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| 250mg |
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Purity: ≥98%
Sildenafil Citrate (formerly also known as UK-92480 citrate; Trade names Revatio;among others), the citrate form of Sildenafil, is a potent and selective inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5) with IC50 of 5.22 nM. Sildenafil Citrate is a well-tolerated and highly effective treatment for erectile dysfunction and pulmonary arterial hypertension.
| Targets |
PDE5/phosphodiesterase 5
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| ln Vitro |
When compared to serotonin stimulation alone, pretreatment with 1 μM sildenafil citrate enhances phosphorylation of ERK1/ERK2, increases the proportion of cells in S phase, and promotes cell proliferation (P<0.05). An abrupt rise in the optical density (OD value) to 0.33 occurs after pretreatment with 1 μM sildenafil citrate and serotonin stimulation. This is significantly different from serotonin stimulation alone (P<0.05). It is evident that 1 μM sildenafil increases the upregulation of serotonin-induced ERK1/ERK2 phosphorylation[2].
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| ln Vivo |
Sildenafil citrate dramatically raises ICP and ICP/BP in the canine erection model, but has no discernible effect on blood pressure when compared to the vehicle[1]. Treatment with sildenafil dramatically reduces TL+-cell counts at 10 mg/kg, but not at 0.5 mg/kg. At this stage, animals treated with PBS have cells positive for the M1-like marker COX-2+ in the ischemic core, while animals treated with 10 mg/kg of sildenafil (but not 0.5 mg/kg) have most of these cells in the penumbra. In contrast, sildenafil therapy (0.5 or 10 mg/kg dosage) significantly reduces the amount of microglia/macrophages stained by Iba-1 eight days after pMCAo[3]. By boosting the release of growth factors (FGF and VEGF), sildenafil citrate has been proven to reduce flap necrosis in preclinical animal models. It has also been demonstrated histologically to be efficacious in rat cavernous nerve architecture[4].
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| Enzyme Assay |
All experiments on ERK1/ERK2 activation, MKP-1, PCNA expression, as well as cell proliferation and cell cycle analysis were performed on cells that were three days in culture at passages 3-5. Thereafter, cells were serum starved for three days in RPMI-1640 containing 0.2% FBS and 1% antibiotics. Cells were then exposed to serotonin or sildenafil at 1 μmol/L then serotonin, as indicated. In some experiments, cells were pretreated with 10 μmol/L of U0126 for 30 minutes before sildenafil and subsequently exposed to serotonin, as indicated. In control groups, an equal volume of phosphate buffered saline (PBS) was substituted for the reagents.[2]
Immunoblotting analysis of ERK1/ERK2 phosphorylation status[2] Subconfluent serum-starved cells were treated with serotonin or 1 μmol/L sildenafil then serotonin stimulation with or without U0126, as indicated above. Protein was extracted at the indicated time as described above. Phosphorylation of ERK1/ERK2 protein was examined by Western blotting. Briefly, equal amounts of proteins (15-20 μg) were separated by SDS-PAGE, transferred to polyvinylidene difluoride membranes, probed with anti-phospho-ERKl/ERK2 antibody, and detected with horseradish peroxidase (HRP)-conjugated secondary antibody. To determine the expression of total ERK1/ERK2, the membrane was washed with stripping buffer at 50°C for 30 minutes, followed by blocking the membrane with 5% bovine serum albumin in PBST for 4 hours. Thereafter, the membrane was re-probed with specific ERK1/ERK2 antibody. Immunoblotting analysis of MKP-1, PCNA[2] Subconfluent serum starved PASMCs were exposed to sildenafil, serotonin or U0126 for different periods of time as described above. At the end of the incubation period, protein was extracted and separated by SDS-PAGE with 12% gels. Then total protein was transferred to polyvinylidene difluoride membrane, and probed with PCNA and MKP-1 antibody (1:1000), glyceraldehydes phosphate dehydrogenase (GAPDH) antibody (1:2000) at 4°C overnight. After being washed, the appropriate secondary antibodies (1:5000) were added for one hour at room temperature. The blots were developed with a Super Signal enhanced chemiluminescence kit and visualized on Kodak-AR film. The bands were quantified by densitometry using image analysis software. The relative expression of protein was normalized to GAPDH. |
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| Cell Assay |
MTT colorimetric assay[2]
Cells at approximately 90% confluence were harvested with 0.1% trypsin/0.01% ethylene diamine tetraacetic acid (EDTA) solution and seeded into a 96-well plate at a density of 2x104 cells/well and grown in RPMI-1640 containing 10% FBS for three days, followed by serum starvation for three days. Cells were then incubated for different time with various concentration of serotonin or 1 μmol/Lsildenafil followed by serotonin with or without U0126, as indicated. Control cells were treated in the same way except sterile PBS replaced the drug. After treatment, medium was changed to fresh medium, and cells were incubated with 5 g/L of MTT for four hours. MTT was then dissolved with 150 μl of 10% dimethylsulfoxide (DMSO) for 20 minutes. The optical densities (OD) in the 96-well plates were determined using a microplate reader at 570 nm. Flow cytometry analysis[2] Cells at approximately 90% confluence were harvested with 0.1% trypsin/0.01% EDTA and seeded into 6-well plates at a density of 5x104 cells/well and grown in RPMI-1640 containing 10% FBS for 3 days, followed by serum starvation for 3 days. Then cells were incubated for 24 hours with serotonin or 1 μmol/L sildenafil followed by serotonin stimulation with or without U0126, as indicated. Cells were rinsed with PBS, trypsinized with 0.1% trypsin/0.01% EDTA solution, and collected by centrifugation at 1000 r/min at 20°C for five minutes. The cell pellets were fixed in 70% ethanol at 4°C for at least 24 hours. The fixed cells were washed twice with PBS, resuspended in PBS containing 50 g/L RNase A and 50 mg/L of propidium iodide (PI). The suspension was incubated at 37°C for 30 minutes, filtered through 200 μm nylon mesh, then analyzed by flow cytometer (FACS Calibur). The ModfitLT software was used for data analysis. The ratio of cells in S phase to all cells that are in G0G1+ S + G2M was calculated by the formula: S phase fraction (SPF) =S/(G0G1+S+G2M) x100% |
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| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
Absorption Sildenafil is known to be quickly absorbed, with maximum plasma concentrations being observed within 30-120 minutes (with a median of 60 minutes) of oral administration in a fasting patient. Moreover, the mean absolute bioavailability observed for sildenafil is about 41% (from a range of 25-63%). In particular, after oral three times a day dosing of sildenafil, the AUC and Cmax increase in proportion with dose over the recommended dosage range of 25-100 mg. When used in pulmonary arterial hypertension patients, however, the oral bioavailability of sildenafil after a dosing regimen of 80 mg three times a day, was on average 43% greater than compared to the lower doses. Finally, if sildenafil is administered orally with food, the rate of absorption is observed to be decreased with a mean delay in Tmax of about 60 minutes and a mean decrease in Cmax of approximately 29%. Regardless, the extent of absorption is not observed to be significantly affected as the recorded AUC decreased by only about 11 %. Route of Elimination After either oral or intravenous administration, sildenafil is excreted as metabolites predominantly in the feces (approximately 80% of the administered oral dose) and to a lesser extent in the urine (approximately 13% of the administered oral dose). Volume of Distribution The mean steady-state volume of distribution documented for sildenafil is approximately 105 L - a value which suggests the medication undergoes distribution into the tissues. Clearance The total body clearance documented for sildenafil is 41 L/h. Sildenafil is rapidly and almost completely absorbed following oral administration. Bioequivalence has been established between the 20-mg tablet and the 10-mg/mL oral suspension when administered as a single oral dose of 20 mg. Although single-dose studies indicate that more than 90% of an oral sildenafil dose is absorbed from the GI tract, the drug undergoes extensive metabolism in the GI mucosa during absorption and on first pass through the liver, with only about 40% of a dose reaching systemic circulation unchanged. Pharmacokinetics of the drug (as determined by peak plasma concentrations or area under the plasma concentration-time curve (AUC)) are dose proportional over the single-dose range of 1.25-200 mg. Peak plasma concentrations of sildenafil and its active N-desmethyl metabolite are achieved within 30-120 (median: 60) minutes following oral administration in fasting adults. Sildenafil appears to be widely distributed in the body, with a reported volume of distribution at steady state averaging 105 L. It is not known whether sildenafil is distributed into milk. Sildenafil and its major circulating N-desmethyl metabolite are each approximately 96% bound to plasma proteins; protein binding reportedly is independent of plasma concentration over the range of 0.01-10 ug/mL. Plasma protein binding of the drug in geriatric adults older than 65 years of age is slightly greater (97%) than that observed in individuals younger than 45 years of age (96%). Sildenafil is distributed to a limited extent in semen following oral administration, with less than 0.001% of a single dose appearing in semen 90 minutes after dosing in healthy individuals Such concentrations are unlikely to cause any effects in sexual partners exposed to the semen. Sildenafil is eliminated mainly in the feces as metabolites. In healthy adults and those with erectile dysfunction, approximately 80% of an oral dose is excreted as metabolites in feces and 13% is excreted in urine. In volunteers with mild (CLcr=50-80 mL/min) and moderate (CLcr=30-49 mL/min) renal impairment, the pharmacokinetics of a single oral dose of Viagra (50 mg) were not altered. In volunteers with severe (CLcr=<30 mL/min) renal impairment, sildenafil clearance was reduced, resulting in approximately doubling of AUC and Cmax compared to age-matched volunteers with no renal impairment. View More
Metabolism / Metabolites
Biological Half-Life The terminal phase half-life observed for sildenafil is approximately 3 to 5 hours. Plasma sildenafil concentrations appear to decline in a biphasic manner following oral administration, with a terminal elimination half-life of about 4 hours (range: 3-5 hours). High clearance was the principal determinant of short elimination half-lives in rodents (0.4-1.3 hr), whereas moderate clearance in dog and man resulted in longer half-lives (6.1 and 3.7 hr respectively). |
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| Toxicity/Toxicokinetics |
Toxicity Summary
IDENTIFICATION AND USE: Sildenafil is a white to off-white crystalline powder that is formulated into film-coated tablets, oral suspension, and parenteral injection. Sildenafil is a phosphodiesterase-5 (PDE-5) inhibitor. It is used both for the treatment of erectile dysfunction and for the treatment of pulmonary arterial hypertension (PAH) in adults to improve exercise ability and delay clinical worsening. HUMAN EXPOSURE AND TOXICITY: In general, overdosage of sildenafil may be expected to produce effects that are extensions of common adverse reactions. In studies of healthy individuals receiving single sildenafil doses up to 800 mg, the types of adverse events (e.g., decreased blood pressure, syncope, and prolonged erection) observed were similar to those observed at lower doses, but the incidences were increased. Serious adverse effects have also been reported at therapeutic dose levels including sudden decrease or loss of hearing, sudden loss of vision in one or both eyes, and prolonged erection lasting greater than 4 hours or priapism (a painful erection lasting greater than 6 hours). Serious cardiovascular, cerebrovascular, and vascular events, including myocardial infarction, sudden cardiac death, ventricular arrhythmia, cerebrovascular hemorrhage, transient ischemic attack, hypertension, subarachnoid and intracerebral hemorrhages, and pulmonary hemorrhage have been reported post-marketing in temporal association with the use of sildenafil for erectile dysfunction. Most, but not all, of these patients had preexisting cardiovascular risk factors. Therefore it was not possible to determine whether these events were related directly to sildenafil, to sexual activity, to the patient's underlying cardiovascular disease, to a combination of these factors, or to other factors. The use of sildenafil is not recommended in children. In a long-term trial in pediatric patients with PAH, an increase in mortality with increasing sildenafil dose was observed. Pulmonary vasodilators such as sildenafil may significantly worsen the cardiovascular status of patients with pulmonary veno-occlusive disease. Sildenafil profoundly potentiates the vasodilatory effects of organic nitrates and nitrites. The drug did not exhibit clastogenic potential in an in vitro human lymphocytes test system. ANIMAL STUDIES: Lethality after oral administration occurred at 1000 mg/kg and 500 mg/kg in rats and 1000 mg/kg in mice. Female rats were more affected than male rats. Acute sildenafil treatment stimulated testosterone production in adult male rats. There was no impairment of fertility in rats given sildenafil up to 60 mg/kg/day for 36 days to females and 102 days to males. However, in another study male rats were gavaged with sildenafil citrate (0.06 mg/0.05 mL) and allowed to mate. Fertilization rates and numbers of embryos were evaluated after treatment. Fertilization rates (day 1) were markedly reduced (approximately 33%) in matings where the male had taken sildenafil citrate. Over days 2-4, the numbers of embryos developing in the treated group were significantly fewer than in the control group. There was also a trend for impaired cleavage rates within those embryos, although this did not reach significance. No evidence of teratogenicity, embryotoxicity or fetotoxicity was observed in rats and rabbits which received up to 200 mg/kg/day during organogenesis. In another study, adult male rabbits received sildenafil at doses up to 9 mg/kg/day for 4 weeks to investigate the testicular histological alterations induced by overdoses of this drug. Abnormality in the germinal epithelium of the seminiferous tubules included spermatocytes karyopyknosis, spermatocytes degeneration, desquamation, spermatid giant cells and arrest of spermatogenesis. Additionally, increased Leydig cells cellularity, tubular degeneration, thickening of the interstitium were also observed. The encountered histological findings indicate that chronic exposure to sildenafil overdoses produces significant morphological and histological alterations in the testes which finally might lead to complete arrest of spermatogenesis. There was no evidence of carcinogenicity when sildenafil was administered orally to rats and mice for up to two years. Sildenafil did not exhibit evidence of mutagenicity in vitro in bacterial and Chinese hamster ovary cell assays. The drug also did not exhibit clastogenic potential in vivo in the mouse micronucleus test. Sildenafil is cleared predominantly by the CYP3A4 (major route) and CYP2C9 (minor route) hepatic microsomal isoenzymes. The major circulating metabolite results from N-desmethylation of sildenafil, and is itself further metabolized. This metabolite has a phosphodiesterase (PDE) selectivity profile similar to sildenafil and an in vitro potency for phosphodiesterase type 5 (PDE-5) approximately 50% of the parent drug. Plasma concentrations of this metabolite are approximately 40% of those seen for sildenafil, so that the metabolite accounts for about 20% of sildenafil's pharmacologic effects. Hepatotoxicity There have been at least 5 reports of acute liver injury attibuted to sildenafil use, but no instances of acute hepatic failure. The latency in most reports has been unclear because of the intermittent and sometimes unacknowledged use of sildenafil, but appears to be within 1 to 8 weeks. The pattern of serum enzyme elevations has ranged from hepatocellular to cholestatic, sometimes evolving from one to the other. The most convincing cases have been a mild cholestatic or "mixed" hepatitis arising within 1 to 3 months of starting sildenafil. Immunoallergic features and autoantibodies were not observed. Cases of acute onset with high serum aminotransferase levels have been reported after use of sildenafil that have some characteristics of ischemic injury. In other instances, the pattern of injury suggested anabolic steroid use. In two cases, re-exposure did not result in recurrence. Thus, the hepatotoxicity of sildenafil is not completely convincing and must be quite rare, if it occurs at all. Likelihood score: C (probable rare cause of clinically apparent liver injury). Effects During Pregnancy and Lactation View More
◉ Summary of Use during Lactation
Interactions Sildenafil and other phosphodiesterase (PDE) type 5 inhibitors (e.g., tadalafil, vardenafil) profoundly potentiate the vasodilatory effects (e.g., a systolic blood pressure reduction exceeding 25 mm Hg with sildenafil) of organic nitrates and nitrites (e.g., nitroglycerin, isosorbide dinitrate), and potentially life-threatening hypotension and/or hemodynamic compromise can result. Nitrates and nitrites promote the formation of cyclic guanosine monophosphate (cGMP) by stimulating guanylate cyclase, and PDE type 5 inhibitors (e.g., sildenafil, tadalafil, vardenafil) act to decrease the degradation of cGMP via phosphodiesterase (PDE) type 5 by inhibiting this enzyme, resulting in increased accumulation of cGMP and more pronounced smooth muscle relaxation and vasodilation than with either PDE type 5 inhibitors or nitrates/nitrites alone. This interaction probably occurs with any organic nitrate, nitrite, or nitric oxide donor (e.g., nitroprusside) regardless of their predominant hemodynamic site of action. Protein Binding It is generally observed that sildenafil and its main circulating N-desmethyl metabolite are both estimated to be about 96% bound to plasma proteins. Nevertheless, it has been determined that protein binding for sildenafil is independent of total drug concentrations. |
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| References |
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| Additional Infomation |
Sildenafil citrate is the citrate salt of sildenafil. It has a role as a vasodilator agent and an EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor. It contains a sildenafil.
Sildenafil Citrate is the citrate salt form of sildenafil, an orally bioavailable pyrazolopyrimidinone derivative structurally related to zaprinast, with vasodilating and potential anti-inflammatory activities. Upon oral administration, sildenafil selectively targets and inhibits cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5), thereby inhibiting the PDE5-mediated degradation of cGMP found in smooth muscle and increasing cGMP availability. This results in prolonged smooth muscle relaxation in the corpus cavernosum of the penis, thereby causing vasodilation, blood engorgement and a prolonged penile erection. In the smooth muscle of the pulmonary vasculature, the increase in cGMP results in smooth muscle relaxation, vasodilation of the pulmonary vascular bed, relieving pulmonary hypertension and increasing blood flow in the lungs. In addition, sildenafil may reduce airway inflammation and mucus production. A PHOSPHODIESTERASE TYPE-5 INHIBITOR; VASODILATOR AGENT and UROLOGICAL AGENT that is used in the treatment of ERECTILE DYSFUNCTION and PRIMARY PULMONARY HYPERTENSION. See also: Sildenafil (has active moiety). Drug Indication AdultsTreatment of adult patients with pulmonary arterial hypertension classified as WHO functional class II and III, to improve exercise capacity. Efficacy has been shown in primary pulmonary hypertension and pulmonary hypertension associated with connective tissue disease. Paediatric populationTreatment of paediatric patients aged 1 year to 17 years old with pulmonary arterial hypertension. Efficacy in terms of improvement of exercise capacity or pulmonary haemodynamics has been shown in primary pulmonary hypertension and pulmonary hypertension associated with congenital heart disease (see section 5. 1). AdultsTreatment of adult patients with pulmonary arterial hypertension classified as WHO functional class II and III, to improve exercise capacity. Efficacy has been shown in primary pulmonary hypertension and pulmonary hypertension associated with connective tissue disease. Paediatric populationTreatment of paediatric patients aged 1 year to 17 years old with pulmonary arterial hypertension. Efficacy in terms of improvement of exercise capacity or pulmonary haemodynamics has been shown in primary pulmonary hypertension and pulmonary hypertension associated with congenital heart disease. |
| Molecular Formula |
C22H30N6O4S.C6H8O7
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| Molecular Weight |
666.7
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| Exact Mass |
666.231
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| Elemental Analysis |
C, 50.44; H, 5.75; N, 12.61; O, 26.40; S, 4.81
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| CAS # |
171599-83-0
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| Related CAS # |
Sildenafil;139755-83-2;Sildenafil citrate-d8;1215071-03-6; 171599-83-0 (citrate); 252951-59-0 (nitrate)
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| PubChem CID |
135413523
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| Appearance |
White to off-white solid powder
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| Density |
1.447g/cm3
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| Boiling Point |
672.4ºC at 760 mmHg
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| Melting Point |
187-189ºC
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| Flash Point |
360.5ºC
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| Vapour Pressure |
0mmHg at 25°C
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| Index of Refraction |
1.683
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| LogP |
1.319
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| Hydrogen Bond Donor Count |
5
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| Hydrogen Bond Acceptor Count |
15
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| Rotatable Bond Count |
12
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| Heavy Atom Count |
46
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| Complexity |
1070
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| Defined Atom Stereocenter Count |
0
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| SMILES |
S(C1C([H])=C([H])C(=C(C2=NC3C(C([H])([H])C([H])([H])C([H])([H])[H])=NN(C([H])([H])[H])C=3C(N2[H])=O)C=1[H])OC([H])([H])C([H])([H])[H])(N1C([H])([H])C([H])([H])N(C([H])([H])[H])C([H])([H])C1([H])[H])(=O)=O.O([H])C(C(=O)O[H])(C([H])([H])C(=O)O[H])C([H])([H])C(=O)O[H]
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| InChi Key |
DEIYFTQMQPDXOT-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C22H30N6O4S.C6H8O7/c1-5-7-17-19-20(27(4)25-17)22(29)24-21(23-19)16-14-15(8-9-18(16)32-6-2)33(30,31)28-12-10-26(3)11-13-28;7-3(8)1-6(13,5(11)12)2-4(9)10/h8-9,14H,5-7,10-13H2,1-4H3,(H,23,24,29);13H,1-2H2,(H,7,8)(H,9,10)(H,11,12)
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| Chemical Name |
5-(2-ethoxy-5-((4-methylpiperazin-1-yl)sulfonyl)phenyl)-1-methyl-3-propyl-1,4-dihydro-7H-pyrazolo[4,3-d]pyrimidin-7-one 2-hydroxypropane-1,2,3-tricarboxylate
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| Synonyms |
UK-92480 citrate; UK 92480 citrate; Sildenafil Citrate; UK92480 citrate; UK 92480-10; 171599-83-0; Revatio; VIAGRA; Caverta; Sildenafil (citrate); Sildenafil citrate [USAN]; LIQREV; UK-92,480-10. Trade names: Revatio.
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 5 mg/mL (7.50 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 50.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 5 mg/mL (7.50 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 50.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 5 mg/mL (7.50 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 30% PEG400+0.5% Tween80+5% propylene glycol:30 mg/mL |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.4999 mL | 7.4996 mL | 14.9993 mL | |
| 5 mM | 0.3000 mL | 1.4999 mL | 2.9999 mL | |
| 10 mM | 0.1500 mL | 0.7500 mL | 1.4999 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT05558176 | Recruiting | Drug: Sildenafil citrate | Foetal Hypoxia | Ladoke Akintola University of Technology Teaching Hospital, Ogbomoso |
April 8, 2022 | Phase 4 |
| NCT02845388 | Completed | Drug: Sildenafil citrate Drug: estradiol valerate |
Infertility | Omar Ahmed El Sayed Saad | September 2015 | Phase 2 |
| NCT05951413 | Recruiting | Drug: Sildenafil Citrate Drug: estradiol |
IVF | Beni-Suef University | June 30, 2023 | Phase 2 Phase 3 |
| NCT03417492 | Terminated | Drug: Sildenafil Citrate | Traumatic Brain Injury Mild Traumatic Brain Injury |
University of Pennsylvania | March 1, 2018 | Phase 1 |
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