Tadalafil - CAS 171596-29-5
Catalog number: 171596-29-5
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
C22H19N3O4
Molecular Weight:
389.4
COA:
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Targets:
Phosphodiesterase (PDE)
Description:
Tadalafil binds to PDE5 with KD of 2.4 nM.
Purity:
>98%
Synonyms:
IC351, IC-351, IC 351, Tadalafil, Adcirca, Cialis
MSDS:
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InChIKey:
WOXKDUGGOYFFRN-IIBYNOLFSA-N
InChI:
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
Canonical SMILES:
CN1CC(=O)N2C(C1=O)CC3=C(C2C4=CC5=C(C=C4)OCO5)NC6=CC=CC=C36
1.A randomized clinical trial investigating treatment choice in Chinese men receiving sildenafil citrate and tadalafil for treating erectile dysfunction.
Bai WJ, Li HJ, Jin JJ, Xu WP, Sebastian S, Wang XF1. Asian J Androl. 2016 Apr 22. doi: 10.4103/1008-682X.175782. [Epub ahead of print]
Sildenafil and tadalafil are efficacious and well tolerated in Chinese men with erectile dysfunction (ED). Recent study results indicate that men with ED in China who were naïve to phosphodiesterase inhibitor type 5 (PDE5) therapy prefer tadalafil 20-mg (on-demand) versus sildenafil 100-mg (on-demand). Differences in psychosocial outcomes may help to explain treatment preference in favor of tadalafil. This open-label, randomized, crossover study compared psychosocial outcomes and drug attribute choices between tadalafil and sildenafil in Chinese men with ED naïve to PDE5 inhibitor therapy. Eligible patients were randomized to sequential 20-mg tadalafil/100-mg sildenafil (n = 190) or 100-mg sildenafil/20-mg tadalafil (n = 193) for 8 weeks each and were asked which treatment they preferred to take for the 8-week extension phase. Psychosocial outcomes were assessed using the Psychological and Interpersonal Relationship Scale (PAIRS), Drug Attributes Questionnaire (DRAQ), and Sexual Life Quality Questionnaire (SLQQ).
2.Efficacy of Continuous Dosing of Tadalafil Once Daily vs Tadalafil On Demand in Clinical Subgroups of Men With Erectile Dysfunction: A Descriptive Comparison Using the Integrated Tadalafil Databases.
Brock G1, Ni X2, Oelke M3, Mulhall J4, Rosenberg M5, Seftel A6, D'Souza D7, Barry J8. J Sex Med. 2016 May;13(5):860-75. doi: 10.1016/j.jsxm.2016.02.171.
INTRODUCTION: Various factors play a role in the development of erectile dysfunction (ED).
3.Saxagliptin and Tadalafil Differentially Alter Cyclic Guanosine Monophosphate (cGMP) Signaling and Left Ventricular Function in Aortic-Banded Mini-Swine.
Hiemstra JA1, Lee DI2, Chakir K2, Gutiérrez-Aguilar M3, Marshall KD3, Zgoda PJ1, Cruz Rivera N1, Dozier DG1, Ferguson BS1, Heublein DM4, Burnett JC4, Scherf C5, Ivey JR1, Minervini G6, McDonald KS7, Baines CP8, Krenz M9, Domeier TL7, Emter CA10. J Am Heart Assoc. 2016 Apr 20;5(4). pii: e003277. doi: 10.1161/JAHA.116.003277.
BACKGROUND: Cyclic guanosine monophosphate-protein kinase G-phosphodiesterase 5 signaling may be disturbed in heart failure (HF) with preserved ejection fraction, contributing to cardiac remodeling and dysfunction. The purpose of this study was to manipulate cyclic guanosine monophosphate signaling using the dipeptidyl-peptidase 4 inhibitor saxagliptin and phosphodiesterase 5 inhibitor tadalafil. We hypothesized that preservation of cyclic guanosine monophosphate cGMP signaling would attenuate pathological cardiac remodeling and improve left ventricular (LV) function.
4.The Effect of Sorafenib, Tadalafil and Macitentan Treatments on Thyroxin-Induced Hemodynamic Changes and Cardiac Abnormalities.
Saad NS1,2,3, Floyd K1,2, Ahmed AA3, Mohler PJ1,2, Janssen PM1,2, Elnakish MT1,2,3. PLoS One. 2016 Apr 15;11(4):e0153694. doi: 10.1371/journal.pone.0153694. eCollection 2016.
Multikinase inhibitors (e.g. Sorafenib), phosphodiesterase-5 inhibitors (e.g. Tadalafil), and endothelin-1 receptor blockers (e.g. Macitentan) exert influential protection in a variety of animal models of cardiomyopathy; however, their effects on thyroxin-induced cardiomyopathy have never been investigated. The goal of the present study was to assess the functional impact of these drugs on thyroxin-induced hemodynamic changes, cardiac hypertrophy and associated altered responses of the contractile myocardium both in-vivo at the whole heart level and ex-vivo at the cardiac tissue level. Control and thyroxin (500 μg/kg/day)-treated mice with or without 2-week treatments of sorafenib (10 mg/kg/day; I.P), tadalafil (1 mg/kg/day; I.P or 4 mg/kg/day; oral), macitentan (30 and 100 mg/kg/day; oral), and their vehicles were studied. Blood pressure, echocardiography and electrocardiogram were non-invasively evaluated, followed by ex-vivo assessments of isolated multicellular cardiac preparations.
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CAS 171596-29-5 Tadalafil

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