogenous protective cGMP-Prkg1 signaling pathway that culminates in the activation of poly (ADP-ribose) polymerase. Vardenafil Dihydrochloride 61-71 phosphodiesterase 5A, cGMP-specific Mus musculus 46-50 22270721-5 2012 Treatment of rats and wild-type mice with the Pde5 inhibitor vardenafil almost completely prevented NIHL and caused a Prkg1-dependent upregulation of poly (ADP-ribose) in hair cells and the spiral ganglion, suggesting an endogenous protective cGMP-Prkg1 signaling pathway that culminates in the activation of poly (ADP-ribose) polymerase. Vardenafil Dihydrochloride 61-71 protein kinase, cGMP-dependent, type I Mus musculus 118-123 22270721-5 2012 Treatment of rats and wild-type mice with the Pde5 inhibitor vardenafil almost completely prevented NIHL and caused a Prkg1-dependent upregulation of poly (ADP-ribose) in hair cells and the spiral ganglion, suggesting an endogenous protective cGMP-Prkg1 signaling pathway that culminates in the activation of poly (ADP-ribose) polymerase. Vardenafil Dihydrochloride 61-71 protein kinase, cGMP-dependent, type I Mus musculus 248-253 22270721-5 2012 Treatment of rats and wild-type mice with the Pde5 inhibitor vardenafil almost completely prevented NIHL and caused a Prkg1-dependent upregulation of poly (ADP-ribose) in hair cells and the spiral ganglion, suggesting an endogenous protective cGMP-Prkg1 signaling pathway that culminates in the activation of poly (ADP-ribose) polymerase. Vardenafil Dihydrochloride 61-71 poly (ADP-ribose) polymerase family, member 1 Mus musculus 309-337 22156704-2 2012 MATERIALS AND METHODS: We present a review of the literature and 2 cases of CSC in 2 men taking PDE5 inhibitors (vardenafil and tadalafil) for erectile dysfunction. Vardenafil Dihydrochloride 113-123 phosphodiesterase 5A Homo sapiens 96-100 22156704-8 2012 CONCLUSION: The 2 presented cases of CSC after intake of vardenafil or tadalafil with positive dechallenge, rechallenge and second dechallenge reactions provide important arguments for considering CSC as a rare PDE5 inhibitor class-specific side effect. Vardenafil Dihydrochloride 57-67 phosphodiesterase 5A Homo sapiens 211-215 22304626-3 2012 AIM: An up-to-date review on oral phosphodiesterase 5 inhibitors (PDE5): sildenafil, tadalafil, and vardenafil for individuals with CND and ED. Vardenafil Dihydrochloride 102-112 phosphodiesterase 5A Homo sapiens 68-72 21552528-9 2011 In addition, vardenafil significantly stimulated the ATPase activity of ABCB1 and inhibited the photolabeling of ABCB1 with [(125)I]-IAAP. Vardenafil Dihydrochloride 13-23 ATP binding cassette subfamily B member 1 Homo sapiens 72-77 22234177-5 2011 METHODS AND MEASUREMENTS: Cultured human omental AT was stimulated with PDE-5 inhibitor, vardenafil, at different concentration for 24 and 72 h. Analysis of the expression of both key-regulator genes of adipocyte metabolism and mitochondria-biogenesis markers was performed. Vardenafil Dihydrochloride 89-99 phosphodiesterase 5A Homo sapiens 72-77 22234177-6 2011 RESULTS: We found an increased gene expression of peroxisome proliferator-activated receptor-gamma (PPAR-gamma), adiponectin, and proliferator- activated receptor gamma coactivator-1 alpha (PGC-1alpha) after a 24-h stimulation with vardenafil at the lowest concentration employed compared to controls (p<0.05). Vardenafil Dihydrochloride 232-242 peroxisome proliferator activated receptor gamma Homo sapiens 50-98 22234177-6 2011 RESULTS: We found an increased gene expression of peroxisome proliferator-activated receptor-gamma (PPAR-gamma), adiponectin, and proliferator- activated receptor gamma coactivator-1 alpha (PGC-1alpha) after a 24-h stimulation with vardenafil at the lowest concentration employed compared to controls (p<0.05). Vardenafil Dihydrochloride 232-242 PPARG coactivator 1 alpha Homo sapiens 190-200 21771280-3 2011 Sildenafil (Viagra(R)), tadalafil (Cialis(R)), and vardenafil (Levitra(R)) are from the same class of drugs that inhibit PDE5. Vardenafil Dihydrochloride 51-61 phosphodiesterase 5A Homo sapiens 121-125 21771281-10 2011 Vardenafil was statistically significantly superior to placebo for all primary efficacy measures (P < 0.0001) and showed nominally statistically significant superiority compared with placebo for SEP1/ejaculation success rates (P = 0.0003 and P < 0.0001, respectively) and the percentage of subjects reporting "return-to-normal" erectile function (P = 0.0004). Vardenafil Dihydrochloride 0-10 septin 1 Homo sapiens 198-202 21460862-7 2011 We found reports on five kinds of PDE-5 inhibitors for the management of ED: sildenafil, vardenafil, tadalafil, udenafil and mirodenafil. Vardenafil Dihydrochloride 89-99 phosphodiesterase 5A Homo sapiens 34-39 21735661-1 2011 Phosphodiesterase type 5 (PDE5) inhibitors, sildenafil, tadalafil and vardenafil, are the first-line drugs for the treatment of erectile dysfunction (ED). Vardenafil Dihydrochloride 70-80 phosphodiesterase 5A Homo sapiens 26-30 21552528-0 2011 The phosphodiesterase-5 inhibitor vardenafil is a potent inhibitor of ABCB1/P-glycoprotein transporter. Vardenafil Dihydrochloride 34-44 ATP binding cassette subfamily B member 1 Homo sapiens 70-75 21552528-0 2011 The phosphodiesterase-5 inhibitor vardenafil is a potent inhibitor of ABCB1/P-glycoprotein transporter. Vardenafil Dihydrochloride 34-44 ATP binding cassette subfamily B member 1 Homo sapiens 76-90 21552528-2 2011 Previously, through the use of an extensive screening process, we found that vardenafil, a phosphodiesterase 5 (PDE-5) inhibitor significantly reverses MDR in ABCB1 overexpressing cancer cells, and its efficacy was greater than that of tadalafil, another PDE-5 inhibitor. Vardenafil Dihydrochloride 77-87 phosphodiesterase 5A Homo sapiens 91-110 21552528-2 2011 Previously, through the use of an extensive screening process, we found that vardenafil, a phosphodiesterase 5 (PDE-5) inhibitor significantly reverses MDR in ABCB1 overexpressing cancer cells, and its efficacy was greater than that of tadalafil, another PDE-5 inhibitor. Vardenafil Dihydrochloride 77-87 phosphodiesterase 5A Homo sapiens 112-117 21552528-2 2011 Previously, through the use of an extensive screening process, we found that vardenafil, a phosphodiesterase 5 (PDE-5) inhibitor significantly reverses MDR in ABCB1 overexpressing cancer cells, and its efficacy was greater than that of tadalafil, another PDE-5 inhibitor. Vardenafil Dihydrochloride 77-87 ATP binding cassette subfamily B member 1 Homo sapiens 159-164 21552528-2 2011 Previously, through the use of an extensive screening process, we found that vardenafil, a phosphodiesterase 5 (PDE-5) inhibitor significantly reverses MDR in ABCB1 overexpressing cancer cells, and its efficacy was greater than that of tadalafil, another PDE-5 inhibitor. Vardenafil Dihydrochloride 77-87 phosphodiesterase 5A Homo sapiens 255-260 21552528-5 2011 However, vardenafil when used in combination with anticancer substrates of ABCB1, significantly potentiated their cytotoxicity in ABCB1 overexpressing cells in a concentration-dependent manner, and this effect was greater than that of tadalafil. Vardenafil Dihydrochloride 9-19 ATP binding cassette subfamily B member 1 Homo sapiens 75-80 21552528-5 2011 However, vardenafil when used in combination with anticancer substrates of ABCB1, significantly potentiated their cytotoxicity in ABCB1 overexpressing cells in a concentration-dependent manner, and this effect was greater than that of tadalafil. Vardenafil Dihydrochloride 9-19 ATP binding cassette subfamily B member 1 Homo sapiens 130-135 21552528-7 2011 The differential effects of vardenafil and tadalafil appear to be specific for the ABCB1 transporter as both vardenafil and tadalafil had no significant effect on the reversal of drug resistance conferred by ABCC1 (MRP1) and ABCG2 (BCRP) transporters. Vardenafil Dihydrochloride 28-38 ATP binding cassette subfamily B member 1 Homo sapiens 83-88 21552528-8 2011 Vardenafil significantly increased the intracellular accumulation of [(3)H]-paclitaxel in the ABCB1 overexpressing KB-C2 cells. Vardenafil Dihydrochloride 0-10 ATP binding cassette subfamily B member 1 Homo sapiens 94-99 21995676-4 2011 Sildenafil, tadalafil, and vardenafil are the most widely used and studied PDE5 inhibitors. Vardenafil Dihydrochloride 27-37 phosphodiesterase 5A Homo sapiens 75-79 21934637-0 2011 The disposition of three phosphodiesterase type 5 inhibitors, vardenafil, sildenafil, and udenafil, is differently influenced by the CYP3A5 genotype. Vardenafil Dihydrochloride 62-72 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 133-139 21934637-3 2011 After each dose, plasma concentrations of the parents and their major metabolites were measured up to 24 or 48 h. RESULTS: The AUC( ) and C(max) of vardenafil were 2.9-fold and 3.1-fold higher in CYP3A5*3/*3 carriers than in individuals with CYP3A5*1/*1 (P=0.003 and 0.002, respectively). Vardenafil Dihydrochloride 148-158 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 196-202 21934637-3 2011 After each dose, plasma concentrations of the parents and their major metabolites were measured up to 24 or 48 h. RESULTS: The AUC( ) and C(max) of vardenafil were 2.9-fold and 3.1-fold higher in CYP3A5*3/*3 carriers than in individuals with CYP3A5*1/*1 (P=0.003 and 0.002, respectively). Vardenafil Dihydrochloride 148-158 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 242-248 21934637-7 2011 The CYP3A5*3 genotype affects the oral disposition of vardenafil significantly. Vardenafil Dihydrochloride 54-64 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 4-10 21839578-0 2011 Combination of BAY 60-4552 and vardenafil exerts proerectile facilitator effects in rats with cavernous nerve injury: a proof of concept study for the treatment of phosphodiesterase type 5 inhibitor failure. Vardenafil Dihydrochloride 31-41 phosphodiesterase 5A Rattus norvegicus 164-188 21839578-10 2011 CONCLUSIONS: The present study supports the concept that the combined administration of a sGC stimulator, BAY 60-4552, and vardenafil provides synergistic beneficial effects and might therefore salvage patients who experience treatment failures with PDE5 inhibitors after RP. Vardenafil Dihydrochloride 123-133 phosphodiesterase 5A Homo sapiens 250-254 21620965-3 2011 A preparation comprised mainly of Band 2 PDE5 was partially converted to Band 3 PDE5 by 1h incubation with cGMP or the PDE5-specific inhibitors sildenafil, vardenafil, or tadalafil, but not with cAMP, milrinone (PDE3-specific), or rolipram (PDE4-specific). Vardenafil Dihydrochloride 156-166 phosphodiesterase 5A Homo sapiens 41-45 21620965-3 2011 A preparation comprised mainly of Band 2 PDE5 was partially converted to Band 3 PDE5 by 1h incubation with cGMP or the PDE5-specific inhibitors sildenafil, vardenafil, or tadalafil, but not with cAMP, milrinone (PDE3-specific), or rolipram (PDE4-specific). Vardenafil Dihydrochloride 156-166 phosphodiesterase 5A Homo sapiens 80-84 21620965-3 2011 A preparation comprised mainly of Band 2 PDE5 was partially converted to Band 3 PDE5 by 1h incubation with cGMP or the PDE5-specific inhibitors sildenafil, vardenafil, or tadalafil, but not with cAMP, milrinone (PDE3-specific), or rolipram (PDE4-specific). Vardenafil Dihydrochloride 156-166 phosphodiesterase 5A Homo sapiens 80-84 21679304-11 2011 Least squares (LS) mean SEP3 overall success rates after 12 weeks of treatment were 9.5 (baseline) vs. 67.2 (week 12) and 12.4 (baseline) vs. 24.2 (week 12) in the vardenafil and placebo groups, respectively (P < 0.0001). Vardenafil Dihydrochloride 164-174 septin 3 Homo sapiens 24-28 20803229-0 2011 Vardenafil, an inhibitor of phosphodiesterase-5, blocks advanced glycation end product (AGE)-induced up-regulation of monocyte chemoattractant protein-1 mRNA levels in endothelial cells by suppressing AGE receptor (RAGE) expression via elevation of cGMP. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 28-47 20803229-0 2011 Vardenafil, an inhibitor of phosphodiesterase-5, blocks advanced glycation end product (AGE)-induced up-regulation of monocyte chemoattractant protein-1 mRNA levels in endothelial cells by suppressing AGE receptor (RAGE) expression via elevation of cGMP. Vardenafil Dihydrochloride 0-10 C-C motif chemokine ligand 2 Homo sapiens 118-152 20803229-0 2011 Vardenafil, an inhibitor of phosphodiesterase-5, blocks advanced glycation end product (AGE)-induced up-regulation of monocyte chemoattractant protein-1 mRNA levels in endothelial cells by suppressing AGE receptor (RAGE) expression via elevation of cGMP. Vardenafil Dihydrochloride 0-10 advanced glycosylation end-product specific receptor Homo sapiens 215-219 20803229-4 2011 Therefore, this study investigated whether and how vardenafil, an inhibitor of PDE-5, could block the deleterious effects of AGE on human umbilical vein endothelial cells (HUVEC). Vardenafil Dihydrochloride 51-61 phosphodiesterase 5A Homo sapiens 79-84 20803229-7 2011 AGE increased receptor for AGE (RAGE) mRNA and protein levels in HUVEC, both of which were significantly inhibited by the treatments with 30 nM vardenafil or 5 muM 8-Br-cGMP, an analogue of cGMP. Vardenafil Dihydrochloride 144-154 advanced glycosylation end-product specific receptor Homo sapiens 32-36 20803229-8 2011 Further, vardenafil reduced the AGE-induced ROS generation and subsequently inhibited up-regulation of monocyte chemoattractant protein-1 (MCP-1) mRNA levels in HUVEC. Vardenafil Dihydrochloride 9-19 C-C motif chemokine ligand 2 Homo sapiens 103-137 20803229-8 2011 Further, vardenafil reduced the AGE-induced ROS generation and subsequently inhibited up-regulation of monocyte chemoattractant protein-1 (MCP-1) mRNA levels in HUVEC. Vardenafil Dihydrochloride 9-19 C-C motif chemokine ligand 2 Homo sapiens 139-144 20803229-9 2011 We demonstrated here for the first time that vardenafil could block the AGE-induced up-regulation of MCP-1 mRNA levels in HUVEC by suppressing RAGE expression and subsequent ROS generation via elevation of cGMP. Vardenafil Dihydrochloride 45-55 C-C motif chemokine ligand 2 Homo sapiens 101-106 20803229-9 2011 We demonstrated here for the first time that vardenafil could block the AGE-induced up-regulation of MCP-1 mRNA levels in HUVEC by suppressing RAGE expression and subsequent ROS generation via elevation of cGMP. Vardenafil Dihydrochloride 45-55 advanced glycosylation end-product specific receptor Homo sapiens 143-147 21552528-9 2011 In addition, vardenafil significantly stimulated the ATPase activity of ABCB1 and inhibited the photolabeling of ABCB1 with [(125)I]-IAAP. Vardenafil Dihydrochloride 13-23 ATP binding cassette subfamily B member 1 Homo sapiens 113-118 21552528-11 2011 Overall, our results suggest that vardenafil reverses ABCB1-mediated MDR by directly blocking the drug efflux function of ABCB1. Vardenafil Dihydrochloride 34-44 ATP binding cassette subfamily B member 1 Homo sapiens 54-59 21552528-11 2011 Overall, our results suggest that vardenafil reverses ABCB1-mediated MDR by directly blocking the drug efflux function of ABCB1. Vardenafil Dihydrochloride 34-44 ATP binding cassette subfamily B member 1 Homo sapiens 122-127 21585174-2 2011 To date, three PDE5 inhibitors are on the market: sildenafil, vardenafil and tadalafil. Vardenafil Dihydrochloride 62-72 phosphodiesterase 5A Homo sapiens 15-19 21573049-4 2011 OBJECTIVES: To review the drug delivery mechanisms of ODTs in general and to review safety and efficacy of vardenafil ODT (a PDE-5 inhibitor) as a treatment option for management of ED. Vardenafil Dihydrochloride 107-121 phosphodiesterase 5A Homo sapiens 125-130 21929518-6 2011 In this laboratory setting study PDE5 inhibitors seem to prolong ELT but the difference from placebo is significant only in vardenafil. Vardenafil Dihydrochloride 124-134 phosphodiesterase 5A Homo sapiens 33-37 21416414-11 2011 To search for new analogues of PDE-5 inhibitors, a precursor ion scan of an expected ion m/z 283, which was one of the mass fragments from the analogues of sildenafil or vardenafil, was performed and fragmentation of the precursor ion, by combining a precursor ion scan with automatic confirmation using EPI spectra, was acquired. Vardenafil Dihydrochloride 170-180 phosphodiesterase 5A Homo sapiens 31-36 21401398-13 2011 CONCLUSION: Vardenafil concentrations of 1 and 10 muM should be considered as appropriate for ureteral relaxation. Vardenafil Dihydrochloride 12-22 latexin Homo sapiens 50-53 20562123-1 2011 Sildenafil and vardenafil, two selective inhibitors of phosphodiesterase type 5 (PDE5) are able, when applied by intraperitoneal injection, to activate chloride transport in cystic fibrosis (CF) mice homozygous for the F508del mutation. Vardenafil Dihydrochloride 15-25 phosphodiesterase 5A, cGMP-specific Mus musculus 55-79 21681286-2 2011 Three highly selective PDE5 inhibitors (PDE5i), sildenafil, vardenafil and tadalafil, have been developed for treatment of erectile dysfunction (ED). Vardenafil Dihydrochloride 60-70 phosphodiesterase 5A, cGMP-specific Mus musculus 23-27 20925442-1 2011 BACKGROUND: Vardenafil is a potent and highly selective oral phosphodiesterase type 5 (PDE-5) inhibitor that has been shown in numerous clinical trials and post-marketing surveillance studies to be safe and effective for improving erectile function in men with erectile dysfunction (ED). Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 61-85 20925442-1 2011 BACKGROUND: Vardenafil is a potent and highly selective oral phosphodiesterase type 5 (PDE-5) inhibitor that has been shown in numerous clinical trials and post-marketing surveillance studies to be safe and effective for improving erectile function in men with erectile dysfunction (ED). Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 87-92 20562123-1 2011 Sildenafil and vardenafil, two selective inhibitors of phosphodiesterase type 5 (PDE5) are able, when applied by intraperitoneal injection, to activate chloride transport in cystic fibrosis (CF) mice homozygous for the F508del mutation. Vardenafil Dihydrochloride 15-25 phosphodiesterase 5A, cGMP-specific Mus musculus 81-85 21179109-1 2011 Results are reported from the first two adequate trials of the PDE-5 inhibitor vardenafil using a stopwatch to precisely measure erection duration in men with ED. Vardenafil Dihydrochloride 79-89 phosphodiesterase 5A Homo sapiens 63-68 22131856-2 2011 Three selective inhibitors of PDE-5 - sildenafil, vardenafil and tadalafil - have been successfully used by millions of men worldwide for the treatment of erectile dysfunction. Vardenafil Dihydrochloride 50-60 phosphodiesterase 5A Homo sapiens 30-35 20859794-5 2011 Several of these inhibitors are highly selective for particular PDEs; potent and largely selective PDE5 inhibitors are used clinically for treatment of erectile dysfunction [sildenafil (Viagra ), tadalafil (Cialis ) and vardenafil (Levitra )] and pulmonary hypertension [sildenafil (Revatio ) and tadalafil (Adenocirca)]. Vardenafil Dihydrochloride 220-230 phosphodiesterase 5A Homo sapiens 99-103 20859794-5 2011 Several of these inhibitors are highly selective for particular PDEs; potent and largely selective PDE5 inhibitors are used clinically for treatment of erectile dysfunction [sildenafil (Viagra ), tadalafil (Cialis ) and vardenafil (Levitra )] and pulmonary hypertension [sildenafil (Revatio ) and tadalafil (Adenocirca)]. Vardenafil Dihydrochloride 232-239 phosphodiesterase 5A Homo sapiens 99-103 21124003-8 2011 The pigs treated with vardenafil (group 3) also showed significantly increased apoptotic cells, iNOS and eNOS levels compared to the sham-operated group. Vardenafil Dihydrochloride 22-32 nitric oxide synthase 2 Sus scrofa 96-100 22469265-2 2011 The mechanism of action of tadalafil is similar to sildenafil and vardenafil through the inhibition of PDE. Vardenafil Dihydrochloride 66-76 aldehyde dehydrogenase 7 family member A1 Homo sapiens 103-106 21253331-4 2010 In the present study, we investigated the effects of vardenafil on oxytocin and c-Fos expression in the paraventricular nucleus (PVN) of conscious rats. Vardenafil Dihydrochloride 53-63 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 80-85 21253331-11 2010 c-Fos in the oxytocin neurons of the PVN was increased by 1 day administration of 2 mg/kg vardenafil, and this effect of vardenafil also appeared in a duration-dependent manner. Vardenafil Dihydrochloride 90-100 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 0-5 21253331-11 2010 c-Fos in the oxytocin neurons of the PVN was increased by 1 day administration of 2 mg/kg vardenafil, and this effect of vardenafil also appeared in a duration-dependent manner. Vardenafil Dihydrochloride 121-131 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 0-5 20939743-2 2010 Phosphodiesterase type 5 (PDE5) inhibitors (sildenafil, tadalafil and vardenafil) are currently the first-line treatment option presented to patients with ED. Vardenafil Dihydrochloride 70-80 phosphodiesterase 5A Homo sapiens 0-24 20919747-2 2010 Phosphodiesterase-5 (PDE-5) inhibitors, sildenafil, vardenafil and tadalafil, are well known oral treatment for males with erectile dysfunction. Vardenafil Dihydrochloride 52-62 phosphodiesterase 5A Homo sapiens 0-19 20919747-2 2010 Phosphodiesterase-5 (PDE-5) inhibitors, sildenafil, vardenafil and tadalafil, are well known oral treatment for males with erectile dysfunction. Vardenafil Dihydrochloride 52-62 phosphodiesterase 5A Homo sapiens 21-26 20939743-2 2010 Phosphodiesterase type 5 (PDE5) inhibitors (sildenafil, tadalafil and vardenafil) are currently the first-line treatment option presented to patients with ED. Vardenafil Dihydrochloride 70-80 phosphodiesterase 5A Homo sapiens 26-30 20471953-6 2010 Additionally, we found that the other two PDE5 inhibitors (vardenafil and tadalafil) and the cGMP analog 8-pCPT-cGMP also increased adipogenesis. Vardenafil Dihydrochloride 59-69 phosphodiesterase 5A, cGMP-specific Mus musculus 42-46 21045254-6 2010 Three of these drugs (namely sildenafil, tadalafil and vardenafil) are inhibitors of the enzyme phosphodiesterase type 5 (PDE5)and work peripherally within the penis to potentiate the smooth muscle relaxation that is needed for a penile erection. Vardenafil Dihydrochloride 55-65 phosphodiesterase 5A Homo sapiens 122-126 20819751-5 2010 The third PDE-5 inhibitor, vardenafil, is currently being investigated in PAH. Vardenafil Dihydrochloride 27-37 phosphodiesterase 5A Homo sapiens 10-15 20413734-0 2010 A phosphodiesterase-5 inhibitor vardenafil enhances angiogenesis through a protein kinase G-dependent hypoxia-inducible factor-1/vascular endothelial growth factor pathway. Vardenafil Dihydrochloride 32-42 phosphodiesterase 5A Homo sapiens 2-21 20413734-0 2010 A phosphodiesterase-5 inhibitor vardenafil enhances angiogenesis through a protein kinase G-dependent hypoxia-inducible factor-1/vascular endothelial growth factor pathway. Vardenafil Dihydrochloride 32-42 vascular endothelial growth factor A Homo sapiens 129-163 20413734-2 2010 METHODS AND RESULTS: Unilateral hindlimb ischemia was generated by resecting right femoral artery in wild-type C3H/He mice, treated with either vehicle or a PDE5 inhibitor vardenafil (10 mg/kg per day). Vardenafil Dihydrochloride 172-182 phosphodiesterase 5A, cGMP-specific Mus musculus 157-161 20413734-4 2010 Vardenafil upregulated protein expression of vascular endothelial growth factor and hypoxia-inducible factor (HIF)-1 alpha in ischemic muscle and enhanced mobilization of Sca-1/Flk-1-positive endothelial progenitor cells (EPCs) in peripheral blood and bone marrow, contributing to neovascularization. Vardenafil Dihydrochloride 0-10 vascular endothelial growth factor A Homo sapiens 45-79 20413734-4 2010 Vardenafil upregulated protein expression of vascular endothelial growth factor and hypoxia-inducible factor (HIF)-1 alpha in ischemic muscle and enhanced mobilization of Sca-1/Flk-1-positive endothelial progenitor cells (EPCs) in peripheral blood and bone marrow, contributing to neovascularization. Vardenafil Dihydrochloride 0-10 hypoxia inducible factor 1 subunit alpha Homo sapiens 84-122 20413734-4 2010 Vardenafil upregulated protein expression of vascular endothelial growth factor and hypoxia-inducible factor (HIF)-1 alpha in ischemic muscle and enhanced mobilization of Sca-1/Flk-1-positive endothelial progenitor cells (EPCs) in peripheral blood and bone marrow, contributing to neovascularization. Vardenafil Dihydrochloride 0-10 ataxin 1 Homo sapiens 171-176 20413734-4 2010 Vardenafil upregulated protein expression of vascular endothelial growth factor and hypoxia-inducible factor (HIF)-1 alpha in ischemic muscle and enhanced mobilization of Sca-1/Flk-1-positive endothelial progenitor cells (EPCs) in peripheral blood and bone marrow, contributing to neovascularization. Vardenafil Dihydrochloride 0-10 kinase insert domain receptor Homo sapiens 177-182 20413734-6 2010 Furthermore, reporter assays showed that vardenafil and cGMP activated the transactivation activity of HIF-1 under hypoxia. Vardenafil Dihydrochloride 41-51 hypoxia inducible factor 1 subunit alpha Homo sapiens 103-108 20394470-7 2010 When co-possessed prescriptions were defined by overlapping exposure periods, the proportion of PDE5-I patients with co-possessed nitrates ranged from 1.44% (tadalafil) to 1.72% (vardenafil) and 2.13% (sildenafil). Vardenafil Dihydrochloride 179-189 phosphodiesterase 5A Homo sapiens 96-100 20394470-8 2010 Co-possession percentages of PDE5-I prescriptions were 0.83% for tadalafil and 1.07% for sildenafil and vardenafil. Vardenafil Dihydrochloride 104-114 phosphodiesterase 5A Homo sapiens 29-33 20102442-8 2010 The potential role of pGC activation and cGMP generation in this effect is reinforced by the potentiation of this effect by phosphodiesterase-5 inhibitor vardenafil (55.0+-7.5-UGN vs. 98.6+-1.4%-UGN+vardenafil; P<0.05). Vardenafil Dihydrochloride 154-164 guanylate cyclase activator 2B Homo sapiens 176-179 20102442-8 2010 The potential role of pGC activation and cGMP generation in this effect is reinforced by the potentiation of this effect by phosphodiesterase-5 inhibitor vardenafil (55.0+-7.5-UGN vs. 98.6+-1.4%-UGN+vardenafil; P<0.05). Vardenafil Dihydrochloride 154-164 guanylate cyclase activator 2B Homo sapiens 195-198 20419092-7 2010 Oral administration of PDE5 inhibitor, vardenafil, to mice with HER2-positive intracranial lung tumors led to an increased tumor permeability to high molecular weight [(14)C]dextran (2.6-fold increase) and to Herceptin (2-fold increase). Vardenafil Dihydrochloride 39-49 phosphodiesterase 5A, cGMP-specific Mus musculus 23-27 20109548-1 2010 In this study we tested whether phosphodiesterase 5 (PDE5) inhibitors, sildenafil and vardenafil, would afford protection against 3-nitropropionic acid (3NP), which produces striatal lesions that closely mimic some of the neuropathological features of Huntington"s Disease (HD). Vardenafil Dihydrochloride 86-96 phosphodiesterase 5A, cGMP-specific Mus musculus 53-57 20109548-3 2010 Animals treated with PDE5 inhibitors (sildenafil or vardenafil) showed improved neurologic scores, reduced the loss of striatal DARPP-32 protein levels and lesion volumes, and decreased calpain activation produced by 3NP. Vardenafil Dihydrochloride 52-62 phosphodiesterase 5A, cGMP-specific Mus musculus 21-25 20109548-3 2010 Animals treated with PDE5 inhibitors (sildenafil or vardenafil) showed improved neurologic scores, reduced the loss of striatal DARPP-32 protein levels and lesion volumes, and decreased calpain activation produced by 3NP. Vardenafil Dihydrochloride 52-62 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 128-136 20456213-8 2010 Vardenafil ODT therapy was statistically significantly superior to placebo for all primary (i.e. IIEF-EF, SEP2, SEP3) and secondary efficacy variables (p < 0.0001). Vardenafil Dihydrochloride 0-14 septin 3 Homo sapiens 112-116 19959201-9 2010 The overall removal efficiency of the STP in Tarragona (Spain) is 68%, 69% and 80% for sildenafil, tadalafil and vardenafil, respectively. Vardenafil Dihydrochloride 113-123 thyroid hormone receptor interactor 10 Homo sapiens 38-41 20233275-9 2010 Vardenafil ODT therapy was statistically significantly superior to placebo for all primary (IIEF-EF, SEP2, SEP3) and secondary efficacy measures (all P < 0.0001). Vardenafil Dihydrochloride 0-14 septin 6 Homo sapiens 101-105 20233275-9 2010 Vardenafil ODT therapy was statistically significantly superior to placebo for all primary (IIEF-EF, SEP2, SEP3) and secondary efficacy measures (all P < 0.0001). Vardenafil Dihydrochloride 0-14 septin 3 Homo sapiens 107-111 19185976-1 2010 BACKGROUND: Sildenafil, vardenafil, and tadalafil are phosphodiesterase type 5 inhibitors (PDE5-Is) usually used in the treatment of erectile dysfunction (ED). Vardenafil Dihydrochloride 24-34 phosphodiesterase 5A Homo sapiens 91-95 19796053-6 2010 Proliferation assay was used as readout of PDE5 activity, evaluated as ability of vardenafil to increase the antiproliferative effect of different nitric oxide (NO)/cGMP pathway activators [the PDE5-resistant cGMP analog Sp-8-Br-PET-cGMPS, the NO donor sodium nitroprusside (SNP), and the soluble guanylate cyclase (sGC) stimulator BAY 41-8543]. Vardenafil Dihydrochloride 82-92 phosphodiesterase 5A Homo sapiens 194-198 19185976-11 2010 Tadalafil in combination with Mox-LDL and TNF-alpha showed a decrease of IL-8 (p<0.05) compared with sildenafil and vardenafil. Vardenafil Dihydrochloride 119-129 tumor necrosis factor Homo sapiens 42-51 19929916-1 2010 INTRODUCTION: Phosphodiesterase type 5 inhibitors (PDE5), such as sildenafil, tadalafil, and vardenafil, have revolutionized the treatment of erectile dysfunction. Vardenafil Dihydrochloride 93-103 phosphodiesterase 5A Homo sapiens 51-55 20103095-1 2010 Vardenafil is a phosphodiesterase-5 (PDE-5) inhibitor for the treatment of erectile dysfunction (ED). Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 16-35 20103095-1 2010 Vardenafil is a phosphodiesterase-5 (PDE-5) inhibitor for the treatment of erectile dysfunction (ED). Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 37-42 19887943-3 2010 PDE5 inhibitors (sildenafil, tadalafil, vardenafil, etc.) Vardenafil Dihydrochloride 40-50 phosphodiesterase 5A Homo sapiens 0-4 19889145-9 2010 Vardenafil treatment dramatically decreased hypoxyprobe staining, as well as VEGF and ETB expression in SHR bladder up to WKY level. Vardenafil Dihydrochloride 0-10 vascular endothelial growth factor A Rattus norvegicus 77-81 20104672-10 2010 At 12 weeks, vardenafil therapy was associated with statistically significant improvements from baseline in IIEF-EF scores, and SEP2 and SEP3 success rates, including patients with ED and diabetes, hypertension, dyslipidemia, or metabolic syndrome. Vardenafil Dihydrochloride 13-23 septin 6 Homo sapiens 128-132 19889145-9 2010 Vardenafil treatment dramatically decreased hypoxyprobe staining, as well as VEGF and ETB expression in SHR bladder up to WKY level. Vardenafil Dihydrochloride 0-10 endothelin receptor type B Rattus norvegicus 86-89 19796053-6 2010 Proliferation assay was used as readout of PDE5 activity, evaluated as ability of vardenafil to increase the antiproliferative effect of different nitric oxide (NO)/cGMP pathway activators [the PDE5-resistant cGMP analog Sp-8-Br-PET-cGMPS, the NO donor sodium nitroprusside (SNP), and the soluble guanylate cyclase (sGC) stimulator BAY 41-8543]. Vardenafil Dihydrochloride 82-92 Sp8 transcription factor Homo sapiens 221-225 19889145-10 2010 Accordingly, in SHR bladder, vardenafil administration significantly blunted relaxation induced by the selective ETB agonist IRL-1620. Vardenafil Dihydrochloride 29-39 endothelin receptor type B Rattus norvegicus 113-116 19936151-4 2009 The availability of three (sildenafil citrate, tadalafil, and vardenafil) well tolerated and effective oral PDE5 inhibitors gives treatment options for men with ED. Vardenafil Dihydrochloride 62-72 phosphodiesterase 5A Homo sapiens 108-112 19889145-12 2010 Conversely, the hypoxia-related induction of smooth muscle-specific genes (alphaSMA, SM22alpha, and desmin) was significantly reduced by vardenafil. Vardenafil Dihydrochloride 137-147 transgelin Rattus norvegicus 85-94 19889145-12 2010 Conversely, the hypoxia-related induction of smooth muscle-specific genes (alphaSMA, SM22alpha, and desmin) was significantly reduced by vardenafil. Vardenafil Dihydrochloride 137-147 desmin Rattus norvegicus 100-106 20030481-1 2010 The phosphodiesterase type 5 (PDE-5) inhibitors-sildenafil, vardenafil, and tadalafil-are used primarily in erectile dysfunction, but sildenafil is also indicated for pulmonary hypertension. Vardenafil Dihydrochloride 60-70 phosphodiesterase 5A Homo sapiens 4-28 20030481-1 2010 The phosphodiesterase type 5 (PDE-5) inhibitors-sildenafil, vardenafil, and tadalafil-are used primarily in erectile dysfunction, but sildenafil is also indicated for pulmonary hypertension. Vardenafil Dihydrochloride 60-70 phosphodiesterase 5A Homo sapiens 30-35 19949666-1 2009 This study was conducted to evaluate the effects of vardenafil (Levitra), a phosphodiesterase-5 (PDE-5) inhibitor, on cell proliferation in the hippocampal dentate gyrus and on 5-hyroxytryptamine (5-HT, serotonin) synthesis and tryptophan hydroxylase (TPH) expression in the rat dorsal raphe nucleus. Vardenafil Dihydrochloride 52-62 tryptophan hydroxylase 1 Rattus norvegicus 228-250 19949666-1 2009 This study was conducted to evaluate the effects of vardenafil (Levitra), a phosphodiesterase-5 (PDE-5) inhibitor, on cell proliferation in the hippocampal dentate gyrus and on 5-hyroxytryptamine (5-HT, serotonin) synthesis and tryptophan hydroxylase (TPH) expression in the rat dorsal raphe nucleus. Vardenafil Dihydrochloride 52-62 tryptophan hydroxylase 1 Rattus norvegicus 252-255 19949666-5 2009 The results revealed that treatment with vardenafil increased cell proliferation in the dentate gyrus and enhanced 5-HT synthesis and TPH expression in the dorsal raphe in a dose- and duration-dependent manner. Vardenafil Dihydrochloride 41-51 tryptophan hydroxylase 1 Rattus norvegicus 134-137 19936152-4 2009 Currently, three PDE5 inhibitors - sildenafil, tadalafil and vardenafil - are approved to be taken as needed in anticipation of sexual activity, but only one of these, tadalafil, has been approved to be taken once daily. Vardenafil Dihydrochloride 61-71 phosphodiesterase 5A Homo sapiens 17-21 19768639-6 2009 Three oral PDE-5 inhibitors are available (sildenafil, tadalafil, and vardenafil) and are the recommended first-line treatment for erectile dysfunction. Vardenafil Dihydrochloride 70-80 phosphodiesterase 5A Homo sapiens 11-16 19427155-2 2009 Currently, three PDE-5 inhibitors have been approved by the U.S. Food and Drug Administration (FDA) for use in the United States: sildenafil citrate, tadalafil, and vardenafil hydrochloride trihydrate. Vardenafil Dihydrochloride 165-200 phosphodiesterase 5A Homo sapiens 17-22 19732311-1 2009 INTRODUCTION: Vardenafil is reported to improve success rates in the maintenance of an erection sufficient for completion of intercourse (SEP-3) compared with placebo in erectile dysfunction (ED) patients who attempted intercourse from as early as 15 minutes after dosing. Vardenafil Dihydrochloride 14-24 septin 3 Homo sapiens 138-143 19732311-11 2009 SEP-3 success rates in patients who inserted in each interval from 0-15 minutes (P = 0.0268), 15-30 minutes (P = 0.0094) through > 120 minutes were all higher in vardenafil-treated patients than those in placebo. Vardenafil Dihydrochloride 165-175 septin 3 Homo sapiens 0-5 19768639-11 2009 The third PDE-5 inhibitor, vardenafil, is currently being investigated in PAH. Vardenafil Dihydrochloride 27-37 phosphodiesterase 5A Homo sapiens 10-15 19570039-1 2009 INTRODUCTION: The three effective, commercially available drugs for the treatment of erectile dysfunction-sildenafil, vardenafil, and tadalafil-inhibit the same substrate, the erectolytic enzyme phosphodiesterase type 5 (PDE5). Vardenafil Dihydrochloride 118-128 phosphodiesterase 5A Homo sapiens 195-219 19570039-1 2009 INTRODUCTION: The three effective, commercially available drugs for the treatment of erectile dysfunction-sildenafil, vardenafil, and tadalafil-inhibit the same substrate, the erectolytic enzyme phosphodiesterase type 5 (PDE5). Vardenafil Dihydrochloride 118-128 phosphodiesterase 5A Homo sapiens 221-225 19624790-3 2009 Phosphodiesterase-type 5 (PDE5) inhibitors have revolutionised treatment for ED and three such drugs are currently available: sildenafil citrate, tadalafil and vardenafil HCl. Vardenafil Dihydrochloride 160-174 phosphodiesterase 5A Homo sapiens 0-24 19624790-3 2009 Phosphodiesterase-type 5 (PDE5) inhibitors have revolutionised treatment for ED and three such drugs are currently available: sildenafil citrate, tadalafil and vardenafil HCl. Vardenafil Dihydrochloride 160-174 phosphodiesterase 5A Homo sapiens 26-30 19464472-11 2009 Vardenafil significantly reduced the stenosis grade (24.64% +/- 7.46% vs 54.12% +/- 10.30% in the control group, P < .05) and expression of transforming growth factor beta1, as well as alpha-smooth muscle actin, in the neointima. Vardenafil Dihydrochloride 0-10 transforming growth factor, beta 1 Rattus norvegicus 143-175 19605329-11 2009 Vardenafil treatment significantly reduced apoptosis protease activating factor 1, endothelial NOS and inducible NOS levels in the vardenafil group compared with the T/D group. Vardenafil Dihydrochloride 0-10 nitric oxide synthase 3 Rattus norvegicus 83-98 19605329-11 2009 Vardenafil treatment significantly reduced apoptosis protease activating factor 1, endothelial NOS and inducible NOS levels in the vardenafil group compared with the T/D group. Vardenafil Dihydrochloride 131-141 nitric oxide synthase 3 Rattus norvegicus 83-98 19473460-0 2009 Vardenafil modulates bladder contractility through cGMP-mediated inhibition of RhoA/Rho kinase signaling pathway in spontaneously hypertensive rats. Vardenafil Dihydrochloride 0-10 ras homolog family member A Rattus norvegicus 79-83 19473460-3 2009 AIM: The aim of this paper was to investigate whether vardenafil-induced cGMP accumulation reduces RhoA/ROCK signaling in bladder. Vardenafil Dihydrochloride 54-64 ras homolog family member A Rattus norvegicus 99-103 19473460-12 2009 Vardenafil prevented RhoA membrane translocation/activation, decreased ROCK activity, and increased cGMP levels in vivo (rat) and in vitro (hBCs). Vardenafil Dihydrochloride 0-10 ras homolog family member A Rattus norvegicus 21-25 19400854-4 2009 Eight patients had normal testosterone levels and were treated with a PDE-5 inhibitor (vardenafil) only; after 6 months of treatment, 6 of these patients (75%) showed significant improvement in erectile function. Vardenafil Dihydrochloride 87-97 phosphodiesterase 5A Homo sapiens 70-75 19400854-7 2009 The five patients receiving CPAP therapy were treated with a combination of parenteral testosterone undecanoate and a PDE-5 inhibitor (vardenafil) and all had normal erectile function after 3 months of therapy. Vardenafil Dihydrochloride 135-145 phosphodiesterase 5A Homo sapiens 118-123 19464472-11 2009 Vardenafil significantly reduced the stenosis grade (24.64% +/- 7.46% vs 54.12% +/- 10.30% in the control group, P < .05) and expression of transforming growth factor beta1, as well as alpha-smooth muscle actin, in the neointima. Vardenafil Dihydrochloride 0-10 actin gamma 2, smooth muscle Rattus norvegicus 188-213 19243765-2 2009 Vardenafil inhibits the activity of phosphodiesterase type 5 (PDE-5), which degrades cyclic guanossine monophosphate (cGMP) and results in relaxation of smooth muscle. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 36-60 19285714-5 2009 The tension induced by ET-1 was dose-dependently reversed by the drugs with the following rank order of efficacy: rolipram, forskolin, tadalafil, sodium nitroprusside, sildenafil, vinpocetine, vardenafil, EHNA. Vardenafil Dihydrochloride 193-203 endothelin 1 Homo sapiens 23-27 19473460-13 2009 Exposing hBCs to vardenafil increased Ser(188) RhoA phosphorylation, to the same extent as the PDE5-insensitive PKG agonist Sp-8-Br-PET-cGMP. Vardenafil Dihydrochloride 17-27 ras homolog family member A Rattus norvegicus 47-51 19473460-14 2009 Moreover, vardenafil inhibited several RhoA-dependent functions in hBCs, including smooth muscle gene transcription and endothelin-1-induced migration. Vardenafil Dihydrochloride 10-20 ras homolog family member A Rattus norvegicus 39-43 19473460-14 2009 Moreover, vardenafil inhibited several RhoA-dependent functions in hBCs, including smooth muscle gene transcription and endothelin-1-induced migration. Vardenafil Dihydrochloride 10-20 endothelin 1 Rattus norvegicus 120-132 19473460-17 2009 CONCLUSIONS: This is the first study demonstrating that the effect of vardenafil on OAB could be partially determined by a cGMP-dependent RhoA/ROCK signaling inhibition. Vardenafil Dihydrochloride 70-80 ras homolog family member A Rattus norvegicus 138-142 19416089-1 2009 Vardenafil is a short-acting PDE5 inhibitor used in the treatment of male erectile dysfunction. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 29-33 19243765-2 2009 Vardenafil inhibits the activity of phosphodiesterase type 5 (PDE-5), which degrades cyclic guanossine monophosphate (cGMP) and results in relaxation of smooth muscle. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 62-67 19860692-2 2009 Three PDE5 inhibitors--sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis)--are currently approved by the FDA and the EMEA for use in ED, whereas sildenafil is also marketed under a different proprietary name (Revatio) for the treatment of pulmonary arterial hypertension (PAH). Vardenafil Dihydrochloride 44-54 phosphodiesterase 5A Homo sapiens 6-10 19368809-0 2009 Effects of the PDE5-inhibitor vardenafil in a mouse stroke model. Vardenafil Dihydrochloride 30-40 phosphodiesterase 5A, cGMP-specific Mus musculus 15-19 20054411-3 2009 The PDE-5 inhibitor, vardenafil, is characterized by a rapid onset of action, increased duration of erection, high rates of first-dose success and reliable efficacy that can be maintained with continued use. Vardenafil Dihydrochloride 21-31 phosphodiesterase 5A Homo sapiens 4-9 19298393-10 2009 Treatment with vardenafil resulted in higher cGMP levels, reduced transforming growth factor-beta1 expression, significantly improved cardiac function (improvement of E(max) by 95%, PRSW by 69%; P < 0.05) and greater vasorelaxation to acetylcholine and sodium nitroprusside in aortae from diabetic animals. Vardenafil Dihydrochloride 15-25 transforming growth factor, beta 1 Rattus norvegicus 66-98 19057210-3 2009 RECENT FINDINGS: All three commonly used PDE-5 inhibitors (sildenafil, vardenafil and tadalafil) appear to improve LUTS as measured by the International Prostate Symptom Score. Vardenafil Dihydrochloride 71-81 phosphodiesterase 5A Homo sapiens 41-46 19860694-5 2009 Its successful introduction into clinical practice was soon followed by the launch of two other PDE5 inhibitors: tadalafil and vardenafil. Vardenafil Dihydrochloride 127-137 phosphodiesterase 5A Homo sapiens 96-100 19860692-2 2009 Three PDE5 inhibitors--sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis)--are currently approved by the FDA and the EMEA for use in ED, whereas sildenafil is also marketed under a different proprietary name (Revatio) for the treatment of pulmonary arterial hypertension (PAH). Vardenafil Dihydrochloride 56-63 phosphodiesterase 5A Homo sapiens 6-10 19860693-2 2009 Phosphodiesterase type 5 (PDE5) inhibitors (sildenafil, tadalafil, vardenafil) are currently the first choice treatment option for ED by most physicians and patients due to their high efficacy rates and favourable safety profiles. Vardenafil Dihydrochloride 67-77 phosphodiesterase 5A Homo sapiens 0-24 19860693-2 2009 Phosphodiesterase type 5 (PDE5) inhibitors (sildenafil, tadalafil, vardenafil) are currently the first choice treatment option for ED by most physicians and patients due to their high efficacy rates and favourable safety profiles. Vardenafil Dihydrochloride 67-77 phosphodiesterase 5A Homo sapiens 26-30 19132801-1 2009 Phosphodiesterase type 5 (PDE-5) inhibitors (sildenafil, vardenafil and tadalafil) have been in widespread use for the safe and effective treatment of erectile dysfunction (ED) for nearly a decade. Vardenafil Dihydrochloride 57-67 phosphodiesterase 5A Homo sapiens 26-31 18854969-2 2008 The development of the PDE5 inhibitors Sildenafil (Viagra), Vardenafil (Levitra), and Tadalafil (Cialis), combining a high response rate and the advantage of on-demand intake, is the result of the scientific characterization of the physiology of penile erectile smooth muscle.The introduction of these compounds as safe and well-tolerated orally active drugs for the treatment of erectile dysfunction has not only become a worldwide clinical success, but it provided the basis for the development and introduction of several new therapeutic modalities into the management of male and female sexual dysfunction. Vardenafil Dihydrochloride 60-70 phosphodiesterase 5A Homo sapiens 23-27 19132801-1 2009 Phosphodiesterase type 5 (PDE-5) inhibitors (sildenafil, vardenafil and tadalafil) have been in widespread use for the safe and effective treatment of erectile dysfunction (ED) for nearly a decade. Vardenafil Dihydrochloride 57-67 phosphodiesterase 5A Homo sapiens 0-24 19125990-0 2009 Improvement in duration of erection following phosphodiesterase type 5 inhibitor therapy with vardenafil in men with erectile dysfunction: the ENDURANCE study. Vardenafil Dihydrochloride 94-104 phosphodiesterase 5A Homo sapiens 46-70 19125990-1 2009 OBJECTIVE: The ENDURANCE study evaluated the efficacy of vardenafil, a phosphodiesterase type 5 (PDE5) inhibitor, in men with erectile dysfunction (ED), by measuring the duration of erection leading to successful intercourse using a stopwatch as the assessment instrument. Vardenafil Dihydrochloride 57-67 phosphodiesterase 5A Homo sapiens 71-95 19125990-1 2009 OBJECTIVE: The ENDURANCE study evaluated the efficacy of vardenafil, a phosphodiesterase type 5 (PDE5) inhibitor, in men with erectile dysfunction (ED), by measuring the duration of erection leading to successful intercourse using a stopwatch as the assessment instrument. Vardenafil Dihydrochloride 57-67 phosphodiesterase 5A Homo sapiens 97-101 18607596-4 2008 The hypothesis that an impaired NO/cGMP-signaling may contribute to the pathophysiology of benign prostatic hyperplasia (BPH) is supported by the results from randomized, placebo-controlled clinical studies, indicating that NO donor drugs and PDE5-inhibitors sildenafil, tadalafil and vardenafil may be useful to treat storage and voiding dysfunctions resulting from LUTS in men. Vardenafil Dihydrochloride 285-295 phosphodiesterase 5A Homo sapiens 243-247 18779324-9 2008 Pgamma1-60 binding to the GAF domain increased vardenafil but not cGMP affinity, indicating that substrate- and inhibitor-binding sites do not totally overlap. Vardenafil Dihydrochloride 47-57 fibroblast growth factor 9 Homo sapiens 26-29 18779324-10 2008 In addition, prolonged incubation of PDE6 with vardenafil or sildenafil (but not 3-isobutyl-1-methylxanthine and zaprinast) induced a distinct conformational change in the catalytic domain without affecting the binding properties of the GAF domains. Vardenafil Dihydrochloride 47-57 fibroblast growth factor 9 Homo sapiens 237-240 18640769-11 2008 On-demand vardenafil treatment resulted in significantly greater IIEF-EF scores and better SEP3 response rates than placebo over the entire treatment period. Vardenafil Dihydrochloride 10-20 septin 3 Homo sapiens 91-95 18596129-9 2008 Due to PDE-5 inhibition, the endogenous TGF-beta-activating protein TSP-1 and the TGF-beta-signalling protein p-smad-2/3 were decreased suggesting this as an antifibrotic mechanism of action of vardenafil in this model. Vardenafil Dihydrochloride 194-204 transforming growth factor, beta 1 Rattus norvegicus 40-48 18596129-9 2008 Due to PDE-5 inhibition, the endogenous TGF-beta-activating protein TSP-1 and the TGF-beta-signalling protein p-smad-2/3 were decreased suggesting this as an antifibrotic mechanism of action of vardenafil in this model. Vardenafil Dihydrochloride 194-204 thrombospondin 1 Rattus norvegicus 68-73 18596129-9 2008 Due to PDE-5 inhibition, the endogenous TGF-beta-activating protein TSP-1 and the TGF-beta-signalling protein p-smad-2/3 were decreased suggesting this as an antifibrotic mechanism of action of vardenafil in this model. Vardenafil Dihydrochloride 194-204 transforming growth factor, beta 1 Rattus norvegicus 82-90 18640769-12 2008 CONCLUSIONS: In this study of men with ED following bilateral NSRP, vardenafil was efficacious when used on demand, supporting a paradigm shift towards on demand dosing with PDE5 inhibitors in this patient group. Vardenafil Dihydrochloride 68-78 phosphodiesterase 5A Homo sapiens 174-178 19144273-4 2008 The aim of this work is to test the action of three common phosphodiesterase inhibitors: Tadalafil, Sildenafil Citrate and Vardenafil at 0.05 microM on human monocytes, analyzing the expression of iNOS protein and mRNA by Western blot and rt-PCR, and production of NO by conversion of L-(2,3,4,5)-[3H]Arginine to L-(3H) citrulline. Vardenafil Dihydrochloride 123-133 nitric oxide synthase 2 Homo sapiens 197-201 18800959-3 2008 We investigated the hemodynamic and intrapulmonary effects of the intravenous dual endothelin A and B receptor blocker tezosentan, and of the phosphodiesterase-5 (PDE-5) antagonist vardenafil in a pig model of acute normobaric hypoxic pulmonary hypertension. Vardenafil Dihydrochloride 181-191 phosphodiesterase 5A Sus scrofa 163-168 18997493-9 2008 This is because sildenafil, vardenafil, and tadalafil are metabolized mainly via the CYP3A4 pathway. Vardenafil Dihydrochloride 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 18281145-2 2008 Phosphodiesterase (type) 5 (PDE5) inhibitors such as vardenafil are commonly used for the treatment of erectile dysfunction (ED), but have also been shown to improve the symptoms of BPH. Vardenafil Dihydrochloride 53-63 phosphodiesterase 5A Homo sapiens 28-32 18656371-0 2008 In silico prediction of novel phosphodiesterase type-5 inhibitors derived from Sildenafil, Vardenafil and Tadalafil. Vardenafil Dihydrochloride 91-101 phosphodiesterase 5A Homo sapiens 30-54 18418391-3 2008 Sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis), treatments for erectile dysfunction, inhibit PDE5 action. Vardenafil Dihydrochloride 21-31 phosphodiesterase 5A Homo sapiens 111-115 18418391-3 2008 Sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis), treatments for erectile dysfunction, inhibit PDE5 action. Vardenafil Dihydrochloride 33-40 phosphodiesterase 5A Homo sapiens 111-115 18331270-9 2008 CCSMCs were also incubated with L-arg and with vardenafil, an inhibitor of PDE-5. Vardenafil Dihydrochloride 47-57 phosphodiesterase 5A Homo sapiens 75-80 18536732-11 2008 Vardenafil, but neither sildenafil nor tadalafil, significantly reduced the Ca2+ mobilization and Ca2+ influx in thrombin-stimulated washed platelets. Vardenafil Dihydrochloride 0-10 coagulation factor II, thrombin Homo sapiens 113-121 18308836-4 2008 Recombinant CYP3A4 and CYP3A5 both produced N-desalkyl metabolites of sildenafil, udenafil, and vardenafil. Vardenafil Dihydrochloride 96-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 18308836-4 2008 Recombinant CYP3A4 and CYP3A5 both produced N-desalkyl metabolites of sildenafil, udenafil, and vardenafil. Vardenafil Dihydrochloride 96-106 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 23-29 18308836-8 2008 The genetic polymorphism of CYP3A5 may contribute to interindividual variability in the disposition of PDE5Is, especially vardenafil. Vardenafil Dihydrochloride 122-132 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 28-34 18331270-16 2008 VEGF and cGMP levels in the L-arg + vardenafil-treated group were significantly greater than those in the L-arg-treated group and the control group. Vardenafil Dihydrochloride 36-46 vascular endothelial growth factor A Homo sapiens 0-4 18331270-19 2008 Combined L-arg and vardenafil treatment, which can enhance VEGF production, may provide a novel therapeutic strategy for the treatment of erectile dysfunction as well as endothelial dysfunction in general. Vardenafil Dihydrochloride 19-29 vascular endothelial growth factor A Homo sapiens 59-63 18953278-4 2008 The US Food and Drug Administration has approved 3 phosphodiesterase-5 (PDE-5) inhibitors for treatment of male sexual dysfunction: sildenafil, tadalafil, and vardenafil. Vardenafil Dihydrochloride 159-169 phosphodiesterase 5A Homo sapiens 51-70 18953278-4 2008 The US Food and Drug Administration has approved 3 phosphodiesterase-5 (PDE-5) inhibitors for treatment of male sexual dysfunction: sildenafil, tadalafil, and vardenafil. Vardenafil Dihydrochloride 159-169 phosphodiesterase 5A Homo sapiens 72-77 18682779-12 2008 CONCLUSION: Vardenafil 20 mg had a high first-dose success rate for both SEP2 (81%) and SEP3 (70%); this was maintained through to the study end point (85% for SEP2 and 78% for SEP3). Vardenafil Dihydrochloride 12-22 septin 3 Homo sapiens 88-92 18682779-12 2008 CONCLUSION: Vardenafil 20 mg had a high first-dose success rate for both SEP2 (81%) and SEP3 (70%); this was maintained through to the study end point (85% for SEP2 and 78% for SEP3). Vardenafil Dihydrochloride 12-22 septin 3 Homo sapiens 177-181 18373526-2 2008 AIM: This is the first prospective, randomized, double-blind, placebo-controlled study to evaluate the efficacy and safety of a PDE-5 inhibitor (i.e., vardenafil) in an exclusive population of men with ED and dyslipidemia. Vardenafil Dihydrochloride 151-161 phosphodiesterase 5A Homo sapiens 128-133 18373526-10 2008 During the 12-week treatment period, the least squares (LS) adjusted mean success rates in patients on vardenafil vs. placebo were: SEP2, 79.09% vs. 51.92%; and SEP3, 66.69% vs. 33.83% (P < 0.001). Vardenafil Dihydrochloride 103-113 septin 6 Homo sapiens 132-136 18373526-10 2008 During the 12-week treatment period, the least squares (LS) adjusted mean success rates in patients on vardenafil vs. placebo were: SEP2, 79.09% vs. 51.92%; and SEP3, 66.69% vs. 33.83% (P < 0.001). Vardenafil Dihydrochloride 103-113 septin 3 Homo sapiens 161-165 17985135-9 2008 The rats treated with vardenafil and sildenafil (groups 2s and 3s) showed significantly increased apoptotic cell, eNOS and iNOS values in ipsilateral testis (P < 0.05). Vardenafil Dihydrochloride 22-32 nitric oxide synthase 2 Rattus norvegicus 123-127 18588760-1 2008 BACKGROUND: Vardenafil, a selective phosphodiesterase 5 (PDE5) inhibitor, may affect nasal patency because of its adverse-effect profile. Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 36-55 18588760-1 2008 BACKGROUND: Vardenafil, a selective phosphodiesterase 5 (PDE5) inhibitor, may affect nasal patency because of its adverse-effect profile. Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 57-61 18385912-1 2008 AIM: To evaluate the efficacy and tolerability of vardenafil, a phosphodiesterase type-5 (PDE-5) inhibitor, in men of Asian ethnicity with erectile dysfunction (ED). Vardenafil Dihydrochloride 50-60 phosphodiesterase 5A Homo sapiens 64-88 18385912-1 2008 AIM: To evaluate the efficacy and tolerability of vardenafil, a phosphodiesterase type-5 (PDE-5) inhibitor, in men of Asian ethnicity with erectile dysfunction (ED). Vardenafil Dihydrochloride 50-60 phosphodiesterase 5A Homo sapiens 90-95 18385912-8 2008 Vardenafil was associated with significant improvements from baseline in least squares (LS) mean success rates for SEP-2 (vardenafil 82.2 vs. placebo 43.6; P<0.001) and SEP-3 (vardenafil 66.1 vs. placebo 24.0; P<0.001). Vardenafil Dihydrochloride 0-10 septin 6 Homo sapiens 115-120 18385912-8 2008 Vardenafil was associated with significant improvements from baseline in least squares (LS) mean success rates for SEP-2 (vardenafil 82.2 vs. placebo 43.6; P<0.001) and SEP-3 (vardenafil 66.1 vs. placebo 24.0; P<0.001). Vardenafil Dihydrochloride 0-10 septin 3 Homo sapiens 172-177 18197727-4 2008 Phosphodiesterase type 5 (PDE5) inhibitors (sildenafil, tadalafil, vardenafil) are currently the first-choice treatment option for ED by most physicians and patients. Vardenafil Dihydrochloride 67-77 phosphodiesterase 5A Homo sapiens 0-24 18197727-4 2008 Phosphodiesterase type 5 (PDE5) inhibitors (sildenafil, tadalafil, vardenafil) are currently the first-choice treatment option for ED by most physicians and patients. Vardenafil Dihydrochloride 67-77 phosphodiesterase 5A Homo sapiens 26-30 17942972-3 2008 Accordingly, PDE5 has been targeted for sexual medicine purposes, and orally administered PDE5 inhibitors such as sildenafil, tadalafil, and vardenafil comprise a foremost intervention for erectile dysfunction (ED). Vardenafil Dihydrochloride 141-151 phosphodiesterase 5A Homo sapiens 90-94 18673225-4 2008 The most intensively examined and marketed PDE5 inhibitor was sildenafil (Viagra) but recently vardenafil (Levitra) and tadalafil (Cialis) were launched with beneficial ADME parameters and PDE5 selectivity. Vardenafil Dihydrochloride 95-105 phosphodiesterase 5A Homo sapiens 189-193 18673225-4 2008 The most intensively examined and marketed PDE5 inhibitor was sildenafil (Viagra) but recently vardenafil (Levitra) and tadalafil (Cialis) were launched with beneficial ADME parameters and PDE5 selectivity. Vardenafil Dihydrochloride 107-114 phosphodiesterase 5A Homo sapiens 189-193 17959709-0 2008 Conformational variations of both phosphodiesterase-5 and inhibitors provide the structural basis for the physiological effects of vardenafil and sildenafil. Vardenafil Dihydrochloride 131-141 phosphodiesterase 5A Homo sapiens 34-53 17959709-1 2008 Vardenafil has higher affinity to phosphodiesterase-5 (PDE5) than sildenafil and lower administered dosage for the treatment of erectile dysfunction. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 34-53 17959709-1 2008 Vardenafil has higher affinity to phosphodiesterase-5 (PDE5) than sildenafil and lower administered dosage for the treatment of erectile dysfunction. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 55-59 17959709-4 2008 The structure shows that the conformation of the H-loop in the PDE5A1-vardenafil complex is different from those of any known structures of the unliganded PDE5 and its complexes with the inhibitors. Vardenafil Dihydrochloride 70-80 phosphodiesterase 5A Homo sapiens 63-67 17959709-5 2008 In addition, the molecular configuration of vardenafil differs from that of sildenafil when bound to PDE5. Vardenafil Dihydrochloride 44-54 phosphodiesterase 5A Homo sapiens 101-105 18174638-5 2007 Currently two more PDE-5 inhibitors, tadalafil and vardenafil, are under study. Vardenafil Dihydrochloride 51-61 phosphodiesterase 5A Homo sapiens 19-24 17727740-7 2007 Similarly, success rates for the ability to maintain erections (SEP3) improved 38.0% (95% CI: 29.5%, 46.6%) compared to placebo, with individual trial values ranging from 41.7% to 88.2% for vardenafil and 20.5% to 51.4% for placebo. Vardenafil Dihydrochloride 190-200 septin 3 Homo sapiens 64-68 17850306-1 2007 AIMS: This report describes patterns of treatment changes with the phosphodiesterase type 5 (PDE5) inhibitors tadalafil, sildenafil and vardenafil, and variables associated with those treatment changes, during the 6-month, prospective, pan-European Erectile Dysfunction Observational Study (EDOS). Vardenafil Dihydrochloride 136-146 phosphodiesterase 5A Homo sapiens 93-97 17706972-1 2007 The PDE-5 inhibitors sildenafil (Viagra) vardenafil (Levitra) and tadalafil (Cialis) have been taken by millions of men for erectile dysfunction. Vardenafil Dihydrochloride 41-51 phosphodiesterase 5A Homo sapiens 4-9 17706972-1 2007 The PDE-5 inhibitors sildenafil (Viagra) vardenafil (Levitra) and tadalafil (Cialis) have been taken by millions of men for erectile dysfunction. Vardenafil Dihydrochloride 53-60 phosphodiesterase 5A Homo sapiens 4-9 17625575-1 2007 The phosphodiesterase type-5 (PDE5) inhibitors sildenafil, vardenafil and tadalafil are widely used first-line therapy for erectile dysfunction (ED). Vardenafil Dihydrochloride 59-69 phosphodiesterase 5A Homo sapiens 4-28 17625575-1 2007 The phosphodiesterase type-5 (PDE5) inhibitors sildenafil, vardenafil and tadalafil are widely used first-line therapy for erectile dysfunction (ED). Vardenafil Dihydrochloride 59-69 phosphodiesterase 5A Homo sapiens 30-34 17690252-2 2007 In the present study, preincubation with cGMP increased PDE5 catalytic activity for cGMP degradation, and it converted the PDE5 catalytic site to a form that was more potently inhibited by each of the three PDE5 catalytic site-specific inhibitors: sildenafil, vardenafil, and tadalafil. Vardenafil Dihydrochloride 260-270 phosphodiesterase 5A Homo sapiens 123-127 17690252-2 2007 In the present study, preincubation with cGMP increased PDE5 catalytic activity for cGMP degradation, and it converted the PDE5 catalytic site to a form that was more potently inhibited by each of the three PDE5 catalytic site-specific inhibitors: sildenafil, vardenafil, and tadalafil. Vardenafil Dihydrochloride 260-270 phosphodiesterase 5A Homo sapiens 123-127 17727740-8 2007 Vardenafil was equally efficacious in improving IIEF-EF, SEP2, and SEP3 in those with and without self-reported HTN. Vardenafil Dihydrochloride 0-10 septin 3 Homo sapiens 67-71 17498108-9 2007 The average per patient penetration (SEP2) success rate was significantly higher in the vardenafil group compared with placebo (88% vs. 58%; P < 0.0001). Vardenafil Dihydrochloride 88-98 septin 6 Homo sapiens 37-41 17694282-3 2007 Three PDE5 inhibitors, sildenafil, vardenafil, and tadalafil, have been approved for the treatment of "erectile dysfunction" (ED). Vardenafil Dihydrochloride 35-45 phosphodiesterase 5A Homo sapiens 6-10 16988721-1 2007 Differences in clinical pharmacology of the currently marketed phosphodiesterase (PDE)5 inhibitors sildenafil, vardenafil and tadalafil are largely determined by their pharmacokinetic (PK) properties and their PDE5 inhibitory activity profile. Vardenafil Dihydrochloride 111-121 phosphodiesterase 5A Homo sapiens 82-87 16988721-1 2007 Differences in clinical pharmacology of the currently marketed phosphodiesterase (PDE)5 inhibitors sildenafil, vardenafil and tadalafil are largely determined by their pharmacokinetic (PK) properties and their PDE5 inhibitory activity profile. Vardenafil Dihydrochloride 111-121 phosphodiesterase 5A Homo sapiens 210-214 17351661-1 2007 BACKGROUND AND PURPOSE: Recently, orthostatic hypotension was observed in patients with benign prostatic hyperplasia who are taking vardenafil (a PDE 5 inhibitor) and terazosin (a long acting alpha blocker). Vardenafil Dihydrochloride 132-142 phosphodiesterase 5A Homo sapiens 146-151 17498108-10 2007 Moreover, the average per patient intercourse completion (SEP3) success rate was significantly higher in the vardenafil group compared with placebo (69% vs. 23%; P < 0.0001). Vardenafil Dihydrochloride 109-119 septin 3 Homo sapiens 58-62 17378845-9 2007 The benefits of vardenafil were greater in men who had undergone previous PDE-5-inhibitor treatment and men aged <45 years, while the overall pattern of benefit was similar in all examined subgroups. Vardenafil Dihydrochloride 16-26 phosphodiesterase 5A Homo sapiens 74-79 17378845-10 2007 There were significant benefits with vardenafil in all other variables (IIEF-EF scores and positive response rates to SEP-2 and SEP-3). Vardenafil Dihydrochloride 37-47 septin 6 Homo sapiens 118-123 17378845-10 2007 There were significant benefits with vardenafil in all other variables (IIEF-EF scores and positive response rates to SEP-2 and SEP-3). Vardenafil Dihydrochloride 37-47 septin 3 Homo sapiens 128-133 17138653-2 2007 Phosphodiesterase type 5 (PDE5) inhibitors (sildenafil, tadalafil, and vardenafil) decrease lower urinary tract symptoms in patients with erectile dysfunction and BPH. Vardenafil Dihydrochloride 71-81 phosphodiesterase 5A Homo sapiens 0-24 17138653-2 2007 Phosphodiesterase type 5 (PDE5) inhibitors (sildenafil, tadalafil, and vardenafil) decrease lower urinary tract symptoms in patients with erectile dysfunction and BPH. Vardenafil Dihydrochloride 71-81 phosphodiesterase 5A Homo sapiens 26-30 17138653-8 2007 However, blocking PDE5 with vardenafil increased SNP antiproliferative and relaxant activity up to the level observed with SP-8-Br-PET-cGMPS. Vardenafil Dihydrochloride 28-38 phosphodiesterase 5A Homo sapiens 18-22 17138653-13 2007 Overall, these results demonstrate that PDE5 regulates bladder smooth muscle tone, strongly limiting the nitric oxide/cGMP signaling, and that vardenafil, by blocking PDE5, may be a possible therapeutic option for bladder dysfunction by ameliorating irritative lower urinary tract symptoms. Vardenafil Dihydrochloride 143-153 phosphodiesterase 5A Homo sapiens 167-171 16801935-9 2007 RESULTS: In clinic trials, PDE5 inhibitors were effective (rigidity enough for penetration) in 85% of the patients on Sildenafil, 74% of the patients on Vardenafil and 72% of the patients on Tadalafil. Vardenafil Dihydrochloride 153-163 phosphodiesterase 5A Homo sapiens 27-31 16738695-1 2007 The phosphodiesterase type 5 (PDE5) inhibitors, sildenafil, tadalafil and vardenafil, are a class of medications that are safe and effective in treating erectile dysfunction (ED). Vardenafil Dihydrochloride 74-84 phosphodiesterase 5A Homo sapiens 4-28 16738695-1 2007 The phosphodiesterase type 5 (PDE5) inhibitors, sildenafil, tadalafil and vardenafil, are a class of medications that are safe and effective in treating erectile dysfunction (ED). Vardenafil Dihydrochloride 74-84 phosphodiesterase 5A Homo sapiens 30-34 16888683-2 2007 Although the development of phosphodiesterase type 5 (PDE5) inhibitors (i.e. sildenafil, tadalafil and vardenafil) has revolutionized the treatment of ED, these oral medications require on-demand access and are not as effective in treating ED related to diabetic, post-prostatectomy and severe veno-occlusive disease states. Vardenafil Dihydrochloride 103-113 phosphodiesterase 5A Homo sapiens 28-52 16888683-2 2007 Although the development of phosphodiesterase type 5 (PDE5) inhibitors (i.e. sildenafil, tadalafil and vardenafil) has revolutionized the treatment of ED, these oral medications require on-demand access and are not as effective in treating ED related to diabetic, post-prostatectomy and severe veno-occlusive disease states. Vardenafil Dihydrochloride 103-113 phosphodiesterase 5A Homo sapiens 54-58 17305584-3 2007 For example, selective PDE5 inhibitors, such as sildenafil (Viagra, Pfizer), tadalafil (Cialis, Lilly-ICOS), and vardenafil (Levitra, Bayer), have been successfully used to treat the condition of human erectile dysfunction. Vardenafil Dihydrochloride 113-123 phosphodiesterase 5A Homo sapiens 23-27 17691956-3 2007 Chemical inhibition of PDE5 by sildenafil, tadalafil or vardenafil recently became a valid therapeutic option aimed at overexpressing the molecular pathway originated from nitric oxide and expressed via increased cell cGMP availability. Vardenafil Dihydrochloride 56-66 phosphodiesterase 5A Homo sapiens 23-27 26627173-3 2007 In this study, we look at the mechanism and thermodynamics of the binding of selective inhibitors sildenafil (Viagra) and vardenafil (Levitra) to PDE5 using molecular dynamics simulations. Vardenafil Dihydrochloride 122-132 phosphodiesterase 5A Homo sapiens 146-150 17127429-0 2007 Phosphorylation of phosphodiesterase-5 is promoted by a conformational change induced by sildenafil, vardenafil, or tadalafil. Vardenafil Dihydrochloride 101-111 phosphodiesterase 5A Homo sapiens 19-38 17127429-1 2007 Phosphodiesterase-5 (PDE5) inhibitors (sildenafil, vardenafil, or tadalafil) or phosphorylation by cyclic nucleotide-dependent protein kinase causes an apparent conformational change in PDE5, as indicated by a shift in migration on non-denaturing PAGE gels and an altered pattern of tryptic digestion. Vardenafil Dihydrochloride 51-61 phosphodiesterase 5A Homo sapiens 0-19 17127429-1 2007 Phosphodiesterase-5 (PDE5) inhibitors (sildenafil, vardenafil, or tadalafil) or phosphorylation by cyclic nucleotide-dependent protein kinase causes an apparent conformational change in PDE5, as indicated by a shift in migration on non-denaturing PAGE gels and an altered pattern of tryptic digestion. Vardenafil Dihydrochloride 51-61 phosphodiesterase 5A Homo sapiens 21-25 17127429-1 2007 Phosphodiesterase-5 (PDE5) inhibitors (sildenafil, vardenafil, or tadalafil) or phosphorylation by cyclic nucleotide-dependent protein kinase causes an apparent conformational change in PDE5, as indicated by a shift in migration on non-denaturing PAGE gels and an altered pattern of tryptic digestion. Vardenafil Dihydrochloride 51-61 phosphodiesterase 5A Homo sapiens 186-190 26627173-3 2007 In this study, we look at the mechanism and thermodynamics of the binding of selective inhibitors sildenafil (Viagra) and vardenafil (Levitra) to PDE5 using molecular dynamics simulations. Vardenafil Dihydrochloride 134-141 phosphodiesterase 5A Homo sapiens 146-150 16979814-5 2006 Orally effective PDE5-Is, such as sildenafil, tadalafil, or vardenafil, may be ineffective depending on the demonstration of testosterone regulation of PDE5 expression in human corpus cavernous, and their efficacy may be enhanced by testosterone adjunction whenever necessary. Vardenafil Dihydrochloride 60-70 phosphodiesterase 5A Homo sapiens 17-21 17471999-0 2007 [Therapeutic efficacy of a course administration of vardenafil--inhibitor of phosphodiesterase-5--in erectile dysfunction]. Vardenafil Dihydrochloride 52-62 phosphodiesterase 5A Homo sapiens 77-96 17471999-1 2007 We studied a therapeutic effect of long-term and regular use of vardenafil which is an inhibitor of phosphodiesterase-5 (PDE-5) in patients with erectile dysfunction (n=32, mean age 35.7 +/- 6.8 years). Vardenafil Dihydrochloride 64-74 phosphodiesterase 5A Homo sapiens 100-119 17471999-1 2007 We studied a therapeutic effect of long-term and regular use of vardenafil which is an inhibitor of phosphodiesterase-5 (PDE-5) in patients with erectile dysfunction (n=32, mean age 35.7 +/- 6.8 years). Vardenafil Dihydrochloride 64-74 phosphodiesterase 5A Homo sapiens 121-126 17201266-2 2006 There are three kinds of PDE5-I available at present, Sildenafil, Vardenafil and Tadalafil. Vardenafil Dihydrochloride 66-76 phosphodiesterase 5A Homo sapiens 25-29 17101732-1 2006 Phosphodiesterase-5 (PDE5) inhibitors (sildenafil, tadalafil, and vardenafil) are agents currently in clinical use for nonmalignant conditions. Vardenafil Dihydrochloride 66-76 phosphodiesterase 5A Homo sapiens 0-19 17101732-1 2006 Phosphodiesterase-5 (PDE5) inhibitors (sildenafil, tadalafil, and vardenafil) are agents currently in clinical use for nonmalignant conditions. Vardenafil Dihydrochloride 66-76 phosphodiesterase 5A Homo sapiens 21-25 16979814-5 2006 Orally effective PDE5-Is, such as sildenafil, tadalafil, or vardenafil, may be ineffective depending on the demonstration of testosterone regulation of PDE5 expression in human corpus cavernous, and their efficacy may be enhanced by testosterone adjunction whenever necessary. Vardenafil Dihydrochloride 60-70 phosphodiesterase 5A Homo sapiens 152-156 17073835-7 2006 Vardenafil demonstrated overall effectiveness, including first-dose SEP-2 and SEP-3 success rates in patients with and without specific comorbidities. Vardenafil Dihydrochloride 0-10 septin 6 Homo sapiens 68-73 17034606-2 2006 OBJECTIVE: To investigate whether the results of the ultrasonographic (US) measurement of post-occlusive changes in the diameters of cavernosal arteries after administering phosphodiesterase type 5 (PDE-5) inhibitor vardenafil could be associated with the response to vardenafil in patients with erectile dysfunction (ED), as currently there are no reliable methods for predicting the success rate of oral PDE-5 inhibitors. Vardenafil Dihydrochloride 216-226 phosphodiesterase 5A Homo sapiens 173-197 17034606-2 2006 OBJECTIVE: To investigate whether the results of the ultrasonographic (US) measurement of post-occlusive changes in the diameters of cavernosal arteries after administering phosphodiesterase type 5 (PDE-5) inhibitor vardenafil could be associated with the response to vardenafil in patients with erectile dysfunction (ED), as currently there are no reliable methods for predicting the success rate of oral PDE-5 inhibitors. Vardenafil Dihydrochloride 216-226 phosphodiesterase 5A Homo sapiens 199-204 16926278-0 2006 A 46-amino acid segment in phosphodiesterase-5 GAF-B domain provides for high vardenafil potency over sildenafil and tadalafil and is involved in phosphodiesterase-5 dimerization. Vardenafil Dihydrochloride 78-88 phosphodiesterase 5A Homo sapiens 27-46 17100937-12 2006 Patients also had a higher percentage of positive responses for vardenafil for SEP2, SEP3, GAQ, and 12 of 19 questions on the TSS. Vardenafil Dihydrochloride 64-74 septin 6 Homo sapiens 79-83 17100937-12 2006 Patients also had a higher percentage of positive responses for vardenafil for SEP2, SEP3, GAQ, and 12 of 19 questions on the TSS. Vardenafil Dihydrochloride 64-74 septin 3 Homo sapiens 85-89 16820261-6 2006 Patients treated with vardenafil 8 hours before sexual activity achieved clinically meaningful (>or=18%) and statistically significantly greater least-squares mean per-patient SEP3 and SEP2 success rates over weeks 2-10, compared with patients receiving placebo (SEP3 69% vs 34%; SEP2 81% vs 51%; both p<0.001). Vardenafil Dihydrochloride 22-32 septin 6 Homo sapiens 188-192 16820261-6 2006 Patients treated with vardenafil 8 hours before sexual activity achieved clinically meaningful (>or=18%) and statistically significantly greater least-squares mean per-patient SEP3 and SEP2 success rates over weeks 2-10, compared with patients receiving placebo (SEP3 69% vs 34%; SEP2 81% vs 51%; both p<0.001). Vardenafil Dihydrochloride 22-32 septin 6 Homo sapiens 283-287 16820261-7 2006 SEP3 and SEP2 measures demonstrated the significant superiority of vardenafil over placebo from week 2 onwards (p<0.001). Vardenafil Dihydrochloride 67-77 septin 6 Homo sapiens 9-13 17100936-0 2006 Vardenafil improves sexual function and treatment satisfaction in couples affected by erectile dysfunction (ED): a randomized, double-blind, placebo-controlled trial in PDE5 inhibitor-naive men with ED and their partners. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 169-173 17100936-2 2006 AIM: The FINDER study aimed to evaluate the efficacy and tolerability of the phosphodiesterase type-5 (PDE5) inhibitor, vardenafil, in a broad population of PDE5-naive men with ED of different etiologies and severity and included their partners" assessments of treatment with vardenafil. Vardenafil Dihydrochloride 120-130 phosphodiesterase 5A Homo sapiens 77-101 17100936-2 2006 AIM: The FINDER study aimed to evaluate the efficacy and tolerability of the phosphodiesterase type-5 (PDE5) inhibitor, vardenafil, in a broad population of PDE5-naive men with ED of different etiologies and severity and included their partners" assessments of treatment with vardenafil. Vardenafil Dihydrochloride 120-130 phosphodiesterase 5A Homo sapiens 103-107 17100936-2 2006 AIM: The FINDER study aimed to evaluate the efficacy and tolerability of the phosphodiesterase type-5 (PDE5) inhibitor, vardenafil, in a broad population of PDE5-naive men with ED of different etiologies and severity and included their partners" assessments of treatment with vardenafil. Vardenafil Dihydrochloride 120-130 phosphodiesterase 5A Homo sapiens 157-161 17100936-2 2006 AIM: The FINDER study aimed to evaluate the efficacy and tolerability of the phosphodiesterase type-5 (PDE5) inhibitor, vardenafil, in a broad population of PDE5-naive men with ED of different etiologies and severity and included their partners" assessments of treatment with vardenafil. Vardenafil Dihydrochloride 276-286 phosphodiesterase 5A Homo sapiens 103-107 16926278-0 2006 A 46-amino acid segment in phosphodiesterase-5 GAF-B domain provides for high vardenafil potency over sildenafil and tadalafil and is involved in phosphodiesterase-5 dimerization. Vardenafil Dihydrochloride 78-88 phosphodiesterase 5A Homo sapiens 146-165 16926278-7 2006 All PDE5 constructs had similar affinities for 3-isobutyl-1-methylxanthine, sildenafil, tadalafil, and UK-122764, but mutants containing a complete GAF-B had 7- to 18-fold higher affinity for vardenafil-based compounds compared with those lacking a complete GAF-B. Vardenafil Dihydrochloride 192-202 phosphodiesterase 5A Homo sapiens 4-8 16884667-3 2006 Phosphodiesterase type 5 (PDE5) inhibitors, sildenafil, vardenafil, and tadalafil, provide effective treatment of erectile dysfunction. Vardenafil Dihydrochloride 56-66 phosphodiesterase 5A Homo sapiens 26-30 16942533-8 2006 Sexual intercourse was successfully completed (SEP3) in 76.3%, 80.1%, and 74.3% of subjects receiving 5, 10, and 20 mg vardenafil compared with 25.9%, 17.9%, and 19.2% at baseline, respectively. Vardenafil Dihydrochloride 119-129 septin 3 Homo sapiens 47-51 16735511-1 2006 Phosphodiesterase-5 (PDE5) is the target for sildenafil, vardenafil, and tadalafil, which are drugs for treatment of erectile dysfunction and pulmonary hypertension. Vardenafil Dihydrochloride 57-67 phosphodiesterase 5A Homo sapiens 0-19 16904479-9 2006 Compared with the BCNX group, vardenafil increased both iNOS and proliferating cell nuclear antigen expression (SM cell replication), with normalization of the dynamic infusion cavernosometry drop rate and SM/collagen ratio. Vardenafil Dihydrochloride 30-40 nitric oxide synthase 2 Rattus norvegicus 56-60 16904479-10 2006 CONCLUSIONS: Long-term treatment with vardenafil may prevent CVOD after radical prostatectomy by preserving SM content and inhibiting corporal fibrosis possibly by its effect on iNOS. Vardenafil Dihydrochloride 38-48 nitric oxide synthase 2 Rattus norvegicus 178-182 16735511-1 2006 Phosphodiesterase-5 (PDE5) is the target for sildenafil, vardenafil, and tadalafil, which are drugs for treatment of erectile dysfunction and pulmonary hypertension. Vardenafil Dihydrochloride 57-67 phosphodiesterase 5A Homo sapiens 21-25 16894950-2 2006 Vardenafil is a potent, highly selective phosphodiesterase 5 (PDE5) inhibitor. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 41-60 16901064-1 2006 Three different phosphodiesterase 5 (PDE5) inhibitors are currently available for the treatment of erectile dysfunction: sildenafil, vardenafil and tadalafil. Vardenafil Dihydrochloride 133-143 phosphodiesterase 5A Homo sapiens 37-41 16894950-2 2006 Vardenafil is a potent, highly selective phosphodiesterase 5 (PDE5) inhibitor. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 62-66 16724576-10 2006 The most frequently reported adverse events were vasodilation and nasal congestion, well-known side effects of PDE-5 inhibitors such as vardenafil. Vardenafil Dihydrochloride 136-146 phosphodiesterase 5A Homo sapiens 111-116 17058681-3 2006 We studied potentialities of ultrasonic investigation (UI) of postcompression increase in cavernous arteries diameter (PICAD) after intake of vardenafil (levitra, Bayer&GlaxoSmithKline) which is a PDE-5 inhibitor in prediction of clinical efficacy of this medicine. Vardenafil Dihydrochloride 142-152 phosphodiesterase 5A Homo sapiens 201-206 16469038-2 2006 MATERIALS AND METHODS: Vardenafil was given to male rats (eight per group) either in the drinking water or as an oral instillation once daily, at approximately 1 and approximately 3 mg/kg/day for 45 days after one injection with TGF-beta1 into the tunica albuginea, as an "early preventive" treatment for TGF-beta1-induced formation of a PD-like plaque. Vardenafil Dihydrochloride 23-33 transforming growth factor, beta 1 Rattus norvegicus 229-238 16683577-1 2006 This paper reviewed the efficacy and safety of vardenafil, a highly selective phosphodiesterase type 5 (PDE 5) inhibitor, in men with erectile dysfunction who were difficult to treat. Vardenafil Dihydrochloride 47-57 phosphodiesterase 5A Homo sapiens 78-102 16683577-1 2006 This paper reviewed the efficacy and safety of vardenafil, a highly selective phosphodiesterase type 5 (PDE 5) inhibitor, in men with erectile dysfunction who were difficult to treat. Vardenafil Dihydrochloride 47-57 phosphodiesterase 5A Homo sapiens 104-109 16281046-0 2006 Tyrosine-612 in PDE5 contributes to higher affinity for vardenafil over sildenafil. Vardenafil Dihydrochloride 56-66 phosphodiesterase 5A Homo sapiens 16-20 16281046-1 2006 Despite close structural similarity, vardenafil (Levitra) is 32-fold more potent than sildenafil (Viagra) to inhibit cGMP-binding cGMP-specific PDE (PDE5); this is due to differences between their heterocyclic rings. Vardenafil Dihydrochloride 37-47 phosphodiesterase 5A Homo sapiens 149-153 16281046-1 2006 Despite close structural similarity, vardenafil (Levitra) is 32-fold more potent than sildenafil (Viagra) to inhibit cGMP-binding cGMP-specific PDE (PDE5); this is due to differences between their heterocyclic rings. Vardenafil Dihydrochloride 49-56 phosphodiesterase 5A Homo sapiens 149-153 16281046-2 2006 In co-crystals with PDE5, one of the rings of vardenafil or sildenafil interacts with Tyr(612), a catalytic site AA, via (1) a hydrogen bond with a water molecule and (2) hydrophobic bonds. Vardenafil Dihydrochloride 46-56 phosphodiesterase 5A Homo sapiens 20-24 16281046-3 2006 For mutant PDE5(Y612F), which ablates hydrogen-bonding potential, vardenafil or sildenafil inhibition was strengthened (2.2- or 3.0-fold, respectively), implying that the Tyr(612) hydroxyl is a negative determinant for these inhibitors. Vardenafil Dihydrochloride 66-76 phosphodiesterase 5A Homo sapiens 11-15 16281046-4 2006 For mutant PDE5(Y612A), which ablates both hydrogen bonding and hydrophobic-bonding potential, vardenafil inhibition was weakened much more than sildenafil inhibition (122- and 26-fold, respectively), suggesting that hydrophobic bonds involving Tyr(612) are stronger for vardenafil than for sildenafil. Vardenafil Dihydrochloride 95-105 phosphodiesterase 5A Homo sapiens 11-15 16281046-4 2006 For mutant PDE5(Y612A), which ablates both hydrogen bonding and hydrophobic-bonding potential, vardenafil inhibition was weakened much more than sildenafil inhibition (122- and 26-fold, respectively), suggesting that hydrophobic bonds involving Tyr(612) are stronger for vardenafil than for sildenafil. Vardenafil Dihydrochloride 271-281 phosphodiesterase 5A Homo sapiens 11-15 16469038-5 2006 RESULTS: Preventative treatment with vardenafil at the higher dose (both continuous and once-daily treatments) reduced the collagen/smooth muscle and collagen III/I ratios, and the numbers of myofibroblasts and TGF-beta1-positive cells, and selectively increased the apoptotic index in the PD-like plaque. Vardenafil Dihydrochloride 37-47 transforming growth factor, beta 1 Rattus norvegicus 211-220 17017939-2 2006 Three PDE5 inhibitors (sildenafil, tadalafil, and vardenafil) are clinically available at this time, and extensive drug design efforts are registered for finding agents with a better activity, enhanced selectivity and reduced side effects. Vardenafil Dihydrochloride 50-60 phosphodiesterase 5A Homo sapiens 6-10 16480739-2 2006 We investigated the cardioprotective effect of vardenafil (VAR) (Levitra), a highly selective and biochemically potent inhibitor of phosphodiesterase-5 (PDE-5) that enhances erectile function in men through up-regulation of cGMP. Vardenafil Dihydrochloride 47-57 phosphodiesterase 5A Homo sapiens 132-151 16480739-2 2006 We investigated the cardioprotective effect of vardenafil (VAR) (Levitra), a highly selective and biochemically potent inhibitor of phosphodiesterase-5 (PDE-5) that enhances erectile function in men through up-regulation of cGMP. Vardenafil Dihydrochloride 47-57 phosphodiesterase 5A Homo sapiens 153-158 16480739-2 2006 We investigated the cardioprotective effect of vardenafil (VAR) (Levitra), a highly selective and biochemically potent inhibitor of phosphodiesterase-5 (PDE-5) that enhances erectile function in men through up-regulation of cGMP. Vardenafil Dihydrochloride 65-72 phosphodiesterase 5A Homo sapiens 132-151 16480739-2 2006 We investigated the cardioprotective effect of vardenafil (VAR) (Levitra), a highly selective and biochemically potent inhibitor of phosphodiesterase-5 (PDE-5) that enhances erectile function in men through up-regulation of cGMP. Vardenafil Dihydrochloride 65-72 phosphodiesterase 5A Homo sapiens 153-158 16526979-11 2006 The recent addition of vardenafil and tadalafil to the market has increased the number of phosphodiesterase type 5 inhibitors (PDE5) to three agents used throughout the world. Vardenafil Dihydrochloride 23-33 phosphodiesterase 5A Homo sapiens 127-131 16755146-2 2006 Recently, vardenafil, a more potent and selective PDE-5 inhibitor than sildenafil, has been approved for the treatment of erectile dysfunction. Vardenafil Dihydrochloride 10-20 phosphodiesterase 5A Homo sapiens 50-55 16204472-2 2006 We aimed to explore the mechanisms underlying the vasorelaxation induced by the selective PDE5 inhibitors sildenafil, vardenafil, and tadalafil in the rat aorta. Vardenafil Dihydrochloride 118-128 phosphodiesterase 5A Rattus norvegicus 90-94 16204472-12 2006 These results suggest that vardenafil, but not sildenafil or tadalafil, affects Ca(2+) handling in the rat aorta in addition to increasing cGMP levels through inhibition of PDE5 to cause relaxation. Vardenafil Dihydrochloride 27-37 phosphodiesterase 5A Rattus norvegicus 173-177 16422806-8 2005 RESULTS: Compared with placebo at LOCF, vardenafil significantly increased least square (LS) mean scores in: (i) overall per-treated male SEP3 success rate, IIEF-EF, and EQS; and (ii) mSLQQ-QOL, total FSFI and sexual desire, subjective arousal, lubrication, orgasm and satisfaction FSFI domains in untreated women partners. Vardenafil Dihydrochloride 40-50 septin 3 Homo sapiens 138-142 16387566-1 2005 Currently, 3 phosphodiesterase 5 (PDE5) inhibitor agents are available worldwide for the treatment of erectile dysfunction (ED): sildenafil, vardenafil, and tadalafil. Vardenafil Dihydrochloride 141-151 phosphodiesterase 5A Homo sapiens 34-38 16273417-6 2005 This review, which is based on the contemporary literature on PDE-5 inhibitors, describes the chemical, pharmacological, and clinical features of sildenafil, vardenafil, and tadalafil. Vardenafil Dihydrochloride 158-168 phosphodiesterase 5A Homo sapiens 62-67 16273418-2 2005 Although a complete pharmacological cure for ED is currently unavailable, the phosphodiesterase 5 (PDE5) inhibitors sildenafil, vardenafil, and tadalafil are efficacious oral therapy for ED. Vardenafil Dihydrochloride 128-138 phosphodiesterase 5A Homo sapiens 78-97 16273418-2 2005 Although a complete pharmacological cure for ED is currently unavailable, the phosphodiesterase 5 (PDE5) inhibitors sildenafil, vardenafil, and tadalafil are efficacious oral therapy for ED. Vardenafil Dihydrochloride 128-138 phosphodiesterase 5A Homo sapiens 99-103 16273419-5 2005 In another set-up, the effects of the PDE4 inhibitor rolipram and PDE5 inhibitors sildenafil and vardenafil (1 nM-10 microM) on the tension induced by 0.1 microM ET-1 of human vaginal wall tissue strips were investigated. Vardenafil Dihydrochloride 97-107 endothelin 1 Homo sapiens 162-166 16817245-2 2006 The Food and Drug Administration (FDA) approved PDE-5 inhibitors include sildenafil citrate, vardenafil hydrochloride and tadalafil. Vardenafil Dihydrochloride 93-117 phosphodiesterase 5A Homo sapiens 48-53 16422809-10 2005 Using logistic regression, the odds of refilling initial PDE5 therapy was significantly lower for vardenafil (odds ratio [OR]: 0.39, 95% confidence interval [CI]: 0.38-0.40; P<0.0001) and tadalafil (OR: 0.38, 95% CI: 0.37-0.40; P<0.0001) compared with sildenafil. Vardenafil Dihydrochloride 98-108 phosphodiesterase 5A Homo sapiens 57-61 16422810-1 2005 INTRODUCTION: Vardenafil, a phosphodiesterase type 5 (PDE5) inhibitor, was evaluated in a prospective trial in the primary care setting involving hypertensive men with ED who were receiving at least one antihypertensive medication. Vardenafil Dihydrochloride 14-24 phosphodiesterase 5A Homo sapiens 28-52 16422810-1 2005 INTRODUCTION: Vardenafil, a phosphodiesterase type 5 (PDE5) inhibitor, was evaluated in a prospective trial in the primary care setting involving hypertensive men with ED who were receiving at least one antihypertensive medication. Vardenafil Dihydrochloride 14-24 phosphodiesterase 5A Homo sapiens 54-58 16422810-2 2005 AIMS: To investigate the safety and efficacy of flexible-dose vardenafil therapy compared with placebo in PDE5 inhibitor-naive subjects with arterial hypertension and ED. Vardenafil Dihydrochloride 62-72 phosphodiesterase 5A Homo sapiens 106-110 16422810-6 2005 RESULTS: Compared with placebo, vardenafil significantly improved mean SEP2 and SEP3 success rates over the 12-week study period (intention-to-treat [ITT] and last observation carried forward [LOCF]) analysis). Vardenafil Dihydrochloride 32-42 septin 6 Homo sapiens 71-75 16422810-6 2005 RESULTS: Compared with placebo, vardenafil significantly improved mean SEP2 and SEP3 success rates over the 12-week study period (intention-to-treat [ITT] and last observation carried forward [LOCF]) analysis). Vardenafil Dihydrochloride 32-42 septin 3 Homo sapiens 80-84 16151756-5 2005 Besides psychotherapy, oral pharmacotherapy with oral PDE-5 inhibitors (sildenafil, tadalafil, vardenafil) is the most effective therapy for erectile dysfunction and is superior to centrally acting drugs (yohimbine). Vardenafil Dihydrochloride 95-105 phosphodiesterase 5A Homo sapiens 54-59 16212141-8 2005 During the double-blind phase, the reliability of penetration and maintenance rates for patients successful during the challenge phase were significantly greater with vardenafil compared with placebo (83.4% vs 55.8% [SEP2] and 76.6% vs 42.1% [SEP3], respectively). Vardenafil Dihydrochloride 167-177 septin 6 Homo sapiens 217-221 16212141-8 2005 During the double-blind phase, the reliability of penetration and maintenance rates for patients successful during the challenge phase were significantly greater with vardenafil compared with placebo (83.4% vs 55.8% [SEP2] and 76.6% vs 42.1% [SEP3], respectively). Vardenafil Dihydrochloride 167-177 septin 3 Homo sapiens 243-247 16123402-6 2005 Vardenafil, a potent PDE5 inhibitor (K(i) = 0.2 nM), was the most potent PDE6 inhibitor tested (K(i) = 0.7 nM). Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 21-25 16088037-2 2005 The cumulative probability of achieving successful penetration and of maintaining an erection increased with the number of attempts for all 3 vardenafil groups. Vardenafil Dihydrochloride 142-152 paired box 5 Homo sapiens 136-141 16088037-3 2005 For the first attempt, the probability of achieving successful penetration was higher in all 3 vardenafil groups compared with placebo; 67% in the 5-mg vardenafil group, 77% in the 10-mg vardenafil group, and 74% in the 20-mg vardenafil group compared with 46% for placebo. Vardenafil Dihydrochloride 95-105 paired box 5 Homo sapiens 89-94 16100293-1 2005 Differences in the clinical pharmacology of the 3 currently available oral phosphodiesterase-5 (PDE5) inhibitors, sildenafil, vardenafil, and tadalafil, are largely determined by their clinical pharmacokinetics as well as their PDE inhibitory activity profile. Vardenafil Dihydrochloride 126-136 phosphodiesterase 5A Homo sapiens 75-94 16100293-1 2005 Differences in the clinical pharmacology of the 3 currently available oral phosphodiesterase-5 (PDE5) inhibitors, sildenafil, vardenafil, and tadalafil, are largely determined by their clinical pharmacokinetics as well as their PDE inhibitory activity profile. Vardenafil Dihydrochloride 126-136 phosphodiesterase 5A Homo sapiens 96-100 16100293-1 2005 Differences in the clinical pharmacology of the 3 currently available oral phosphodiesterase-5 (PDE5) inhibitors, sildenafil, vardenafil, and tadalafil, are largely determined by their clinical pharmacokinetics as well as their PDE inhibitory activity profile. Vardenafil Dihydrochloride 126-136 aldehyde dehydrogenase 7 family member A1 Homo sapiens 96-99 16123402-6 2005 Vardenafil, a potent PDE5 inhibitor (K(i) = 0.2 nM), was the most potent PDE6 inhibitor tested (K(i) = 0.7 nM). Vardenafil Dihydrochloride 0-10 aldehyde dehydrogenase 7 family member A1 Homo sapiens 73-77 15941818-9 2005 Sildenafil, vardenafil, and tadalafil are selective PDE5 inhibitors currently available for treatment of ED. Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 52-56 16922644-4 2005 Vardenafil is a highly selective, potent PDE5 inhibitor developed for the treatment of ED. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 41-45 16922644-5 2005 The potency and selectivity of vardenafil for PDE5 and other PDE isoforms have been evaluated in vitro and in vivo and compared with other compounds in the class. Vardenafil Dihydrochloride 31-41 phosphodiesterase 5A Homo sapiens 46-50 15941818-11 2005 CONCLUSIONS: Sildenafil, vardenafil, and tadalafil are safe and effective PDE5 inhibitors for the treatment of ED. Vardenafil Dihydrochloride 25-35 phosphodiesterase 5A Homo sapiens 74-78 16011816-10 2005 CONCLUSION: In this retrospective analysis of two pivotal trials, vardenafil improved success rates compared with placebo in ED patients who attempted intercourse from as early as 15 minutes or less and through 4-8 hours after dosing in ability to penetrate (SEP2) and from as early as 15 minutes or less and through 8-12 hours after dosing in maintenance of erection (SEP3). Vardenafil Dihydrochloride 66-76 septin 3 Homo sapiens 369-373 16078679-4 2005 In recent years, new PDE5 inhibitors--vardenafil and tadalafil came into market in succession, providing more options available for oral therapy. Vardenafil Dihydrochloride 38-48 phosphodiesterase 5A Homo sapiens 21-25 16156422-4 2005 The PDE5 inhibitors, sildenafil, tadalafil, and vardenafil, have proven to be effective and well tolerated and facilitate erectile function. Vardenafil Dihydrochloride 48-58 phosphodiesterase 5A Homo sapiens 4-8 15766322-3 2005 Two PDE5 inhibitors, vardenafil and tadalafil, have since joined sildenafil to compete in the ERD market. Vardenafil Dihydrochloride 21-31 phosphodiesterase 5A Homo sapiens 4-8 15766322-15 2005 However, vardenafil is the only PDE5 inhibitor with a cardiac conduction precaution. Vardenafil Dihydrochloride 9-19 phosphodiesterase 5A Homo sapiens 32-36 15934858-1 2005 Therapy of erectile dysfunction has been revolutionised in recent years, as specific pharmacological inhibitors of phosphodiesterase 5 (PDE5), such as sildenafil, tadalafil, or vardenafil, were shown to be highly effective in the treatment of erectile dysfunction. Vardenafil Dihydrochloride 177-187 phosphodiesterase 5A Homo sapiens 115-134 15934858-1 2005 Therapy of erectile dysfunction has been revolutionised in recent years, as specific pharmacological inhibitors of phosphodiesterase 5 (PDE5), such as sildenafil, tadalafil, or vardenafil, were shown to be highly effective in the treatment of erectile dysfunction. Vardenafil Dihydrochloride 177-187 phosphodiesterase 5A Homo sapiens 136-140 15934468-2 2005 Recent molecular studies have demonstrated that vardenafil has high affinity for PDE5 and low dissociation rate from PDE5, which serves to explain why vardenafil works with low dosage, onsets quickly and has curative action in clinical practice. Vardenafil Dihydrochloride 48-58 phosphodiesterase 5A Homo sapiens 81-85 15934468-2 2005 Recent molecular studies have demonstrated that vardenafil has high affinity for PDE5 and low dissociation rate from PDE5, which serves to explain why vardenafil works with low dosage, onsets quickly and has curative action in clinical practice. Vardenafil Dihydrochloride 48-58 phosphodiesterase 5A Homo sapiens 117-121 15934468-2 2005 Recent molecular studies have demonstrated that vardenafil has high affinity for PDE5 and low dissociation rate from PDE5, which serves to explain why vardenafil works with low dosage, onsets quickly and has curative action in clinical practice. Vardenafil Dihydrochloride 151-161 phosphodiesterase 5A Homo sapiens 81-85 15934468-2 2005 Recent molecular studies have demonstrated that vardenafil has high affinity for PDE5 and low dissociation rate from PDE5, which serves to explain why vardenafil works with low dosage, onsets quickly and has curative action in clinical practice. Vardenafil Dihydrochloride 151-161 phosphodiesterase 5A Homo sapiens 117-121 16739369-4 2005 The effectiveness of vardenafil was analysed on the basis of the parameters Sexual Encounter Profile (SEP) 2 (vaginal penetration) and SEP3 (erection maintenance) as also the "erectile function score" and overall satisfaction. Vardenafil Dihydrochloride 21-31 septin 6 Homo sapiens 76-108 16739369-4 2005 The effectiveness of vardenafil was analysed on the basis of the parameters Sexual Encounter Profile (SEP) 2 (vaginal penetration) and SEP3 (erection maintenance) as also the "erectile function score" and overall satisfaction. Vardenafil Dihydrochloride 21-31 septin 3 Homo sapiens 135-139 16378510-4 2005 This knowledge has led to the development and current availability of effective oral treatments for erectile dysfunction, the selective phosphodiesterase type 5 (PDE5) inhibitors-sildenafil, vardenafil and tadalafil. Vardenafil Dihydrochloride 191-201 phosphodiesterase 5A Homo sapiens 136-160 16378510-4 2005 This knowledge has led to the development and current availability of effective oral treatments for erectile dysfunction, the selective phosphodiesterase type 5 (PDE5) inhibitors-sildenafil, vardenafil and tadalafil. Vardenafil Dihydrochloride 191-201 phosphodiesterase 5A Homo sapiens 162-166 15538396-0 2005 High biochemical selectivity of tadalafil, sildenafil and vardenafil for human phosphodiesterase 5A1 (PDE5) over PDE11A4 suggests the absence of PDE11A4 cross-reaction in patients. Vardenafil Dihydrochloride 58-68 phosphodiesterase 5A Homo sapiens 79-100 16060698-4 2005 Phosphodiesterase type 5 (PDE5) inhibitors (sildenafil, tadalafil, vardenafil) are currently the first-choice of most physicians and patients for the treatment of ED. Vardenafil Dihydrochloride 67-77 phosphodiesterase 5A Homo sapiens 0-24 16060698-4 2005 Phosphodiesterase type 5 (PDE5) inhibitors (sildenafil, tadalafil, vardenafil) are currently the first-choice of most physicians and patients for the treatment of ED. Vardenafil Dihydrochloride 67-77 phosphodiesterase 5A Homo sapiens 26-30 15538396-0 2005 High biochemical selectivity of tadalafil, sildenafil and vardenafil for human phosphodiesterase 5A1 (PDE5) over PDE11A4 suggests the absence of PDE11A4 cross-reaction in patients. Vardenafil Dihydrochloride 58-68 phosphodiesterase 5A Homo sapiens 102-106 16422913-1 2005 INTRODUCTION: Vardenafil is a potent and selective phosphodiesterase 5 (PDE5) inhibitor developed for the treatment of erectile dysfunction (ED). Vardenafil Dihydrochloride 14-24 phosphodiesterase 5A Homo sapiens 51-70 16042360-4 2005 In facts, inhibition of phosphodiesterase type 5 (PDE5) isoenzyme with sildenafil, tadalafil and vardenafil enhances vasodilatation in the corpus cavernosum and subsequent penile erection. Vardenafil Dihydrochloride 97-107 phosphodiesterase 5A Homo sapiens 24-48 16042360-4 2005 In facts, inhibition of phosphodiesterase type 5 (PDE5) isoenzyme with sildenafil, tadalafil and vardenafil enhances vasodilatation in the corpus cavernosum and subsequent penile erection. Vardenafil Dihydrochloride 97-107 phosphodiesterase 5A Homo sapiens 50-54 16422913-1 2005 INTRODUCTION: Vardenafil is a potent and selective phosphodiesterase 5 (PDE5) inhibitor developed for the treatment of erectile dysfunction (ED). Vardenafil Dihydrochloride 14-24 phosphodiesterase 5A Homo sapiens 72-76 15312980-2 2004 Two commercialized PDE5 inhibitors, sildenafil and vardenafil, are being used to treat erectile dysfunction. Vardenafil Dihydrochloride 51-61 phosphodiesterase 5A Homo sapiens 19-23 15988068-2 2005 Phosphodiesterase-5 (PDE5), which is highly specific for guanosine 3"-5"-cyclic-monophosphate (cGMP) at both its catalytic site and its allosteric sites, has generated particular interest because it is potently and specifically inhibited by three drugs: sildenafil (Viagra, Pfizer), tadalafil (Cialis, Lilly-ICOS), and vardenafil (Levitra, Bayer GSK). Vardenafil Dihydrochloride 319-329 phosphodiesterase 5A Homo sapiens 0-19 15988068-2 2005 Phosphodiesterase-5 (PDE5), which is highly specific for guanosine 3"-5"-cyclic-monophosphate (cGMP) at both its catalytic site and its allosteric sites, has generated particular interest because it is potently and specifically inhibited by three drugs: sildenafil (Viagra, Pfizer), tadalafil (Cialis, Lilly-ICOS), and vardenafil (Levitra, Bayer GSK). Vardenafil Dihydrochloride 319-329 phosphodiesterase 5A Homo sapiens 21-25 15988068-2 2005 Phosphodiesterase-5 (PDE5), which is highly specific for guanosine 3"-5"-cyclic-monophosphate (cGMP) at both its catalytic site and its allosteric sites, has generated particular interest because it is potently and specifically inhibited by three drugs: sildenafil (Viagra, Pfizer), tadalafil (Cialis, Lilly-ICOS), and vardenafil (Levitra, Bayer GSK). Vardenafil Dihydrochloride 319-329 inducible T cell costimulator Homo sapiens 308-312 15672122-6 2004 PDE5 is selectively inhibited by sildenafil, vardenafil and tadalafil, and less selectively by zaprinast and dipyridamole. Vardenafil Dihydrochloride 45-55 phosphodiesterase 5A Rattus norvegicus 0-4 16422960-1 2004 BACKGROUND: Vardenafil (Levitra) is a potent and selective phosphodiesterase 5 (PDE5) inhibitor used in the management of erectile dysfunction (ED). Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 59-78 16422960-1 2004 BACKGROUND: Vardenafil (Levitra) is a potent and selective phosphodiesterase 5 (PDE5) inhibitor used in the management of erectile dysfunction (ED). Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 80-84 16422960-1 2004 BACKGROUND: Vardenafil (Levitra) is a potent and selective phosphodiesterase 5 (PDE5) inhibitor used in the management of erectile dysfunction (ED). Vardenafil Dihydrochloride 24-31 phosphodiesterase 5A Homo sapiens 59-78 16422960-1 2004 BACKGROUND: Vardenafil (Levitra) is a potent and selective phosphodiesterase 5 (PDE5) inhibitor used in the management of erectile dysfunction (ED). Vardenafil Dihydrochloride 24-31 phosphodiesterase 5A Homo sapiens 80-84 16422960-8 2004 For all classifications and for mild-to-moderate to severe ED, men treated with 10 or 20 mg of vardenafil showed statistically and clinically significant improvements (P < 0.001) in IIEF-EF scores, diary response rates to the SEP-2 and SEP-3 questions, and GAQ as compared with those given placebo. Vardenafil Dihydrochloride 95-105 septin 6 Homo sapiens 229-234 16422960-8 2004 For all classifications and for mild-to-moderate to severe ED, men treated with 10 or 20 mg of vardenafil showed statistically and clinically significant improvements (P < 0.001) in IIEF-EF scores, diary response rates to the SEP-2 and SEP-3 questions, and GAQ as compared with those given placebo. Vardenafil Dihydrochloride 95-105 septin 3 Homo sapiens 239-244 15312980-0 2004 Vardenafil: structural basis for higher potency over sildenafil in inhibiting cGMP-specific phosphodiesterase-5 (PDE5). Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 92-111 15312980-0 2004 Vardenafil: structural basis for higher potency over sildenafil in inhibiting cGMP-specific phosphodiesterase-5 (PDE5). Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 113-117 15522526-1 2004 A liquid chromatography-electrospray ionisation-mass spectrometry (LC-ESI-MS) method was developed to screen for the presence of synthetic phosphodiesterase type 5 (PDE-5) inhibitors including sildenafil, tadalafil and vardenafil. Vardenafil Dihydrochloride 219-229 phosphodiesterase 5A Homo sapiens 139-163 15522526-1 2004 A liquid chromatography-electrospray ionisation-mass spectrometry (LC-ESI-MS) method was developed to screen for the presence of synthetic phosphodiesterase type 5 (PDE-5) inhibitors including sildenafil, tadalafil and vardenafil. Vardenafil Dihydrochloride 219-229 phosphodiesterase 5A Homo sapiens 165-170 15312980-5 2004 Although these are the only two structural differences, vardenafil has more than 20-fold greater potency than sildenafil for inhibiting purified PDE5. Vardenafil Dihydrochloride 56-66 phosphodiesterase 5A Homo sapiens 145-149 15312980-8 2004 Similarly, the EC50 of methyl-sildenafil for inhibiting [3H]vardenafil binding to PDE5 indicated that it was 84 times less potent than demethyl-vardenafil, while the EC50 for sildenafil indicated that it was 31 times less potent than vardenafil. Vardenafil Dihydrochloride 60-70 phosphodiesterase 5A Homo sapiens 82-86 15595695-3 2004 Recently, DRIVER (Depression Related Improvement with Vardenafil for Erectile Response) trials showed that, phosphodiesterase 5 (PDE 5) inhibitor vardenafil could improve not only erectile function but also depressive symptoms and quality of life in men with ED and depression. Vardenafil Dihydrochloride 54-64 phosphodiesterase 5A Homo sapiens 108-127 15533493-7 2004 Two placebo patients and 1 vardenafil 10-mg patient had a drop of 20 mm Hg or more in standing DBP; 1 vardenafil 10-mg patient had a standing SBP drop of 30 mm Hg or more. Vardenafil Dihydrochloride 27-37 DEAH-box helicase 15 Homo sapiens 95-101 15533493-7 2004 Two placebo patients and 1 vardenafil 10-mg patient had a drop of 20 mm Hg or more in standing DBP; 1 vardenafil 10-mg patient had a standing SBP drop of 30 mm Hg or more. Vardenafil Dihydrochloride 102-112 DEAH-box helicase 15 Homo sapiens 95-101 15595695-3 2004 Recently, DRIVER (Depression Related Improvement with Vardenafil for Erectile Response) trials showed that, phosphodiesterase 5 (PDE 5) inhibitor vardenafil could improve not only erectile function but also depressive symptoms and quality of life in men with ED and depression. Vardenafil Dihydrochloride 54-64 phosphodiesterase 5A Homo sapiens 129-134 15595695-3 2004 Recently, DRIVER (Depression Related Improvement with Vardenafil for Erectile Response) trials showed that, phosphodiesterase 5 (PDE 5) inhibitor vardenafil could improve not only erectile function but also depressive symptoms and quality of life in men with ED and depression. Vardenafil Dihydrochloride 146-156 phosphodiesterase 5A Homo sapiens 108-127 15595695-3 2004 Recently, DRIVER (Depression Related Improvement with Vardenafil for Erectile Response) trials showed that, phosphodiesterase 5 (PDE 5) inhibitor vardenafil could improve not only erectile function but also depressive symptoms and quality of life in men with ED and depression. Vardenafil Dihydrochloride 146-156 phosphodiesterase 5A Homo sapiens 129-134 15464333-9 2004 CONCLUSIONS: In PAH patients, the three PDE5 inhibitors differ markedly in their kinetics of pulmonary vasorelaxation (most rapid effect by vardenafil), their selectivity for the pulmonary circulation (sildenafil and tadalafil, but not vardenafil), and their impact on arterial oxygenation (improvement with sildenafil only). Vardenafil Dihydrochloride 236-246 phosphodiesterase 5A Homo sapiens 40-44 15476742-4 2004 We studied the ability of three compounds that inhibit PDE5--sildenafil, tadalafil, and vardenafil--to block the HERG channel. Vardenafil Dihydrochloride 88-98 potassium voltage-gated channel subfamily H member 2 Homo sapiens 113-117 15476742-9 2004 Tadalafil had the weakest capacity to block the HERG channel, producing a 50.9% blockade at the maximum soluble concentration (100 microM), compared with 86.2% for vardenafil (100 microM) and 75.2% for sildenafil (100 microM). Vardenafil Dihydrochloride 164-174 potassium voltage-gated channel subfamily H member 2 Homo sapiens 48-52 15464333-3 2004 Vardenafil and tadalafil are new PDE5 inhibitors, recently being approved for the treatment of erectile dysfunction. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 33-37 15497716-1 2004 Vardenafil is an oral, potent, highly selective phosphodiesterase 5 (PDE5) inhibitor. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 48-67 15464333-6 2004 RESULTS: All three PDE5 inhibitors caused significant pulmonary vasorelaxation, with maximum effects being obtained after 40 to 45 min (vardenafil), 60 min (sildenafil), and 75 to 90 min (tadalafil). Vardenafil Dihydrochloride 136-146 phosphodiesterase 5A Homo sapiens 19-23 15464333-9 2004 CONCLUSIONS: In PAH patients, the three PDE5 inhibitors differ markedly in their kinetics of pulmonary vasorelaxation (most rapid effect by vardenafil), their selectivity for the pulmonary circulation (sildenafil and tadalafil, but not vardenafil), and their impact on arterial oxygenation (improvement with sildenafil only). Vardenafil Dihydrochloride 140-150 phosphodiesterase 5A Homo sapiens 40-44 16422971-1 2004 INTRODUCTION: Vardenafil, a potent and selective oral PDE5 inhibitor, is efficacious and generally well-tolerated in men with erectile dysfunction (ED). Vardenafil Dihydrochloride 14-24 phosphodiesterase 5A Homo sapiens 54-58 15562797-1 2004 Vardenafil is a new type of PDE5 inhibitor (PDE5I) with great inhibiting potential on PDE5 (IC50: 0.01 nmol/L) for enhancing erectile function. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 28-32 15562797-1 2004 Vardenafil is a new type of PDE5 inhibitor (PDE5I) with great inhibiting potential on PDE5 (IC50: 0.01 nmol/L) for enhancing erectile function. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 44-48 15497716-1 2004 Vardenafil is an oral, potent, highly selective phosphodiesterase 5 (PDE5) inhibitor. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 69-73 15497717-1 2004 Vardenafil is a potent and highly selective phosphodiesterase type 5 (PDE5) inhibitor with a potency about 10-fold higher than sildenafil. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 44-68 15497717-1 2004 Vardenafil is a potent and highly selective phosphodiesterase type 5 (PDE5) inhibitor with a potency about 10-fold higher than sildenafil. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 70-74 15497717-3 2004 Vardenafil is a PDE5 inhibitor with the fastest onset of action among its kind so far found and works as early as 10 minutes after oral administration, providing patients with penile erection sufficient to complete an intercourse. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 16-20 15224129-3 2004 Sildenafil, vardenafil, and tadalafil are selective for PDE5, with vardenafil exhibiting the highest potency and minimal inhibition of other PDEs, with the exception of PDE6. Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 56-60 15223851-0 2004 Cardiovascular parameter changes in patients with erectile dysfunction using pde-5 inhibitors: a study with sildenafil and vardenafil. Vardenafil Dihydrochloride 123-133 phosphodiesterase 5A Homo sapiens 77-82 15223851-2 2004 Vardenafil is a new phosphodiesterase type 5 (Pde-5) inhibitor that was approved by the US Food and Drug Administration last year to treat patients with ED of various causes. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 20-44 15223851-2 2004 Vardenafil is a new phosphodiesterase type 5 (Pde-5) inhibitor that was approved by the US Food and Drug Administration last year to treat patients with ED of various causes. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 46-51 15223851-13 2004 With vardenafil, we recorded a greater variation for SBP and DBP. Vardenafil Dihydrochloride 5-15 selenium binding protein 1 Homo sapiens 53-56 15223851-13 2004 With vardenafil, we recorded a greater variation for SBP and DBP. Vardenafil Dihydrochloride 5-15 D-box binding PAR bZIP transcription factor Homo sapiens 61-64 15197447-4 2004 Because all three PDE 5 inhibitors sildenafil, tadalafil, and vardenafil have a common mode of action, i.e., inhibition of PDE 5, they are not different in terms of their efficacy and safety profile except for color vision disturbances which are more common after sildenafil and back pain/myalgia more often observed after tadalafil. Vardenafil Dihydrochloride 62-72 phosphodiesterase 5A Homo sapiens 123-128 21224902-5 2004 The introduction of PDE-5 inhibitors like sildenafil, vardenafil and tadalafil has revolutionized the treatment of sexual dysfunctions.This review focuses on the recent pharmacological advances in the treatment of common sexual dysfunctions like ED and PME with special focus on the role of PDE-5 inhibitors. Vardenafil Dihydrochloride 54-64 phosphodiesterase 5A Homo sapiens 20-25 15242361-1 2004 AIM: Vardenafil is a selective and highly potent phosphodiesterase type 5 (PDE5) inhibitor for the treatment of erectile dysfunction (ED), with improved selectivity for PDE5 and demonstrated efficacy for improving sexual function in men with ED. Vardenafil Dihydrochloride 5-15 phosphodiesterase 5A Homo sapiens 49-73 15242361-1 2004 AIM: Vardenafil is a selective and highly potent phosphodiesterase type 5 (PDE5) inhibitor for the treatment of erectile dysfunction (ED), with improved selectivity for PDE5 and demonstrated efficacy for improving sexual function in men with ED. Vardenafil Dihydrochloride 5-15 phosphodiesterase 5A Homo sapiens 75-79 15242361-1 2004 AIM: Vardenafil is a selective and highly potent phosphodiesterase type 5 (PDE5) inhibitor for the treatment of erectile dysfunction (ED), with improved selectivity for PDE5 and demonstrated efficacy for improving sexual function in men with ED. Vardenafil Dihydrochloride 5-15 phosphodiesterase 5A Homo sapiens 169-173 15213306-0 2004 Binding of tritiated sildenafil, tadalafil, or vardenafil to the phosphodiesterase-5 catalytic site displays potency, specificity, heterogeneity, and cGMP stimulation. Vardenafil Dihydrochloride 47-57 phosphodiesterase 5A Homo sapiens 65-84 15213306-1 2004 Sildenafil, tadalafil, and vardenafil each competitively inhibit cGMP hydrolysis by phosphodiesterase-5 (PDE5), thereby fostering cGMP accumulation and relaxation of vascular smooth muscle. Vardenafil Dihydrochloride 27-37 phosphodiesterase 5A Homo sapiens 84-103 15213306-1 2004 Sildenafil, tadalafil, and vardenafil each competitively inhibit cGMP hydrolysis by phosphodiesterase-5 (PDE5), thereby fostering cGMP accumulation and relaxation of vascular smooth muscle. Vardenafil Dihydrochloride 27-37 phosphodiesterase 5A Homo sapiens 105-109 15224134-5 2004 M1, an active metabolite of vardenafil, is a four-fold-less potent inhibitor of PDE5 than its parent compound, contributing approximately 7% to vardenafil"s overall efficacy. Vardenafil Dihydrochloride 28-38 phosphodiesterase 5A Homo sapiens 80-84 15373085-5 2004 For the treatment of erectile dysfunction, the new PDE5 inhibitors vardenafil and tadalafil are now available in addition to sildenafil. Vardenafil Dihydrochloride 67-77 phosphodiesterase 5A Homo sapiens 51-55 15281210-6 2004 Oral PDE-5-inhibitors(sildenafil, tadalafil, vardenafil) are superior in effectiveness to centrally acting drugs (apomorphin, yohimbine). Vardenafil Dihydrochloride 45-55 phosphodiesterase 5A Homo sapiens 5-10 15115191-1 2004 The mechanism of action of the phosphodiesterase type 5 (PDE5) inhibitors (i.e., sildenafil, tadalafil, and vardenafil) involves inhibition of the PDE5 isoenzyme located in penile vascular smooth muscle cells. Vardenafil Dihydrochloride 108-118 phosphodiesterase 5A Homo sapiens 31-55 15155143-4 2004 Tadalafil (Cialis; Eli Lilly & Co., ICOS) and vardenafil (Levitra; Bayer Pharmaceuticals, GlaxoSmithKline) are new PDE5 inhibitors that have recently been approved worldwide. Vardenafil Dihydrochloride 50-60 phosphodiesterase 5A Homo sapiens 119-123 15082207-8 2004 Successful SEP2 rates increased after vardenafil, reaching 84% at weeks 8 and 12 vs. 49-53% receiving placebo (p<0.005 vs. placebo). Vardenafil Dihydrochloride 38-48 septin 6 Homo sapiens 11-15 15082207-9 2004 Vardenafil improved successful SEP3 rates ranging from 58% to 74% compared to 22-34% for placebo. Vardenafil Dihydrochloride 0-10 septin 3 Homo sapiens 31-35 15115191-1 2004 The mechanism of action of the phosphodiesterase type 5 (PDE5) inhibitors (i.e., sildenafil, tadalafil, and vardenafil) involves inhibition of the PDE5 isoenzyme located in penile vascular smooth muscle cells. Vardenafil Dihydrochloride 108-118 phosphodiesterase 5A Homo sapiens 57-61 15115191-1 2004 The mechanism of action of the phosphodiesterase type 5 (PDE5) inhibitors (i.e., sildenafil, tadalafil, and vardenafil) involves inhibition of the PDE5 isoenzyme located in penile vascular smooth muscle cells. Vardenafil Dihydrochloride 108-118 phosphodiesterase 5A Homo sapiens 147-151 15115191-7 2004 Differences in pharmacokinetic properties among the PDE5 inhibitors include the fact that sildenafil and vardenafil have a shorter duration of action (approximately 4 h) compared with the longer period of responsiveness observed with tadalafil (up to 36 h). Vardenafil Dihydrochloride 105-115 phosphodiesterase 5A Homo sapiens 52-56 15148932-4 2004 The development of two new PDE-5 inhibitors, vardenafil and tadalafil, has added to the options for the treatment of ED. Vardenafil Dihydrochloride 45-55 phosphodiesterase 5A Homo sapiens 27-32 15075013-6 2004 Three PDE5 inhibitors are currently available, sildenafil, vardenafil and tadalafil. Vardenafil Dihydrochloride 59-69 phosphodiesterase 5A Homo sapiens 6-10 14871543-1 2004 Phosphodiesterase type-5 (PDE-5) inhibitors including sildenafil, vardenafil and tadalafil are a new class of vasoactive drugs that have been developed for treatment of erectile dysfunction in patients. Vardenafil Dihydrochloride 66-76 phosphodiesterase 5A Homo sapiens 0-24 15102574-2 2004 Vardenafil is a potent and highly selective PDE5 inhibitor developed as an oral therapy for ED. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 44-48 15102574-9 2004 Vardenafil is well-tolerated, with an adverse event profile typical of this class of PDE5 inhibitors. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 85-89 15117087-0 2004 Vardenafil--PDE5 inhibitor number 3. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 12-16 15083994-1 2004 Clinical evidence in men with erectile dysfunction (ED) shows that the phosphodiesterase type 5 (PDE5) inhibitors sildenafil citrate, tadalafil, and vardenafil hydrochloride have favorable safety and efficacy profiles. Vardenafil Dihydrochloride 149-173 phosphodiesterase 5A Homo sapiens 71-95 15083994-1 2004 Clinical evidence in men with erectile dysfunction (ED) shows that the phosphodiesterase type 5 (PDE5) inhibitors sildenafil citrate, tadalafil, and vardenafil hydrochloride have favorable safety and efficacy profiles. Vardenafil Dihydrochloride 149-173 phosphodiesterase 5A Homo sapiens 97-101 14871543-1 2004 Phosphodiesterase type-5 (PDE-5) inhibitors including sildenafil, vardenafil and tadalafil are a new class of vasoactive drugs that have been developed for treatment of erectile dysfunction in patients. Vardenafil Dihydrochloride 66-76 phosphodiesterase 5A Homo sapiens 26-31 15260511-10 2004 New PDE5 inhibitors such as vardenafil should be tried first as therapy for sildenafil nonresponders before exploring any combination therapy options. Vardenafil Dihydrochloride 28-38 phosphodiesterase 5A Homo sapiens 4-8 14742800-6 2004 DATA SYNTHESIS: Vardenafil is a potent and selective inhibitor of the phosphodiesterase 5 (PDE5) enzyme that has been shown to improve erectile function in several populations of men with ED. Vardenafil Dihydrochloride 16-26 phosphodiesterase 5A Homo sapiens 70-89 14742800-6 2004 DATA SYNTHESIS: Vardenafil is a potent and selective inhibitor of the phosphodiesterase 5 (PDE5) enzyme that has been shown to improve erectile function in several populations of men with ED. Vardenafil Dihydrochloride 16-26 phosphodiesterase 5A Homo sapiens 91-95 14960129-1 2004 UNLABELLED: Vardenafil (Levitra) is a potent and highly selective oral phosphodiesterase type 5 (PDE5) inhibitor. Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 71-95 15323315-0 2004 [Levitra (vardenafil)--a new PDE 5 inhibitor for the treatment of erectile dysfunction]. Vardenafil Dihydrochloride 1-8 phosphodiesterase 5A Homo sapiens 29-34 15323315-0 2004 [Levitra (vardenafil)--a new PDE 5 inhibitor for the treatment of erectile dysfunction]. Vardenafil Dihydrochloride 10-20 phosphodiesterase 5A Homo sapiens 29-34 14960129-10 2004 The most commonly reported adverse events (typical of those seen with PDE5 inhibitors) in vardenafil 5-20mg recipients included headache, flushing, rhinitis, dyspepsia and sinusitis. Vardenafil Dihydrochloride 90-100 phosphodiesterase 5A Homo sapiens 70-74 14960129-12 2004 CONCLUSION: Vardenafil is a potent and highly selective oral PDE5 inhibitor. Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 61-65 14960129-14 2004 Vardenafil should be considered a first-line treatment option in men with ED who are suitable candidates for oral PDE5 inhibitor therapy. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 114-118 14960129-1 2004 UNLABELLED: Vardenafil (Levitra) is a potent and highly selective oral phosphodiesterase type 5 (PDE5) inhibitor. Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 97-101 14960129-1 2004 UNLABELLED: Vardenafil (Levitra) is a potent and highly selective oral phosphodiesterase type 5 (PDE5) inhibitor. Vardenafil Dihydrochloride 24-31 phosphodiesterase 5A Homo sapiens 71-95 14960129-1 2004 UNLABELLED: Vardenafil (Levitra) is a potent and highly selective oral phosphodiesterase type 5 (PDE5) inhibitor. Vardenafil Dihydrochloride 24-31 phosphodiesterase 5A Homo sapiens 97-101 14569380-3 2003 The later PDE-5 inhibitors Tadalafil and Vardenafil show, as far as it is currently possible to judge, a similar profile to Sildenafil. Vardenafil Dihydrochloride 41-51 phosphodiesterase 5A Homo sapiens 10-15 14622499-2 2003 Three potent and selective PDE-5 inhibitors (sildenafil, tadalafil, and vardenafil) have been approved for clinical use. Vardenafil Dihydrochloride 72-82 phosphodiesterase 5A Homo sapiens 27-32 14622502-1 2003 Vardenafil is a phosphodiesterase type-5 (PDE-5) inhibitor developed as an oral therapy for erectile dysfunction (ED). Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 16-40 14622502-1 2003 Vardenafil is a phosphodiesterase type-5 (PDE-5) inhibitor developed as an oral therapy for erectile dysfunction (ED). Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 42-47 14622502-9 2003 Vardenafil is well tolerated, with an adverse event profile typical of the class of PDE-5 inhibitors. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 84-89 14693300-1 2003 BACKGROUND: Three inhibitors of phosphodiesterase 5 (PDE5) are now available for the treatment of erectile dysfunction (ED): sildenafil citrate, vardenafil, and tadalafil. Vardenafil Dihydrochloride 145-155 phosphodiesterase 5A Homo sapiens 32-51 14551572-3 2003 This article examines the correlation between the available biochemical and clinical data for the PDE 5 inhibitors sildenafil (Viagra), tadalafil (Cialis) and vardenafil (Levitra). Vardenafil Dihydrochloride 171-178 phosphodiesterase 5A Homo sapiens 98-103 14626653-9 2003 Contra-indications (co-administration with drugs increasing nitric oxide) and side-effects (headache and flushing due to vasodilatation) of vardenafil are similar to those of other PDE5 inhibitors. Vardenafil Dihydrochloride 140-150 phosphodiesterase 5A Homo sapiens 181-185 12955149-6 2003 Here we present the three-dimensional structures of the catalytic domain (residues 537-860) of human PDE5 complexed with the three drug molecules sildenafil, tadalafil (Cialis) and vardenafil (Levitra). Vardenafil Dihydrochloride 181-191 phosphodiesterase 5A Homo sapiens 101-105 12955149-6 2003 Here we present the three-dimensional structures of the catalytic domain (residues 537-860) of human PDE5 complexed with the three drug molecules sildenafil, tadalafil (Cialis) and vardenafil (Levitra). Vardenafil Dihydrochloride 193-200 phosphodiesterase 5A Homo sapiens 101-105 14626653-2 2003 Vardenafil (Levitra), recently launched in Belgium by Bayer and Glaxo-SmithKline, is a new drug that potently and selectively inhibits phosphodiesterase type 5 (PDE5) in the cavernosum tissue of the penis. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 135-159 12508460-12 2002 There are two new PDE 5 inhibitors (tadalafil and vardenafil) that will be released on the market 2003, which will provide better selectivity. Vardenafil Dihydrochloride 50-60 phosphodiesterase 5A Homo sapiens 18-23 14626653-2 2003 Vardenafil (Levitra), recently launched in Belgium by Bayer and Glaxo-SmithKline, is a new drug that potently and selectively inhibits phosphodiesterase type 5 (PDE5) in the cavernosum tissue of the penis. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 161-165 14626653-2 2003 Vardenafil (Levitra), recently launched in Belgium by Bayer and Glaxo-SmithKline, is a new drug that potently and selectively inhibits phosphodiesterase type 5 (PDE5) in the cavernosum tissue of the penis. Vardenafil Dihydrochloride 12-19 phosphodiesterase 5A Homo sapiens 135-159 14626653-2 2003 Vardenafil (Levitra), recently launched in Belgium by Bayer and Glaxo-SmithKline, is a new drug that potently and selectively inhibits phosphodiesterase type 5 (PDE5) in the cavernosum tissue of the penis. Vardenafil Dihydrochloride 12-19 phosphodiesterase 5A Homo sapiens 161-165 14626653-7 2003 Vardenafil has a more potent inhibitory activity of PDE5 in vitro than sildenafil or tadalafil while its pharmacokinetics in vivo is somewhat more rapid than that of the two other compounds. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 52-56 12934045-10 2003 First-line therapy for other patients is typically oral PDE5 inhibitors, such as sildenafil, tadalafil, or vardenafil. Vardenafil Dihydrochloride 107-117 phosphodiesterase 5A Homo sapiens 56-60 14636086-1 2003 UNLABELLED: Vardenafil (Levitra) is a potent and highly selective oral phosphodiesterase type 5 (PDE5) inhibitor. Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 71-95 14636086-1 2003 UNLABELLED: Vardenafil (Levitra) is a potent and highly selective oral phosphodiesterase type 5 (PDE5) inhibitor. Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 97-101 14636086-1 2003 UNLABELLED: Vardenafil (Levitra) is a potent and highly selective oral phosphodiesterase type 5 (PDE5) inhibitor. Vardenafil Dihydrochloride 24-31 phosphodiesterase 5A Homo sapiens 71-95 14636086-1 2003 UNLABELLED: Vardenafil (Levitra) is a potent and highly selective oral phosphodiesterase type 5 (PDE5) inhibitor. Vardenafil Dihydrochloride 24-31 phosphodiesterase 5A Homo sapiens 97-101 14636086-10 2003 The most commonly reported adverse events (typical of those seen with PDE5 inhibitors) in vardenafil 5-20 mg recipients included headache, flushing, rhinitis, dyspepsia and sinusitis. Vardenafil Dihydrochloride 90-100 phosphodiesterase 5A Homo sapiens 70-74 14636086-12 2003 CONCLUSION: Vardenafil is a potent and highly selective oral PDE5 inhibitor. Vardenafil Dihydrochloride 12-22 phosphodiesterase 5A Homo sapiens 61-65 14636086-14 2003 Vardenafil should be considered a first-line treatment option in men with ED who are suitable candidates for oral PDE5 inhibitor therapy. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 114-118 12475462-0 2002 The effect of vardenafil, a potent and highly selective phosphodiesterase-5 inhibitor for the treatment of erectile dysfunction, on the cardiovascular response to exercise in patients with coronary artery disease. Vardenafil Dihydrochloride 14-24 phosphodiesterase 5A Homo sapiens 56-75 12475462-1 2002 OBJECTIVES: The effect of vardenafil, a potent and highly selective phosphodiesterase-5 (PDE5) inhibitor, on symptom-limited exercise time, time to first awareness of angina, and time to ischemic threshold (ST-segment depression > or =1 mm from baseline) during exercise tolerance testing (ETT) was examined in patients with stable coronary artery disease (CAD). Vardenafil Dihydrochloride 26-36 phosphodiesterase 5A Homo sapiens 68-87 12475462-1 2002 OBJECTIVES: The effect of vardenafil, a potent and highly selective phosphodiesterase-5 (PDE5) inhibitor, on symptom-limited exercise time, time to first awareness of angina, and time to ischemic threshold (ST-segment depression > or =1 mm from baseline) during exercise tolerance testing (ETT) was examined in patients with stable coronary artery disease (CAD). Vardenafil Dihydrochloride 26-36 phosphodiesterase 5A Homo sapiens 89-93 12494279-3 2002 Two novel PDE5 inhibitors, tadalafil (Lilly ICOS) and vardenafil (Bayer), have recently completed efficacy and safety clinical trials in "general" and diabetic study populations and are now candidates for US FDA approval. Vardenafil Dihydrochloride 54-64 phosphodiesterase 5A Homo sapiens 10-14 12825147-10 2003 The phosphodiesterase type 5 (PDE-5) inhibitors sildenafil, vardenafil, and taldalafil are peripheral conditioners. Vardenafil Dihydrochloride 60-70 phosphodiesterase 5A Homo sapiens 4-28 12825147-10 2003 The phosphodiesterase type 5 (PDE-5) inhibitors sildenafil, vardenafil, and taldalafil are peripheral conditioners. Vardenafil Dihydrochloride 60-70 phosphodiesterase 5A Homo sapiens 30-35 12825147-14 2003 Vardenafil, another selective PDE-5 inhibitor with potentially higher selectivity and efficacy compared to sildenafil was just approved. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 30-35 12789394-2 2003 Vardenafil is a type 5 phosphodiesterase (PDE5) inhibitor that potentiates the nitric oxide (NO)/cGMP pathway facilitating penile smooth muscle relaxation and improving penile erection in men. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 42-46 12789394-11 2003 These results emphasize the role of the NO/cGMP pathway in the local vasodilatory response in female sexual organs and provide a rationale for testing PDE5 inhibitors, such as vardenafil, as a treatment for certain forms of female sexual dysfunction. Vardenafil Dihydrochloride 176-186 phosphodiesterase 5A Canis lupus familiaris 151-155 12625845-4 2003 Sildenafil, tadalafil, and vardenafil are all potent inhibitors of PDE5 and show the same mechanism of action, although they have some pharmacological differences that may translate into varying clinical effects. Vardenafil Dihydrochloride 27-37 phosphodiesterase 5A Homo sapiens 67-71 12393651-7 2003 Vardenafil- or sildenafil-treated B-CLL cells displayed up to 30% intracellular active caspase 3. Vardenafil Dihydrochloride 0-10 caspase 3 Homo sapiens 87-96 12435622-3 2002 - The development of the PDE-5 inhibitors vardenafil and tadalafil prompts the question of whether and how these three substances differ in terms of their efficacy and adverse effects. Vardenafil Dihydrochloride 42-52 phosphodiesterase 5A Homo sapiens 25-30 12027779-1 2002 Vardenafil selectively inhibits phosphodiesterase type 5 (PDE5), an enzyme which hydrolyses cyclic guanosine monophosphate in the cavernosum tissue of the penis. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 32-56 12002434-1 2002 Vardenafil and sildenafil are potent and specific phosphodiesterase type 5 (PDE 5) inhibitors. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 50-74 12002434-1 2002 Vardenafil and sildenafil are potent and specific phosphodiesterase type 5 (PDE 5) inhibitors. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 76-81 12358156-10 2002 Other oral medications for ED include apomorphine, phentolamine, yohimbine, trazodone, testosterone and new PDE-5 inhibitors in Phase III clinical trials, such as vardenafil and tadalafil. Vardenafil Dihydrochloride 163-173 phosphodiesterase 5A Homo sapiens 108-113 12027779-1 2002 Vardenafil selectively inhibits phosphodiesterase type 5 (PDE5), an enzyme which hydrolyses cyclic guanosine monophosphate in the cavernosum tissue of the penis. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 58-62 12027779-12 2002 Adverse events associated with vardenafil were those commonly associated with PDE5 inhibitors: headache, flushing, dyspepsia and rhinitis. Vardenafil Dihydrochloride 31-41 phosphodiesterase 5A Homo sapiens 78-82 11669467-0 2001 Inhibition of cyclic GMP hydrolysis in human corpus cavernosum smooth muscle cells by vardenafil, a novel, selective phosphodiesterase type 5 inhibitor. Vardenafil Dihydrochloride 86-96 5'-nucleotidase, cytosolic II Homo sapiens 21-24 11890515-0 2001 The phosphodiesterase inhibitory selectivity and the in vitro and in vivo potency of the new PDE5 inhibitor vardenafil. Vardenafil Dihydrochloride 108-118 phosphodiesterase 5A Homo sapiens 93-97 11890515-6 2001 Vardenafil specifically inhibited the hydrolysis of cGMP by PDE5 with an IC50 of 0.7 nM (6.6 nM). Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 60-64 11890515-7 2001 In contrast, the IC50 of vardenafil for PDE1 was 180 nM; for PDE6, 11 nM; for PDE2, PDE3 and PDE4, more than 1000 nM. Vardenafil Dihydrochloride 25-35 phosphodiesterase 4A Homo sapiens 93-97 11890515-14 2001 The selectivity for PDE5, the potentiation of NO-induced relaxation and cGMP accumulation in human trabecular smooth muscle and the ability to enhance NO-induced erection in vivo indicate that vardenafil has the appropriate properties to be a potential compound for the treatment of erectile dysfunction. Vardenafil Dihydrochloride 193-203 phosphodiesterase 5A Homo sapiens 20-24 11890515-15 2001 Vardenafil was more potent and selective than sildenafil on its inhibitory activity on PDE5. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 87-91 11669467-0 2001 Inhibition of cyclic GMP hydrolysis in human corpus cavernosum smooth muscle cells by vardenafil, a novel, selective phosphodiesterase type 5 inhibitor. Vardenafil Dihydrochloride 86-96 phosphodiesterase 5A Homo sapiens 117-141 11669467-4 2001 Vardenafil is a novel, high affinity PDE5 inhibitor currently under clinical development. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 37-41 11669467-11 2001 These observations suggest that vardenafil is a more potent PDE5 inhibitor, than sildenafil in vitro. Vardenafil Dihydrochloride 32-42 phosphodiesterase 5A Homo sapiens 60-64 34875337-0 2022 Phosphodiesterase (PDE) 5 inhibitors sildenafil, tadalafil and vardenafil impact cAMP-specific PDE8 isoforms-linked second messengers and steroid production in a mouse Leydig tumor cell line. Vardenafil Dihydrochloride 63-73 phosphodiesterase 5A, cGMP-specific Mus musculus 0-25 33777681-5 2021 Moreover, based on virtual screening and biological verification, vardenafil and linagliptin as GPR35 and AHR agonists respectively were discovered from 2388 approved drugs. Vardenafil Dihydrochloride 66-76 G protein-coupled receptor 35 Homo sapiens 96-101 33777681-5 2021 Moreover, based on virtual screening and biological verification, vardenafil and linagliptin as GPR35 and AHR agonists respectively were discovered from 2388 approved drugs. Vardenafil Dihydrochloride 66-76 aryl hydrocarbon receptor Homo sapiens 106-109 34875337-7 2022 cAMP binding to PDE8A/B was displaced upon cell treatment with PDE5i, revealing that sildenafil, tadalafil and vardenafil have similar effectiveness in live cells, in vitro. Vardenafil Dihydrochloride 111-121 phosphodiesterase 8A Homo sapiens 16-23 11528196-6 2001 RESULTS: After 20 and 40 mg vardenafil, the mean duration of >60% rigidity of the base of the penis was greater than after placebo by 42.9 min (95% Cl 29.3-56.4) and by 49.3 min (95% Cl 35.7-62.9), respectively (p<0.001), and greater than after placebo by 34.6 min (95% Cl 22.1-47.1) for both doses at the tip. Vardenafil Dihydrochloride 28-38 TOR signaling pathway regulator Homo sapiens 312-315 26410556-6 2015 Moreover, potential synergisms of BAY 41-2272 or BAY 60-2770 and inhibition of cGMP degradation by the PDE5 inhibitor vardenafil were investigated. Vardenafil Dihydrochloride 118-128 phosphodiesterase 5A Homo sapiens 103-107 26410556-11 2015 Moreover, administration of BAY 41-2272 or BAY 60-2770 enhanced the efficiency of the PDE5 inhibitor vardenafil to inhibit and revert myofibroblast differentiation in vitro. Vardenafil Dihydrochloride 101-111 phosphodiesterase 5A Homo sapiens 86-90 34875337-0 2022 Phosphodiesterase (PDE) 5 inhibitors sildenafil, tadalafil and vardenafil impact cAMP-specific PDE8 isoforms-linked second messengers and steroid production in a mouse Leydig tumor cell line. Vardenafil Dihydrochloride 63-73 phosphodiesterase 8A Mus musculus 95-99 33359621-2 2021 The present ex-vivo study evaluated the combination of the endothelin receptor antagonists (ERA) macitentan and bosentan with the phosphodiesterase-5 (PDE-5) inhibitor vardenafil in pulmonary arteries from patients suffering from terminal lung disease as a model of PAH. Vardenafil Dihydrochloride 168-178 phosphodiesterase 5A Homo sapiens 130-149 34829647-2 2021 Here we aimed to characterize RV and left ventricular (LV) remodeling and its prevention by vardenafil (a long-acting phosphodiesterase-5A (PDE-5A) inhibitor) administration in a diabetic HFpEF model. Vardenafil Dihydrochloride 92-102 phosphodiesterase 5A Rattus norvegicus 118-138 34829647-2 2021 Here we aimed to characterize RV and left ventricular (LV) remodeling and its prevention by vardenafil (a long-acting phosphodiesterase-5A (PDE-5A) inhibitor) administration in a diabetic HFpEF model. Vardenafil Dihydrochloride 92-102 phosphodiesterase 5A Rattus norvegicus 140-146 35119252-6 2022 Different drugs inhibiting PDE5 (PDE5i) exist, the main of which commercially available are sildenafil, vardenafil, tadalafil, and avanafil. Vardenafil Dihydrochloride 104-114 phosphodiesterase 5A Homo sapiens 27-31 35119252-6 2022 Different drugs inhibiting PDE5 (PDE5i) exist, the main of which commercially available are sildenafil, vardenafil, tadalafil, and avanafil. Vardenafil Dihydrochloride 104-114 phosphodiesterase 5A Homo sapiens 33-38 33948561-8 2021 Inhibition of ABCB1 was mediated by vardenafil, and TWIST1 expression was reduced by either Harmine or shRNA. Vardenafil Dihydrochloride 36-46 ATP-binding cassette, sub-family B (MDR/TAP), member 1B Mus musculus 14-19 33948561-13 2021 TWIST1 bound to the ABCB1 promoter (P = .03) and induced cell aggregation in metastatic and TWIST1-overexpressing, non-metastatic (MED6-TWIST1) cells, which was significantly attenuated by vardenafil (P < .05). Vardenafil Dihydrochloride 189-199 twist family bHLH transcription factor 1 Homo sapiens 0-6 33948561-13 2021 TWIST1 bound to the ABCB1 promoter (P = .03) and induced cell aggregation in metastatic and TWIST1-overexpressing, non-metastatic (MED6-TWIST1) cells, which was significantly attenuated by vardenafil (P < .05). Vardenafil Dihydrochloride 189-199 ATP binding cassette subfamily B member 1 Homo sapiens 20-25 33948561-13 2021 TWIST1 bound to the ABCB1 promoter (P = .03) and induced cell aggregation in metastatic and TWIST1-overexpressing, non-metastatic (MED6-TWIST1) cells, which was significantly attenuated by vardenafil (P < .05). Vardenafil Dihydrochloride 189-199 twist family bHLH transcription factor 1 Homo sapiens 92-98 33948561-13 2021 TWIST1 bound to the ABCB1 promoter (P = .03) and induced cell aggregation in metastatic and TWIST1-overexpressing, non-metastatic (MED6-TWIST1) cells, which was significantly attenuated by vardenafil (P < .05). Vardenafil Dihydrochloride 189-199 mediator complex subunit 6 Homo sapiens 131-135 33948561-13 2021 TWIST1 bound to the ABCB1 promoter (P = .03) and induced cell aggregation in metastatic and TWIST1-overexpressing, non-metastatic (MED6-TWIST1) cells, which was significantly attenuated by vardenafil (P < .05). Vardenafil Dihydrochloride 189-199 twist family bHLH transcription factor 1 Homo sapiens 92-98 33948561-14 2021 Conclusions: In this study, we identified a TWIST1-ABCB1 signaling axis during medulloblastoma migration, which can be therapeutically targeted with the clinically approved ABCB1 inhibitor, vardenafil. Vardenafil Dihydrochloride 190-200 twist family bHLH transcription factor 1 Homo sapiens 44-50 33948561-14 2021 Conclusions: In this study, we identified a TWIST1-ABCB1 signaling axis during medulloblastoma migration, which can be therapeutically targeted with the clinically approved ABCB1 inhibitor, vardenafil. Vardenafil Dihydrochloride 190-200 ATP binding cassette subfamily B member 1 Homo sapiens 51-56 33948561-14 2021 Conclusions: In this study, we identified a TWIST1-ABCB1 signaling axis during medulloblastoma migration, which can be therapeutically targeted with the clinically approved ABCB1 inhibitor, vardenafil. Vardenafil Dihydrochloride 190-200 ATP binding cassette subfamily B member 1 Homo sapiens 173-178 33718200-5 2021 Sildenafil, tadalafil, and vardenafil are PDE5 inhibitors and potent vasodilators, that extend the physiological effects of nitric oxide and cyclic guanosine monophosphate (cGMP) signaling. Vardenafil Dihydrochloride 27-37 phosphodiesterase 5A Homo sapiens 42-46 34944010-4 2021 However, recent data suggest certain PDE5-Is, particularly vardenafil, may also reduce transforming growth factor beta 1 (TGF-beta1) activation and extracellular matrix (ECM) accumulation, making them a potential target for therapy for IPF. Vardenafil Dihydrochloride 59-69 phosphodiesterase 5A, cGMP-specific Mus musculus 37-41 34944010-4 2021 However, recent data suggest certain PDE5-Is, particularly vardenafil, may also reduce transforming growth factor beta 1 (TGF-beta1) activation and extracellular matrix (ECM) accumulation, making them a potential target for therapy for IPF. Vardenafil Dihydrochloride 59-69 transforming growth factor, beta 1 Mus musculus 87-120 34944010-4 2021 However, recent data suggest certain PDE5-Is, particularly vardenafil, may also reduce transforming growth factor beta 1 (TGF-beta1) activation and extracellular matrix (ECM) accumulation, making them a potential target for therapy for IPF. Vardenafil Dihydrochloride 59-69 transforming growth factor, beta 1 Mus musculus 122-131 33359621-2 2021 The present ex-vivo study evaluated the combination of the endothelin receptor antagonists (ERA) macitentan and bosentan with the phosphodiesterase-5 (PDE-5) inhibitor vardenafil in pulmonary arteries from patients suffering from terminal lung disease as a model of PAH. Vardenafil Dihydrochloride 168-178 phosphodiesterase 5A Homo sapiens 151-156 32771352-12 2020 Tamoxifen could prevent myofibroblast transformation until 36 hours after TGF-beta1 treatment, whereas vardenafil could prevent only 24 hours after TGF-beta1 treatment. Vardenafil Dihydrochloride 103-113 transforming growth factor beta 1 Homo sapiens 148-157 33248641-4 2021 Meanwhile, this method could also accomplish semi-quantitative analysis of vardenafil with a cut-off value of 0.625 ng mL-1. Vardenafil Dihydrochloride 75-85 L1 cell adhesion molecule Mus musculus 119-123 33166302-14 2020 Also, Vardenafil and Sildenafil induced the activity of superoxide dismutase and catalase whereas, glutathione S-transferase, glutathione reductase, and glutathione peroxidase activities inhibited in livers of rabbits. Vardenafil Dihydrochloride 6-16 catalase Oryctolagus cuniculus 81-89 33166302-17 2020 In addition, the protein expressions of CYP11A1 and CYP 19C in both livers and testes were down-regulated after treatment of rabbits with Sildenafil, Vardenafil, and Tadalafil for 12 weeks. Vardenafil Dihydrochloride 150-160 LOW QUALITY PROTEIN: cholesterol side-chain cleavage enzyme, mitochondrial Oryctolagus cuniculus 40-47 32747447-2 2020 We have shown that therapeutic doses of vardenafil, a phosphodiesterase type 5 (PDE5) inhibitor, corrects CF Transmembrane conductance Regulator (CFTR)-dependent chloride transport in respiratory and intestinal tissues of F508del homozygous mice. Vardenafil Dihydrochloride 40-50 cystic fibrosis transmembrane conductance regulator Mus musculus 106-144 32794708-4 2020 This movement directly blocks the binding of substrate/inhibitors to the PDE5 active site, which is different from all traditional PDE5 inhibitors such as sildenafil, tadalafil, and vardenafil. Vardenafil Dihydrochloride 182-192 phosphodiesterase 5A Homo sapiens 73-77 32794708-4 2020 This movement directly blocks the binding of substrate/inhibitors to the PDE5 active site, which is different from all traditional PDE5 inhibitors such as sildenafil, tadalafil, and vardenafil. Vardenafil Dihydrochloride 182-192 phosphodiesterase 5A Homo sapiens 131-135 32747447-2 2020 We have shown that therapeutic doses of vardenafil, a phosphodiesterase type 5 (PDE5) inhibitor, corrects CF Transmembrane conductance Regulator (CFTR)-dependent chloride transport in respiratory and intestinal tissues of F508del homozygous mice. Vardenafil Dihydrochloride 40-50 cystic fibrosis transmembrane conductance regulator Mus musculus 146-150 32747447-0 2020 Vardenafil increases intracellular accumulation of the most prevalent mutant CFTR in human bronchial epithelial cells. Vardenafil Dihydrochloride 0-10 CF transmembrane conductance regulator Homo sapiens 77-81 32747447-3 2020 Here, we studied the effect of vardenafil on CFTR in 16HBE14o- and CFBE41o- cell lines. Vardenafil Dihydrochloride 31-41 cystic fibrosis transmembrane conductance regulator Mus musculus 45-49 32747447-2 2020 We have shown that therapeutic doses of vardenafil, a phosphodiesterase type 5 (PDE5) inhibitor, corrects CF Transmembrane conductance Regulator (CFTR)-dependent chloride transport in respiratory and intestinal tissues of F508del homozygous mice. Vardenafil Dihydrochloride 40-50 phosphodiesterase 5A, cGMP-specific Mus musculus 54-78 32747447-2 2020 We have shown that therapeutic doses of vardenafil, a phosphodiesterase type 5 (PDE5) inhibitor, corrects CF Transmembrane conductance Regulator (CFTR)-dependent chloride transport in respiratory and intestinal tissues of F508del homozygous mice. Vardenafil Dihydrochloride 40-50 phosphodiesterase 5A, cGMP-specific Mus musculus 80-84 32747447-9 2020 A fast and transient rise in cGMP intracellular contents followed treatment with vardenafil, confirming its PDE5 inhibitory effect. Vardenafil Dihydrochloride 81-91 phosphodiesterase 5A, cGMP-specific Mus musculus 108-112 32747447-12 2020 These findings support the view that vardenafil partially rescues F508del through cGMP/PKG-independent mechanisms. Vardenafil Dihydrochloride 37-47 protein kinase cGMP-dependent 1 Homo sapiens 87-90 32850387-7 2020 Sildenafil-mediated synergistic effects were mimicked by other PDE5 inhibitors including vardenafil and tadalafil, and also by PDE5A knockdown in cells, suggesting PDE5-involved mechanism. Vardenafil Dihydrochloride 89-99 phosphodiesterase 5A Homo sapiens 63-67 32126313-4 2020 From this screen, we identified sildenafil and vardenafil (both PDE5 inhibitors) having the least osteogenic EC50. Vardenafil Dihydrochloride 47-57 phosphodiesterase 5A, cGMP-specific Mus musculus 64-68 32229414-5 2020 Vardenafil is a potent inhibitor of both PDE5 and ABCC5-mediated cGMP cellular efflux. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 41-45 32229414-5 2020 Vardenafil is a potent inhibitor of both PDE5 and ABCC5-mediated cGMP cellular efflux. Vardenafil Dihydrochloride 0-10 ATP binding cassette subfamily C member 5 Homo sapiens 50-55 32229414-6 2020 Nineteen novel vardenafil analogs that have been predicted as potent inhibitors by VLS were chosen for tests of their ability to inhibit ATP- dependent transport of cGMP by measuring the accumulation of cyclic GMP in inside-out vesicles. Vardenafil Dihydrochloride 15-25 5'-nucleotidase, cytosolic II Homo sapiens 166-169 32513693-7 2020 Structural modeling revealed a higher binding energy of tadalafil to mouse PDE5A compared with vardenafil, due to steric clashes of vardenafil with a single methionine residue at position 806 in mouse PDE5A. Vardenafil Dihydrochloride 95-105 phosphodiesterase 5A, cGMP-specific Mus musculus 201-206 32513693-7 2020 Structural modeling revealed a higher binding energy of tadalafil to mouse PDE5A compared with vardenafil, due to steric clashes of vardenafil with a single methionine residue at position 806 in mouse PDE5A. Vardenafil Dihydrochloride 132-142 phosphodiesterase 5A, cGMP-specific Mus musculus 75-80 32126313-6 2020 Sunitinib, a tyrosine receptor kinase inhibitor that also blocks VEGFR2 blocked sildenafil-/vardenafil-induced osteoblast differentiation. Vardenafil Dihydrochloride 92-102 kinase insert domain protein receptor Mus musculus 65-71 32314927-1 2020 Objective: This study investigated the effect of vardenafil, tadalafil, and udenafil from phosphodiesterase-5 inhibitors (PDE-5Is) on bone morphogenic-protein (BMP)2 and 4 levels, along with angiogenesis in ovariectomized rat"s kidney.Method: Rats were randomly divided into five groups (n = 10). Vardenafil Dihydrochloride 49-59 bone morphogenetic protein 2 Rattus norvegicus 134-171 32314927-6 2020 However, BMP4 levels were only high in the OVX + tadalafil group (p < .05).Conclusion: The results indicated that vardenafil, udenafil, and especially tadalafil increased VEGF, BMP2, and VitaminD3 levels. Vardenafil Dihydrochloride 114-124 bone morphogenetic protein 4 Rattus norvegicus 9-13 32314927-6 2020 However, BMP4 levels were only high in the OVX + tadalafil group (p < .05).Conclusion: The results indicated that vardenafil, udenafil, and especially tadalafil increased VEGF, BMP2, and VitaminD3 levels. Vardenafil Dihydrochloride 114-124 vascular endothelial growth factor A Rattus norvegicus 171-175 32314927-6 2020 However, BMP4 levels were only high in the OVX + tadalafil group (p < .05).Conclusion: The results indicated that vardenafil, udenafil, and especially tadalafil increased VEGF, BMP2, and VitaminD3 levels. Vardenafil Dihydrochloride 114-124 bone morphogenetic protein 2 Rattus norvegicus 177-181 31350821-5 2019 RESULTS: The main reasons for patient dissatisfaction when using PDE5is on demand are the relatively long Tonset after taking vardenafil and sildenafil, including formulations such as film-coated tablets, fine granules, orally disintegrating tablets (ODTs), and oral thin films (ODFs). Vardenafil Dihydrochloride 126-136 phosphodiesterase 5A Homo sapiens 65-69 31250549-11 2020 DISCUSSION AND CONCLUSION: Early treated rats with vardenafil had preserved erection and normal cavernosal structure, ultrastructure and gene expression of iNOS, nNOS, eNOS, and TGF-beta1. Vardenafil Dihydrochloride 51-61 nitric oxide synthase 2 Rattus norvegicus 156-160 31250549-11 2020 DISCUSSION AND CONCLUSION: Early treated rats with vardenafil had preserved erection and normal cavernosal structure, ultrastructure and gene expression of iNOS, nNOS, eNOS, and TGF-beta1. Vardenafil Dihydrochloride 51-61 nitric oxide synthase 1 Rattus norvegicus 162-166 31250549-11 2020 DISCUSSION AND CONCLUSION: Early treated rats with vardenafil had preserved erection and normal cavernosal structure, ultrastructure and gene expression of iNOS, nNOS, eNOS, and TGF-beta1. Vardenafil Dihydrochloride 51-61 nitric oxide synthase 3 Rattus norvegicus 168-172 31250549-11 2020 DISCUSSION AND CONCLUSION: Early treated rats with vardenafil had preserved erection and normal cavernosal structure, ultrastructure and gene expression of iNOS, nNOS, eNOS, and TGF-beta1. Vardenafil Dihydrochloride 51-61 transforming growth factor, beta 1 Rattus norvegicus 178-187 31860994-0 2019 The safety and efficacy of PDE5-inhibitors-vardenafil on treating diabetes mellitus erectile dysfunction: A protocol for systematic review and meta analysis. Vardenafil Dihydrochloride 43-53 phosphodiesterase 5A Homo sapiens 27-31 31860994-3 2019 Many clinical trials have proven that PDE5-inhibitors-vardenafil has a significant effect in the treatment of Diabetic mellitus erectile dysfunction. Vardenafil Dihydrochloride 54-64 phosphodiesterase 5A Homo sapiens 38-42 31860994-4 2019 In this systematic review, we aim to evaluate the effectiveness and safety of PDE5-inhibitors-vardenafil for Diabetic mellitus erectile dysfunction. Vardenafil Dihydrochloride 94-104 phosphodiesterase 5A Homo sapiens 78-82 31860994-7 2019 ETHICS AND DISSEMINATION: This systematic review will evaluate the efficacy and safety of PDE5-inhibitors-vardenafil for treating Diabetic mellitus erectile dysfunction. Vardenafil Dihydrochloride 106-116 phosphodiesterase 5A Homo sapiens 90-94 32096002-0 2020 The Phosphodiesterase-5 Inhibitor Vardenafil Improves the Activation of BMP Signaling in Response to Hydrogen Peroxide. Vardenafil Dihydrochloride 34-44 bone morphogenetic protein 1 Homo sapiens 72-75 32096002-4 2020 METHODS AND RESULTS: Vardenafil decreased the number of TUNEL-positive cells, increased the Bcl2/Bax ratio, and ameliorated the numbers of BrdU-positive cells in H2O2-treated HUVECs. Vardenafil Dihydrochloride 21-31 BCL2 apoptosis regulator Homo sapiens 92-96 32096002-4 2020 METHODS AND RESULTS: Vardenafil decreased the number of TUNEL-positive cells, increased the Bcl2/Bax ratio, and ameliorated the numbers of BrdU-positive cells in H2O2-treated HUVECs. Vardenafil Dihydrochloride 21-31 BCL2 associated X, apoptosis regulator Homo sapiens 97-100 32096002-5 2020 The bone morphogenetic protein receptor (BMPR)/p-Smad/MSX2 pathway was enhanced in response to H2O2, and vardenafil treatment could normalize this pathway. Vardenafil Dihydrochloride 105-115 SMAD family member 1 Homo sapiens 49-53 32096002-5 2020 The bone morphogenetic protein receptor (BMPR)/p-Smad/MSX2 pathway was enhanced in response to H2O2, and vardenafil treatment could normalize this pathway. Vardenafil Dihydrochloride 105-115 msh homeobox 2 Homo sapiens 54-58 32096002-6 2020 To determine whether the BMP pathway is involved, we blocked the BMP pathway using dorsomorphin, which abolished the protective effects of vardenafil. Vardenafil Dihydrochloride 139-149 bone morphogenetic protein 1 Homo sapiens 65-68 32096002-7 2020 We found that vardenafil improved the H2O2-induced downregulation of BMP-binding endothelial regulator protein (BMPER), which possibly intersects with the BMP pathway in the regulation of endothelial cell injury in response to oxidative stress. Vardenafil Dihydrochloride 14-24 BMP binding endothelial regulator Homo sapiens 69-110 32096002-7 2020 We found that vardenafil improved the H2O2-induced downregulation of BMP-binding endothelial regulator protein (BMPER), which possibly intersects with the BMP pathway in the regulation of endothelial cell injury in response to oxidative stress. Vardenafil Dihydrochloride 14-24 BMP binding endothelial regulator Homo sapiens 112-117 32096002-7 2020 We found that vardenafil improved the H2O2-induced downregulation of BMP-binding endothelial regulator protein (BMPER), which possibly intersects with the BMP pathway in the regulation of endothelial cell injury in response to oxidative stress. Vardenafil Dihydrochloride 14-24 bone morphogenetic protein 1 Homo sapiens 69-72 32096002-10 2020 Vardenafil decreases apoptosis through an improved Bcl-2/Bax ratio and increases cell proliferation. Vardenafil Dihydrochloride 0-10 BCL2 apoptosis regulator Homo sapiens 51-56 32096002-10 2020 Vardenafil decreases apoptosis through an improved Bcl-2/Bax ratio and increases cell proliferation. Vardenafil Dihydrochloride 0-10 BCL2 associated X, apoptosis regulator Homo sapiens 57-60 32096002-11 2020 Vardenafil protects against endothelial cell injury through ameliorating the intracellular oxidative stress level and BMPER expression. Vardenafil Dihydrochloride 0-10 BMP binding endothelial regulator Homo sapiens 118-123 32096002-12 2020 The protective role of vardenafil on H2O2-induced endothelial cell injury is mediated through BMPR/p-Smad/MSX2 in HUVECs. Vardenafil Dihydrochloride 23-33 SMAD family member 1 Homo sapiens 101-105 32096002-12 2020 The protective role of vardenafil on H2O2-induced endothelial cell injury is mediated through BMPR/p-Smad/MSX2 in HUVECs. Vardenafil Dihydrochloride 23-33 msh homeobox 2 Homo sapiens 106-110 32504853-1 2020 OBJECTIVE: Levitra, a phosphodiesterase-5 (PDE5) inhibitor, is the trade name of vardenafil. Vardenafil Dihydrochloride 11-18 phosphodiesterase 5A Homo sapiens 22-41 32504853-1 2020 OBJECTIVE: Levitra, a phosphodiesterase-5 (PDE5) inhibitor, is the trade name of vardenafil. Vardenafil Dihydrochloride 11-18 phosphodiesterase 5A Homo sapiens 43-47 32504853-1 2020 OBJECTIVE: Levitra, a phosphodiesterase-5 (PDE5) inhibitor, is the trade name of vardenafil. Vardenafil Dihydrochloride 81-91 phosphodiesterase 5A Homo sapiens 22-41 32504853-1 2020 OBJECTIVE: Levitra, a phosphodiesterase-5 (PDE5) inhibitor, is the trade name of vardenafil. Vardenafil Dihydrochloride 81-91 phosphodiesterase 5A Homo sapiens 43-47 31085245-8 2019 Apart from their known PDE inhibition, up-regulation of vascular AMPK and eNOS coupled with down-regulation of Ang-II, ET-1, P-selectin, VCAM-1 and MMP-2 may explain vardenafil and cilostazol protective effect against RA/DM-co-morbidity-induced endothelial dysfunction and vascular reactivity defects. Vardenafil Dihydrochloride 166-176 angiotensinogen Rattus norvegicus 111-117 31311995-4 2019 Functional inhibition of ABCB1 using vardenafil or verapamil significantly (p <= 0.05-0.001) potentiated the response to three chemotherapeutic drugs (vincristine, etoposide and methotrexate). Vardenafil Dihydrochloride 37-47 ATP binding cassette subfamily B member 1 Homo sapiens 25-30 31085245-8 2019 Apart from their known PDE inhibition, up-regulation of vascular AMPK and eNOS coupled with down-regulation of Ang-II, ET-1, P-selectin, VCAM-1 and MMP-2 may explain vardenafil and cilostazol protective effect against RA/DM-co-morbidity-induced endothelial dysfunction and vascular reactivity defects. Vardenafil Dihydrochloride 166-176 matrix metallopeptidase 2 Rattus norvegicus 148-153 29724533-11 2018 The marker for endothelial integrity (CD-31) was also higher in the vardenafil group (control 74 +- 4%, saline 22 +- 2% vs. vardenafil 40 +- 3%, p = .008). Vardenafil Dihydrochloride 68-78 platelet and endothelial cell adhesion molecule 1 Rattus norvegicus 38-43 30542775-1 2019 Vardenafil is a potent phosphodiesterase-5 (PDE-5) inhibitor used in the treatment of erectile dysfunction. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 23-42 30542775-1 2019 Vardenafil is a potent phosphodiesterase-5 (PDE-5) inhibitor used in the treatment of erectile dysfunction. Vardenafil Dihydrochloride 0-10 phosphodiesterase 5A Homo sapiens 44-49 30265267-8 2018 The method displays a linear response for the determination of vardenafil and ROS in the 4.88-488 mug mL-1 and 4.74-94.7 mug mL-1 concentration ranges, and the limit of detection is as low as 1.63 mug mL-1 and 2.20 mug mL-1, respectively. Vardenafil Dihydrochloride 63-73 L1 cell adhesion molecule Mus musculus 102-106 30826900-8 2019 Combination of 1E-7 M macitentan and 1E-6 M vardenafil inhibited sequential constriction with endothelin-1 and norepinephrine of PA significantly more than either compound alone. Vardenafil Dihydrochloride 44-54 endothelin 1 Homo sapiens 94-106 30705876-7 2018 The data demonstrated that sildenafil or vardenafil (two structure-related PDE5 inhibitors) but not tadalafil (structure-unrelated to sildenafil) sensitized doxorubicin-induced apoptosis in CRPC cells with deteriorating the down-regulation of anti-apoptotic Bcl-2 family members, including Bcl-xL and Mcl-1, and amplifying caspase activation. Vardenafil Dihydrochloride 41-51 phosphodiesterase 5A Homo sapiens 75-79 30705876-11 2018 In conclusion, the data suggest that sildenafil and vardenafil induce PDE5-independent apoptotic sensitization to doxorubicin (or other topoisomerase II inhibitors) through impairment of both HR and NHEJ repair systems that are evident by a decrease of nuclear Rad51 levels and their foci formation in the nucleus, and an inhibition of Ku80 DNA end-binding capability. Vardenafil Dihydrochloride 52-62 phosphodiesterase 5A Homo sapiens 70-74 30705876-11 2018 In conclusion, the data suggest that sildenafil and vardenafil induce PDE5-independent apoptotic sensitization to doxorubicin (or other topoisomerase II inhibitors) through impairment of both HR and NHEJ repair systems that are evident by a decrease of nuclear Rad51 levels and their foci formation in the nucleus, and an inhibition of Ku80 DNA end-binding capability. Vardenafil Dihydrochloride 52-62 RAD51 recombinase Homo sapiens 261-266 30705876-11 2018 In conclusion, the data suggest that sildenafil and vardenafil induce PDE5-independent apoptotic sensitization to doxorubicin (or other topoisomerase II inhibitors) through impairment of both HR and NHEJ repair systems that are evident by a decrease of nuclear Rad51 levels and their foci formation in the nucleus, and an inhibition of Ku80 DNA end-binding capability. Vardenafil Dihydrochloride 52-62 X-ray repair cross complementing 5 Homo sapiens 336-340 30265267-8 2018 The method displays a linear response for the determination of vardenafil and ROS in the 4.88-488 mug mL-1 and 4.74-94.7 mug mL-1 concentration ranges, and the limit of detection is as low as 1.63 mug mL-1 and 2.20 mug mL-1, respectively. Vardenafil Dihydrochloride 63-73 L1 cell adhesion molecule Mus musculus 125-129 30265267-8 2018 The method displays a linear response for the determination of vardenafil and ROS in the 4.88-488 mug mL-1 and 4.74-94.7 mug mL-1 concentration ranges, and the limit of detection is as low as 1.63 mug mL-1 and 2.20 mug mL-1, respectively. Vardenafil Dihydrochloride 63-73 L1 cell adhesion molecule Mus musculus 201-211 30265267-8 2018 The method displays a linear response for the determination of vardenafil and ROS in the 4.88-488 mug mL-1 and 4.74-94.7 mug mL-1 concentration ranges, and the limit of detection is as low as 1.63 mug mL-1 and 2.20 mug mL-1, respectively. Vardenafil Dihydrochloride 63-73 L1 cell adhesion molecule Mus musculus 125-129 29113829-8 2018 One of the compounds, vardenafil, resulted in a complete motor neuron protection, an effect that was reversed by blocking receptors of IGF-II. Vardenafil Dihydrochloride 22-32 insulin-like growth factor 2 Mus musculus 135-141 29395941-1 2018 BACKGROUND: Levitra, a phosphodiesterase-5 (PDE5) inhibitor, is the trade name of vardenafil. Vardenafil Dihydrochloride 12-19 phosphodiesterase 5A Homo sapiens 23-42 29395941-1 2018 BACKGROUND: Levitra, a phosphodiesterase-5 (PDE5) inhibitor, is the trade name of vardenafil. Vardenafil Dihydrochloride 12-19 phosphodiesterase 5A Homo sapiens 44-48 29395941-1 2018 BACKGROUND: Levitra, a phosphodiesterase-5 (PDE5) inhibitor, is the trade name of vardenafil. Vardenafil Dihydrochloride 82-92 phosphodiesterase 5A Homo sapiens 23-42 29395941-1 2018 BACKGROUND: Levitra, a phosphodiesterase-5 (PDE5) inhibitor, is the trade name of vardenafil. Vardenafil Dihydrochloride 82-92 phosphodiesterase 5A Homo sapiens 44-48 29113829-9 2018 When administered to naive rats vardenafil was present in the cerebrospinal fluid and increased IGF-II mRNA expression in the spinal cord. Vardenafil Dihydrochloride 32-42 insulin-like growth factor 2 Rattus norvegicus 96-102 29113829-11 2018 Vardenafil also increased IGF-II mRNA and protein levels in motor neurons derived from healthy subject and ALS patient iPSCs, activated a human IGF-II promoter and improved survival of ALS-patient derived motor neurons in culture. Vardenafil Dihydrochloride 0-10 insulin like growth factor 2 Homo sapiens 26-32 29113829-11 2018 Vardenafil also increased IGF-II mRNA and protein levels in motor neurons derived from healthy subject and ALS patient iPSCs, activated a human IGF-II promoter and improved survival of ALS-patient derived motor neurons in culture. Vardenafil Dihydrochloride 0-10 insulin like growth factor 2 Homo sapiens 144-150 29391766-5 2018 In the acute setting, the PDE-5-inhibitor Vardenafil lowered portal pressure by 13%. Vardenafil Dihydrochloride 42-52 phosphodiesterase 5A Homo sapiens 26-31 29794447-20 2018 The hepatoprotective activity of vardenafil in LCA-induced cholestatic damage may result from the drug"s ability to activate Nrf2 signaling and prevent the activation of NLRP3, which could suppress the inflammatory responses in hepatic tissue. Vardenafil Dihydrochloride 33-43 nuclear factor, erythroid derived 2, like 2 Mus musculus 125-129 29794447-20 2018 The hepatoprotective activity of vardenafil in LCA-induced cholestatic damage may result from the drug"s ability to activate Nrf2 signaling and prevent the activation of NLRP3, which could suppress the inflammatory responses in hepatic tissue. Vardenafil Dihydrochloride 33-43 NLR family, pyrin domain containing 3 Mus musculus 170-175 27581752-4 2017 Patch clamp experiments showed that the IC50 values of the human ether-a-go-go-related gene (hERG1) potassium (K) ion channel blocking affinity of PDE5 inhibitors sildenafil, vardenafil, and tadalafil as 33, 12, and 100 muM, respectively. Vardenafil Dihydrochloride 175-185 potassium voltage-gated channel subfamily H member 2 Homo sapiens 93-98 29094165-7 2017 Results: As in dark-reared zebrafish, shedding was reduced in larvae and adults treated with the PDE5/6 inhibitors sildenafil and vardenafil but not with the PDE5 inhibitor tadalafil. Vardenafil Dihydrochloride 130-140 phosphodiesterase 5A, cGMP-specific, b Danio rerio 97-101 27338710-4 2017 The great success of synthetic phosphodiesterase type-5 (PDE-5) inhibitory drugs like sildenafil, vardenafil and tadalafil, used for the treatment of erectile dysfunction has made them, as well as their unapproved analogues, popular as adulterants in herbal dietary supplements. Vardenafil Dihydrochloride 98-108 phosphodiesterase 5A Homo sapiens 31-55 27338710-4 2017 The great success of synthetic phosphodiesterase type-5 (PDE-5) inhibitory drugs like sildenafil, vardenafil and tadalafil, used for the treatment of erectile dysfunction has made them, as well as their unapproved analogues, popular as adulterants in herbal dietary supplements. Vardenafil Dihydrochloride 98-108 phosphodiesterase 5A Homo sapiens 57-62 28150511-4 2017 Due to the amino acid sequence and the secondary structural similarity of PDE6 and PDE11 with the catalytic domain of PDE5, first-generation PDE5 inhibitors (i.e. sildenafil and vardenafil) are also competitive inhibitors of PDE6 and PDE11. Vardenafil Dihydrochloride 178-188 phosphodiesterase 5A Homo sapiens 118-122 28150511-4 2017 Due to the amino acid sequence and the secondary structural similarity of PDE6 and PDE11 with the catalytic domain of PDE5, first-generation PDE5 inhibitors (i.e. sildenafil and vardenafil) are also competitive inhibitors of PDE6 and PDE11. Vardenafil Dihydrochloride 178-188 phosphodiesterase 5A Homo sapiens 141-145 28414103-5 2017 The apoptosis induction effect of low dose Poly-SNO-HSA on C26 cells in vitro under hypoxia can be restored by a phosphodiesterase 5 (PDE5) inhibitor, vardenafil. Vardenafil Dihydrochloride 151-161 phosphodiesterase 5A, cGMP-specific Mus musculus 113-132 28414103-5 2017 The apoptosis induction effect of low dose Poly-SNO-HSA on C26 cells in vitro under hypoxia can be restored by a phosphodiesterase 5 (PDE5) inhibitor, vardenafil. Vardenafil Dihydrochloride 151-161 phosphodiesterase 5A, cGMP-specific Mus musculus 134-138