Tideglusib
10mM in DMSO
- Product Code: 239138
CAS:
865854-05-3
| Molecular Weight: | 334.39 g./mol | Molecular Formula: | C₁₉H₁₄N₂O₂S |
|---|---|---|---|
| EC Number: | MDL Number: | MFCD18633296 | |
| Melting Point: | Boiling Point: | ||
| Density: | Storage Condition: | -20°C |
Product Description:
Tideglusib is primarily investigated for its potential in treating neurodegenerative diseases, especially Alzheimer's disease. It functions as a non-ATP competitive inhibitor of glycogen synthase kinase-3 (GSK-3), an enzyme involved in the formation of neurofibrillary tangles, a hallmark of Alzheimer's pathology. By inhibiting GSK-3, tideglusib helps reduce tau protein hyperphosphorylation, which may slow down neuronal damage and cognitive decline.
In addition to Alzheimer's, tideglusib has shown promise in preclinical studies for other conditions involving GSK-3 overactivity, such as progressive supranuclear palsy and certain muscular dystrophies. It has also been explored for its neuroprotective and anti-inflammatory effects in models of brain injury and stroke.
Another emerging application is in regenerative dentistry. Studies indicate that tideglusib can stimulate dentin regeneration by promoting the differentiation of dental pulp stem cells, offering a potential treatment for tooth repair without the need for synthetic fillings.
Despite promising results in early trials, clinical development has faced challenges related to efficacy and safety at higher doses. However, its unique mechanism continues to support interest in repurposing and optimizing tideglusib for targeted therapies.
Sizes / Availability / Pricing:
| Size | Availability | Price | Quantity |
|---|---|---|---|
| 1ml | 10-20 days | ฿4,630.00 |
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Tideglusib
Tideglusib is primarily investigated for its potential in treating neurodegenerative diseases, especially Alzheimer's disease. It functions as a non-ATP competitive inhibitor of glycogen synthase kinase-3 (GSK-3), an enzyme involved in the formation of neurofibrillary tangles, a hallmark of Alzheimer's pathology. By inhibiting GSK-3, tideglusib helps reduce tau protein hyperphosphorylation, which may slow down neuronal damage and cognitive decline.
In addition to Alzheimer's, tideglusib has shown promise in preclinical studies for other conditions involving GSK-3 overactivity, such as progressive supranuclear palsy and certain muscular dystrophies. It has also been explored for its neuroprotective and anti-inflammatory effects in models of brain injury and stroke.
Another emerging application is in regenerative dentistry. Studies indicate that tideglusib can stimulate dentin regeneration by promoting the differentiation of dental pulp stem cells, offering a potential treatment for tooth repair without the need for synthetic fillings.
Despite promising results in early trials, clinical development has faced challenges related to efficacy and safety at higher doses. However, its unique mechanism continues to support interest in repurposing and optimizing tideglusib for targeted therapies.
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