479073-79-5

Basic information

• Product Name: Thiosildenafil
• Synonyms: Thiosildenafil;Demethyltadalafil Solution, 100ppm
• CAS NO: 479073-79-5
• Molecular Formula: C₂₂H₃₀N₆O₃S₂
• Molecular Weight: 490.642
• Product Categories: Drug Analogues;Heterocycles;Intermediates & Fine Chemicals;Pharmaceuticals;Sulfur & Selenium Compounds;Isotope Labelled Compounds
• Mol File: 479073-79-5.mol
• Article Data: 1

Chemical Properties

• Melting Point: 172-174?C
• Boiling Point: 676.064°C at 760 mmHg
• Flash Point: 362.671°C
• Appearance: /
• Density: 1.398g/cm³
• Vapor Pressure: 0mmHg at 25°C
• Refractive Index: 1.679
• Storage Temp.: Refrigerator
• Solubility: Chloroform (Slightly), Ethyl Acetate (Slightly), Methanol (Slightly, Heated)
• PKA: 5.97±0.42(Predicted)
• CAS DataBase Reference: Thiosildenafil(CAS DataBase Reference)
• NIST Chemistry Reference: Thiosildenafil(479073-79-5)
• EPA Substance Registry System: Thiosildenafil(479073-79-5)

Safety Data

• Hazardous Substances Data: 479073-79-5(Hazardous Substances Data)

Usage

Description

Thiosildenafil is a derivative of the phosphodiesterase 5 (PDE5) inhibitor sildenafil, which is a potent cGMP-specific phosphodiesterase inhibitor. It is a pale yellow solid and has been found as an adulterant in dietary supplements advertising sexual enhancement for men. However, the biological characteristics of thiosildenafil have not been reported.

Uses

Used in Pharmaceutical Industry:
Thiosildenafil is used as a PDE5 inhibitor for its vasorelaxant properties, which can be beneficial in controlling vascular tone in various conditions such as erectile dysfunction, pulmonary arterial hypertension, and high-altitude pulmonary edema associated with altitude sickness.
Used in Research and Development:
As an analog of sildenafil, thiosildenafil is used in the development of novel pyrazolopyrimidinethiones as PDE5 inhibitors. This application is particularly relevant in the research and development of new drugs targeting PDE5 for various therapeutic purposes.
Used in Diagnostic Applications:
An analog of labeled sildenafil, thiosildenafil can be utilized in diagnostic applications to study the interactions and effects of PDE5 inhibitors on biological systems, potentially leading to a better understanding of their mechanisms of action and the development of more targeted therapies.

InChI:InChI=1/C22H30N6O3S2/c1-5-7-17-19-20(27(4)25-17)22(32)24-21(23-19)16-14-15(8-9-18(16)31-6-2)33(29,30)28-12-10-26(3)11-13-28/h8-9,14H,5-7,10-13H2,1-4H3,(H,23,24,32)

Upstream product

• 109-01-3 1-methyl-piperazine 
• 479074-06-1 2-(2-ethoxy)-phenyl-1-methyl-3-n-propyl-1,6-dihydro-7H-pyrazolo[4,3-d]pyrimidine-7-thione 
• 139756-21-1 5-(2-ethoxy)-phenyl-1-methyl-3-n-propyl-1,6-dihydro-7H-pyrazolo[4,3-d]pyrimidine-7-one 

Relevant articles and documents

The phosphodiesterase 5 inhibitor, KJH-1002, reverses a mouse model of amnesia by activating a cGMP/cAMP response element binding protein pathway and decreasing oxidative damage

Background and Purpose: Inhibition of PDE5 improves synaptic plasticity and memory via enhancing cGMP expression, thus activating the cGMP/cAMP response element binding protein (CREB) signalling pathway. This study investigated the effects of a PDE5 inhibitor on scopolamine-induced cognitive dysfunction, using memory-related behavioural tests and biochemical assays. Experimental Approach: In mice were pretreated with PDE5 inhibitor, amnesia was induced by scopolamine. The learning and memory abilities of mice were tested using the Morris water maze test, the Y-maze test, the passive avoidance test and the novel object recognition test in sequence. Expression of memory-related bio-molecules and oxidative stress parameters in brain tissue were measured using Western blot and spectrophotometry respectively. Key Results: KJH-1002, a novel and potent inhibitor of PDE5 (IC50 0.059?±?0.04?nmol·L?1), was synthesized. In the behavioural tests, it markedly improved the memory performance impaired by scopolamine, indicating a restoration of cognitive function in the mice. Moreover, KJH-1002 increased cGMP levels in the cortex and the scopolamine-reduced expression of phosphorylated CREB, Levels of ERK 1/2, Akt and brain-derived neurotrophic factor in the cortex and hippocampus were restored by KJH-1002 treatment. In addition, KJH-1002 administration increased the activities of SOD, glutathione peroxidase and glutathione reductase, and decreased the level of malondialdehyde. Conclusion and Implications: KJH-1002 restored cognitive function in scopolamine-induced amnesia mice by activating the cGMP/CREB signalling pathway and attenuating oxidative stress. The beneficial effects of KJH-1002 on cognition indicate its potential as a therapeutic candidate for Alzheimer's disease.