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Home   »   Product Pathways  »  GSK-3  »  Tideglusib

Products are for research use only. Not for human use. We do not sell to patients.


CS-0613 Tideglusib


(NP-12;NP031112;NP 031112;NP-031112)
Structure Price and Availability of    Tideglusib
United States
Size Price Stock
10mg $83 In-stock Inquiry
50mg $140 In-stock
100mg $266 In-stock
200 mg Get quote
500 mg Get quote
 Distributor In Japan:  フナコシ株式会社 www.funakoshi.co.jp    電話番号:81-3-5684-1620   
 FAX番号:81-3-5684-1775
Inquiry for price and availability only. Please place your order via our email or fax.
Contact us for competitive discounts on bulk quantities .
  • Data Sheet
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Tideglusib  M.Wt:  334.39
Tideglusib  Formula: C19H14N2O2S
Tideglusib  Solubility: DMSO: 12 mg/mL
Tideglusib  Purity: >98%
Tideglusib  Storage:  Please store the product under the recommended conditions in the Certificate of Analysis.
CAS: 865854-05-3

View current batch:

Tideglusib(NP-031112) is an irreversible, non ATP-competitive GSK-3β inhibitor with IC50 of 60 nM. IC50 value: 60 nM [1] Target: GSK-3β in vitro: Tideglusib irreversibly inhibits GSK-3, reduces tau phosphorylation, and prevents apoptotic death in human neuroblastoma cells and murineprimary neurons [1]. Tideglusib (2.5 μM) inhibits glutamate-induced glial activation as evidenced by decreased TNF-α and COX-2 expression in rat primary astrocyte or microglial cultures. Tideglusib (2.5 μM) also exerts a potent neuroprotective effect on cortical neurons from glutamate-induced excitotoxicity as evidenced by significant reduction in the number of Annexin-V-positive cells in rat primary astrocyte or microglial cultures [2]. in vivo: Tideglusib (50 mg/kg) injected into the adult male Wistar rats hippocampus dramatically reduces kainic acid-induced inflammation and has a neuroprotective effect in the damaged areas of the hippocampus [2]. Tideglusib (200 mg/kg, oral) results in lower levels of tau phosphorylation, decreased amyloid deposition and plaque-associated astrocytic proliferation, protection of neurons in the entorhinal cortex and CA1 hippocampal subfield against cell death, and prevention of memory deficits in APP/tau double transgenic mice [3].

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