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Tadalafil (IC 351; Cialis)

Alias: C-351; IC 351; Tadalafil; Cialis; 171596-29-5; Ic351; Tadanafil; ADCIRCA; ICOS 351; IC351; Trade names: Adcirca, Cialis
Cat No.:V0780 Purity: ≥98%
Tadalafil (formerly known as IC351; IC-351;trade name Cialis) is a potent, orally bioavailable, reversible and competitive small-molecule inhibitor of PDE-5 (phosphodiesterase 5) with the potential to treat erectile dysfunction (ED), benign prostatic hyperplasia (BPH), and pulmonary arterial hypertension.
Tadalafil (IC 351; Cialis)
Tadalafil (IC 351; Cialis) Chemical Structure CAS No.: 171596-29-5
Product category: PDE
This product is for research use only, not for human use. We do not sell to patients.
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Other Forms of Tadalafil (IC 351; Cialis):

  • Nortadalafil
  • Tadalafil, (6R ,12aS)-
  • ent-Tadalafil
  • cis-ent-Tadalafil (cis-ent-IC-351; Tadalafil, (6S,12aR)-)
  • Tadalafil-d3 (IC-351-d3)
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Description: Tadalafil (formerly known as IC351; IC-351; trade name Cialis) is a potent, orally bioavailable, reversible and competitive small-molecule inhibitor of PDE-5 (phosphodiesterase 5) with the potential to treat erectile dysfunction (ED), benign prostatic hyperplasia (BPH), and pulmonary arterial hypertension. It inhibits PDE5 with an IC50 of 1.8 nM in a cell-free assay, and shows >10000-fold selectivity for PDE5 over other isoforms of PDE such as PDE1/47/8/9/10. Tadalafil is mainly used for the treatment of erectile dysfunction (ED) via oral administration, but also improves the vasoconstrictive-predominate condition of PAH through elevating cGMP levels in pulmonary vessels resulted from PDE5 inhibition, therefore, it is also a medication used to treat benign prostatic hyperplasia (BPH), and pulmonary arterial hypertension.

Biological Activity I Assay Protocols (From Reference)
Targets
PDE5 (IC50 = 1.8 nM)
ln Vitro
The assays IC (50), K (D) (isotherm), K (D) (dissociation rate), and K (D) ((1/2) EC (50)) were utilized to ascertain the biochemical potency (affinity) of these compounds for PDE5. The results showed that the following compounds met the criteria: sildenafil (3.7 +/-1.4, 4.8 +/-0.80, 3.7 +/-0.29 and 11.7 +/-0.70 nM), Tadalafil (1.8 +/-0.40, 2.4 +/-0.60, 1.9 +/-0.37 and 2.7 +/-0.25 nM); and vardenafil (0.091 +/-0.031, 0.38 +/-0.07, 0.27 +/-0.01 and 0.42 +/-0.10 nM). As a result, each inhibitor has comparable absolute potency values, with vardenafil having the highest relative potency followed by tadalafil and sildenafil [1]. The semen samples were mixed with 0.5 ml of Tadalafil solutions at varying concentrations (0.2, 0.1, 0.05, and 0.025 μg ml-1, respectively). After two hours of incubation, samples treated with 0.2 μg ml-1 Tadalafil demonstrated a significant increase in sperm motility in both groups [2].
ln Vivo
The Tadalafil-treated group's erectile function (intocavernosal pressure/mean arterial pressure) at 0.3, 0.5, 1, 3, and 5 Hz was higher than the diabetic group's values at comparable frequencies that were near to the control values [3]. Orally administer 20 mg of Tadalafil or 100 mg of Sildenafil. In neither group were there statistically significant variations in the parameters of computer-assisted semen analysis. After taking sildenafil for one hour and tadalafil for two hours, there was no discernible change in the frequency of acrosome preterm response [2].
Diabetic rats demonstrated dilated cavernous spaces, smooth muscles with heterochromatic nuclei, degenerated mitochondria, vacuolated cytoplasm, and negative smooth muscle immunoreactivity. Nerve fibers demonstrated a thick myelin sheath and intra-axonal edema, where blood capillaries exhibited thick basement membrane. Diabetic rats on Td showed improved cavernous organization with significant morphometric increases in the area percentage of smooth muscles and elastic tissue and a significant decrease of fibrous tissue. The Td-treated group showed enhanced erectile function (intracavernosal pressure/mean arterial pressure) at 0.3, 0.5, 1, 3, and 5 Hz compared with diabetic group values at the respective frequencies (P <.05) that approached control values. Conclusion: Chronic low-dose administration of Td in diabetic rats is associated with substantial improvement of the structure of penile cavernous tissue, with increased smooth muscles and elastic tissue, decreased fibrous tissue, and functional enhancement of the erectile function. This raises the idea that the change in penile architecture with Td treatment improves erectile function beyond its half-life and its direct pharmacologic action on phosphodiesterase type 5.[3]
For in vivo part, oral administration of tadalafil (20 mg) or sildenafil (100 mg) was given. In both groups, computer-assisted semen analysis parameters showed no significant difference. After the administration of tadalafil (2 h) and sildenafil (1 h), there was no significant difference observed in premature acrosome reaction incidence rate. Taking both in vitro and in vivo results into consideration, acute on-demand administration of tadalafil would have no adverse effect on semen parameters[2].
Enzyme Assay
Sildenafil, tadalafil, and vardenafil each competitively inhibit cGMP hydrolysis by phosphodiesterase-5 (PDE5), thereby fostering cGMP accumulation and relaxation of vascular smooth muscle. Biochemical potencies (affinities) of these compounds for PDE5 determined by IC(50), K(D) (isotherm), K(D) (dissociation rate), and K(D) ((1/2) EC(50)), respectively, were the following: sildenafil (3.7 +/- 1.4, 4.8 +/- 0.80, 3.7 +/- 0.29, and 11.7 +/- 0.70 nM), tadalafil (1.8 +/- 0.40, 2.4 +/- 0.60, 1.9 +/- 0.37, and 2.7 +/- 0.25 nM); and vardenafil (0.091 +/- 0.031, 0.38 +/- 0.07, 0.27 +/- 0.01, and 0.42 +/- 0.10 nM). Thus, absolute potency values were similar for each inhibitor, and relative potencies were vardenafil >> tadalafil > sildenafil. Binding of each (3)H inhibitor to PDE5 was specific as determined by effects of unlabeled compounds. (3)H Inhibitors did not bind to isolated PDE5 regulatory domain. Close correlation of EC(50) values using all three (3)H inhibitors competing against one another indicated that each occupies the same site on PDE5. Studies of sildenafil and vardenafil analogs demonstrated that higher potency of vardenafil is caused by differences in its double ring. Exchange-dissociation studies revealed two binding components for each inhibitor. Excess unlabeled inhibitor did not significantly affect (3)H inhibitor dissociation after infinite dilution, suggesting the absence of subunit-subunit cooperativity. cGMP addition increased binding affinity of [(3)H]tadalafil or [(3)H]vardenafil, an effect presumably mediated by cGMP binding to PDE5 allosteric sites, implying that either inhibitor potentiates its own binding to PDE5 in intact cells by elevating cGMP. Without inhibitor present, cGMP accumulation would stimulate cGMP degradation, but with inhibitor present, this negative feedback process would be blocked[1].
Cell Assay
In vitro[2]
Ten normozoospermic patients and ten asthenozoospermic patients were randomly picked up from our andrological outpatient department respectively. Normozoospermic samples were defined according to the guidelines of World Health Organization (1999): sperm count >20 × 106 ml 1−1, sperm motility >70 per cent, abnormal sperm morphology <70 per cent, vitality >75 per cent and leucocytes<106 ml 1−1. Enrolled patients (age ranged from 26 to 40 years) underwent detailed medical history and physical examination. Patients receiving PDE5 inhibitor treatment, with chronic prostatitis, leucocytospermia or varicocele were excluded.
Every participant was asked to keep sexual abstinence for 4–6 days and to refrain from caffeine, alcohol or nicotine-containing agents 12 h before attendance. Ejaculates were obtained by masturbation into a dry wide-mouth sterile plastic container between 8 and 10 AM in the morning. Immediately after liquefaction, routine semen analyses were performed according to WHO recommendations to obtain initial results.
Samples were then divided into six equal volumes (0.5 ml each) in 3-ml falcon tubes. One was kept as blank control, and one was added with 1 mg ml−1 pentoxifylline as positive control (Nassar et al., 1999). For the other tubes, 0.5 ml tadalafil solutions with different concentrations were added (0.2, 0.1, 0.05 and 0.025 μg ml−1, respectively). Tadalafil solutions were prepared by dissolving its powder in normal saline, and the maximum concentration (0.2 μg ml−1) was determined by the maximum semen content, 2 h after 20 mg tadalafil intake (the maximum recommended dose). Pentoxifylline solution was prepared by adding its parenteral solution (100 mg 5 ml−1) into 95 ml−1 normal saline to reach a final concentration of 1 mg ml−1.
Animal Protocol
The study investigaged 48 adult male albino rats, comprising a control group, sham controls, streptozotocin-induced diabetic rats, and induced diabetic rats that received Td low-dose daily (0.09 mg/200 g weight) for 2 months. The rats were euthanized 1 day after the last dose. Cavernous tissues were subjected to histologic, immunohistochemical, morphometric studies, and measurement of intracavernosal pressure and mean arterial pressure in anesthetized rats.[3]
Ten normozoospermic patients and ten asthenozoospermic patients were randomly picked up from our andrological outpatient department respectively. Inclusion and exclusion criteria were the same with in vitro part. Patients were randomly assigned to receive either drug: sildenafil (100 mg) or tadalafil (20 mg). They were then asked to collect semen samples 1 h or 2 h after sildenafil or tadalafil administration respectively. After a washout period for 7 days, each patient was crossed over to receive the other drug. Ejaculates obtain and requirements were the same with in vitro part. Specifically, sperm acrosome status was assessed by fluorescein isothiocyanate labelled peanut agglutinin (FITC-PNA) and propidium iodide (PI) (Sigma, Dorset, UK) staining and flow cytometry.[2]
Dissovled in saline; 2 mg/kg; oral gavage
Sham-operated rats
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Tadalafil has a tmax of 0.5-6h with a median of 2h in healthy adults. The tmax in adults with PAH is reported as 2-8h with a median of 4h. There does not appear to be a significant effect on absorption when tadalafil is taken with food.
Tadalafil is primarily eliminated via hepatic metabolism. These metabolites are mainly excreted in the feces (61%) and to a lesser extent in the urine (36%)
Tadalafil has a mean apparent volume of distribution of 63L in healthy adults. The mean apparent volume of distribution is reported as 77L in adults with PAH.
The mean apparent oral clearance of tadalafil is 2.5-3.4L/h in healthy adults. The mean apparent oral clearance in adults with PAH is reported as 3.5L/h
Tmax: 30 minutes to 6 hours (median 2 hours). Absolute bioavailability has not been determined; rate and extent of absorption are not influenced by food.
Volume of distribution: 63 L; indicating distribution into tissues. Less than 0.0005% of administered dose was found in the semen of healthy subjects. 94% protein bound.
Over a dose range of 2.5 to 20 mg, tadalafil exposure (AUC) increases proportionally with dose in healthy subjects. Steady-state plasma concentrations are attained within 5 days of once-daily dosing, and exposure is approximately 1.6-fold greater than after a single dose.
Elimination: Mean oral clearance: 2.5 L per hour. Fecal: 61%. Urine: 36%.
For more Absorption, Distribution and Excretion (Complete) data for TADALAFIL (11 total), please visit the HSDB record page.
Metabolism / Metabolites
Tadalafil undergoes hepatic metabolism via CYP3A4 to a catechol metabolite. This catechol metabolite undergoes subsequent methylation and glucuronidation with the methyl-glucuronide metabolite becoming the primary metabolite in circulation. None of the known metabolites are considered to be active.
Biotransformation: Hepatic metabolism, mainly by CYP3A4. Tadalafil is predominantly metabolized by CYP3A4 to a catechol metabolite. The catechol metabolite undergoes extensive methylation and glucuronidation to form the methylcatechol and methylcatechol glucuronide conjugate, respectively. The major circulating metabolite is the methylcatechol glucuronide. Methylcatechol concentrations are less than 10% of glucuronide concentrations. In vitro data suggests that metabolites are not expected to be pharmacologically active at observed metabolite concentrations.
Biological Half-Life
The mean half-life of elimination of tadalafil is 15-17.5h in healthy adults. The mean half-life of elimination in adults with PAH is reported as 35h.
Terminal: 17.5 hours
Toxicity/Toxicokinetics
Hepatotoxicity
Despite fairly extensive use, tadalafil has been linked to only rare reports of serum aminotransferase elevations and clinically apparent liver injury. In a single case report, tadalafil was linked to cholestatic hepatitis arising within a few days of starting the medication. Immunoallergic features and autoantibodies were not present. The injury was self-limiting without residual evidence of bile duct injury. The related PDE5 inhibitor, sildenafil, has also been associated with rare cases of acute cholestatic liver injury with jaundice.
Likelihood score: D (possible rare cause of clinically apparent liver injury).
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
No published information is available on the use of tadalafil during breastfeeding. An alternate agent may be preferred.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.
Protein Binding
Tadalafil is 94% bound to plasma proteins.
References

[1]. Binding of tritiated sildenafil, tadalafil, or vardenafil to the phosphodiesterase-5 catalytic site displays potency,specificity, heterogeneity, and cGMP stimulation. Mol Pharmacol. 2004 Jul;66(1):144-52.

[2]. Effect of acute tadalafil on sperm motility and acrosome reaction: in vitro and in vivo studies. Andrologia. 2013 Apr 14. [Epub ahead of print].

[3]. Effect of Chronic Low-dose Tadalafil on Penile Cavernous Tissues in Diabetic Rats. Urology. 2013 Jun;81(6):1253-60.

Additional Infomation
Tadalafil is a pyrazinopyridoindole that is 2,3,6,7,12,12a-hexahydropyrazino[1',2':1,6]pyrido[3,4-b]indole-1,4-dione substituted at position 2 by a methyl group and at position 6 by a 1,3-benzodioxol-5-yl group (the 6R,12aR-diastereomer). A phosphodiesterase V inhibitor inhibitor, currently marketed in pill form for treating erectile dysfunction under the name Cialis; and under the name Adcirca for the treatment of pulmonary arterial hypertension. It has a role as an EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor and a vasodilator agent. It is a pyrazinopyridoindole and a member of benzodioxoles.
Tadalafil is a selective phosphodiesterase-5 inhibitor that is used in the treatment of erectile dysfunction (ED), pulmonary arterial hypertension (PAH), and benign prostatic hypertrophy. It was first approved in 2003 by the FDA for use in ED and later in 2009 for PAH. In contrast to other PDE5 inhibitors like [sildenafil], tadalafil has greater selectivity for PDE5 and a longer half-life which has made it a more suitable option for chronic once-daily dosing in the treatment of PAH.
Tadalafil is a Phosphodiesterase 5 Inhibitor. The mechanism of action of tadalafil is as a Phosphodiesterase 5 Inhibitor.
Tadalafil is a carboline-based compound with vasodilatory activity. Tadalafil selectively inhibits the cyclic guanosine monophosphate (cGMP)-specific type 5 phosphodiesterase- (PDE-5)-mediated degradation of cGMP, which is found in the smooth muscle of the corpus cavernosa and corpus spongiosum of the penis. Inhibition of cGMP degradation by tadalafil results in prolonged muscle relaxation, vasodilation, and blood engorgement of the corpus cavernosa, and, so, prolonged penile erection.
A carboline derivative and PHOSPHODIESTERASE 5 INHIBITOR that is used primarily to treat ERECTILE DYSFUNCTION; BENIGN PROSTATIC HYPERPLASIA and PRIMARY PULMONARY HYPERTENSION.
See also: Finasteride; tadalafil (component of).
Drug Indication
Tadalafil is indicated for the treatment of erectile dysfunction (ED) and either alone or in combination with [finasteride] for the treatment of benign prostatic hypertrophy (BPH). It is also indicated for the treatment of pulmonary arterial hypertension (PAH) both alone and in combination with [macitentan] or other endothelin-1 antagonists.
FDA Label
Treatment of erectile dysfunction. In order for tadalafil to be effective, sexual stimulation is required. Cialis is not indicated for use by women.
Talmanco is indicated in adults for the treatment of pulmonary arterial hypertension (PAH) classified as WHO functional class II and III, to improve exercise capacity. Efficacy has been shown in idiopathic PAH (IPAH) and in PAH related to collagen vascular disease.
AdultsTreatment of pulmonary arterial hypertension (PAH) classified as WHO functional class II and III, to improve exercise capacity (see section 5. 1). Efficacy has been shown in idiopathic PAH (IPAH) and in PAH related to collagen vascular disease. Paediatric populationTreatment of paediatric patients aged 2 years and above with pulmonary arterial hypertension (PAH) classified as WHO functional class II and III.
Treatment of erectile dysfunction in adult males. In order for tadalafil to be effective, sexual stimulation is required. Tadalafil Lilly is not indicated for use by women. Treatment of the signs and symptoms of benign prostatic hyperplasia in adult males.
Treatment of erectile dysfunction in adult males. In order for tadalafil to be effective, sexual stimulation is required. Tadalafil Mylan is not indicated for use by women.
Treatment of pulmonary arterial hypertension
Mechanism of Action
Tadalafil is a selective phosphodiesterase-5 (PDE5) inhibitor that produces several downstream effects with the most common therapeutic effect being smooth muscle relaxation. Patients may experience ED due to a variety of causes including psychogenic, neurogenic, vasculogenic, iatrogenic, or endocrine. These causes result in dysfunction of penile smooth muscle relaxation through either disrupted neuronal signaling or direct influence on smooth muscle cells. During sexual arousal, non-adrenergic non-cholinergic (NANC) neurons release nitric oxide (NO). Nitric oxide stimulates guanylate cyclase which converts guanosine triphosphate to cyclic guanosine monophosphate (cGMP). cGMP activates the cGMP-dependent kinase (PKG) in a signal cascade which activates K+ channels leading to inhibition of Ca2+ channels, inhibits platelet activation, and inhibits smooth muscle cell proliferation while inducing apoptosis. This signal cascade is attenuated by PDE5 which breaks the phosphodiester bond of cGMP, converting it to GMP. Inhibition of PDE5 by tadalafil increases signaling via the PKG cascade which supports penile smooth muscle relaxation during sexual arousal by decreasing Ca2+ entry into smooth muscle cells. This smooth muscle relaxation allows blood to fill the corpus cavernosum thereby producing an erection. In PAH, blood pressure in the pulmonary arteries is raised due to a variety of mechanisms stemming from endothelial dysfunction. Decreased production of NO and prostacyclin reduce vasodilatory signaling while overproduction of endothelin-1 and thromboxane increase vasoconstriction. Inflammation, thromboses, and hypoxia later contribute to vascular remodeling which further reduces luminal size. The resultant increase in blood pressure reduces the capacity for gas exchange and increases afterload at the right ventricle, producing symptoms of dyspnea, fatigue, and dizziness as well as leading to right-sided heart failure. Tadalafil exerts its therapeutic effect in PAH through boosting NO-cGMP signaling to contribute to smooth muscle relaxation as with ED. Lastly, tadalafil is used to treat BPH. BPH produces urinary dysfunction through hyperproliferation of the epithelial and smooth muscle layers of the prostate. The increased size of the prostate blocks urine flow through the urethra resulting in higher residual volumes due to incomplete emptying. Tadalafil does not appear to exert its benefit via smooth muscle relaxation of the prostate. It may instead exert its effect through a mix of increased oxygenation and decreased inflammation, which decreases tissue remodeling, and inhibition of cell proliferation through the cGMP cascade. The decreased affinity for PDE6 compared to other PDE5 inhibitors may explain the decreased incidence of visual side effects as PDE6 is present in the eye and contributes to color vision.
In vitro studies have shown that the effect of tadalafil is more potent on phosphodiesterase type 5 (PDE5) than on other phosphodiesterases. These studies have shown that tadalafil is >10,000-fold more potent for PDE5 than for PDE1, PDE2, PDE4, and PDE7 enzymes, which are found in the heart, brain, blood vessels, liver, leukocytes, skeletal muscle, and other organs. Tadalafil is >10,000-fold more potent for PDE5 than for PDE3, an enzyme found in the heart and blood vessels. Additionally, tadalafil is 700-fold more potent for PDE5 than for PDE8, PDE9, PDE10 and 14-fold more potent for PDE5 than for PDE11A1, an enzyme found in human skeletal muscle. Tadalafil inhibits human recombinant PDE11A1 activity at concentrations within the therapeutic range. The physiological role and clinical consequence of PDE11 inhibition in humans have not been defined.
Studies in vitro have demonstrated that tadalafil is a selective inhibitor of phosphodiesterase type 5 (PDE5). PDE5 is found in corpus cavernosum smooth muscle, vascular and visceral smooth muscle, skeletal muscle, platelets, kidney, lung, cerebellum, and pancreas.
Penile erection during sexual stimulation is caused by increased penile blood flow resulting from the relaxation of penile arteries and corpus cavernosum smooth muscle. This response is mediated by the release of nitric oxide (NO) from nerve terminals and endothelial cells, which stimulates the synthesis of cyclic GMP in smooth muscle cells. Cyclic GMP causes smooth muscle relaxation and increased blood flow into the corpus cavernosum. The inhibition of phosphodiesterase type 5 (PDE5) enhances erectile function by increasing the amount of cyclic GMP. Tadalafil inhibits PDE5. Because sexual stimulation is required to initiate the local release of nitric oxide, the inhibition of PDE5 by tadalafil has no effect on the absence of sexual stimulation.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C22H19N3O4
Molecular Weight
389.4
Exact Mass
389.137
Elemental Analysis
C, 67.86; H, 4.92; N, 10.79; O, 16.43
CAS #
171596-29-5
Related CAS #
Nortadalafil;171596-36-4;cis-Tadalafil;171596-27-3;ent-Tadalafil;629652-72-8;cis-ent-Tadalafil;171596-28-4;Tadalafil-d3;960226-55-5
PubChem CID
110635
Appearance
White to off-white solid powder
Density
1.5±0.1 g/cm3
Boiling Point
679.1±55.0 °C at 760 mmHg
Melting Point
298-300ºC
Flash Point
364.5±31.5 °C
Vapour Pressure
0.0±2.1 mmHg at 25°C
Index of Refraction
1.758
LogP
1.43
Hydrogen Bond Donor Count
1
Hydrogen Bond Acceptor Count
4
Rotatable Bond Count
1
Heavy Atom Count
29
Complexity
702
Defined Atom Stereocenter Count
2
SMILES
CN1CC(=O)N2[C@@H](C1=O)CC3=C([C@H]2C4=CC5=C(C=C4)OCO5)NC6=CC=CC=C36
InChi Key
WOXKDUGGOYFFRN-IIBYNOLFSA-N
InChi Code
InChI=1S/C22H19N3O4/c1-24-10-19(26)25-16(22(24)27)9-14-13-4-2-3-5-15(13)23-20(14)21(25)12-6-7-17-18(8-12)29-11-28-17/h2-8,16,21,23H,9-11H2,1H3/t16-,21-/m1/s1
Chemical Name
(6R,12aR)-6-(benzo[d][1,3]dioxol-5-yl)-2-methyl-2,3,6,7,12,12a-hexahydropyrazino[1',2':1,6]pyrido[3,4-b]indole-1,4-dione
Synonyms
C-351; IC 351; Tadalafil; Cialis; 171596-29-5; Ic351; Tadanafil; ADCIRCA; ICOS 351; IC351; Trade names: Adcirca, Cialis
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: 78 mg/mL (200.3 mM)
Water:<1 mg/mL
Ethanol: 50 mg/mL (145.6 mM)
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.5 mg/mL (6.42 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (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 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

Solubility in Formulation 2: 30% propylene glycol, 5% Tween 80, 65% D5W:30 mg/mL

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.5681 mL 12.8403 mL 25.6805 mL
5 mM 0.5136 mL 2.5681 mL 5.1361 mL
10 mM 0.2568 mL 1.2840 mL 2.5681 mL

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Clinical Trial Information
NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT05709574 Recruiting Drug: Tadalafil 20 MG Gastric Adenocarcinoma University of Arizona April 20, 2023 Phase 2
NCT05195775 Recruiting Drug: Tadalafil Duchenne Muscular Dystrophy University of Florida December 14, 2021 Phase 2
Phase 3
NCT04491773 Completed Drug: Tadalafil 20 MG Erectile Dysfunction Following
Radical Prostatectomy
Federico II University November 1, 2019
NCT04164355 Completed Drug: Tadalafil 20 MG Erectile Dysfunction Following
Radical Prostatectomy
Federico II University July 4, 2020
Biological Data
  • Tadalafil


    Potency of inhibition of PDE catalytic activity by PDE5 inhibitors.




    Tadalafil

    Affinity of PDE5 for binding 3H inhibitors. Mol Pharmacol.2004 Jul;66(1):144-52.
  • Tadalafil

    Effects of nucleotides and inhibitors on binding of 3H inhibitors to PDE5.Mol Pharmacol.2004 Jul;66(1):144-52.




    Tadalafil

    Effect of cGMP on [3H]tadalafil binding.

  • Tadalafil

    Dissociation of 3H inhibitors from PDE5 after infinite dilution.Mol Pharmacol.2004 Jul;66(1):144-52.
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