CAS 865854-05-3 Tideglusib - Analytical Products / Alfa Chemistry

CAT	AP865854053
CAS	865854-05-3
Structure
MDL Number	MFCD18633296
Molecular Weight	334.39
InChI Key	PMJIHLSCWIDGMD-UHFFFAOYSA-N

Description	≥98% (HPLC)
Solubility	DMSO: >15 mg/mL
Assay	≥98% (HPLC)
Color	white to beige
Form	powder
Size	10MG, 50MG
Storage Conditions	2-8°C

A Phase II Trial of Tideglusib in Alzheimer's Disease

Simon Lovestone, Mercè Boada, Bruno Dubois, Michael Hüll, Juha O Rinne, Hans-Jürgen Huppertz, Miguel Calero, María V Andrés, Belén Gómez-Carrillo, Teresa León, Teodoro del Ser, ARGO investigators

J Alzheimers Dis. 2015;45(1):75-88.

PMID: 25537011

Available and Future Treatments for Atypical Parkinsonism. A Systematic Review

Davide Vito Moretti

CNS Neurosci Ther. 2019 Feb;25(2):159-174.

PMID: 30294976

Nuclear GSK3β Promotes Tumorigenesis by Phosphorylating KDM1A and Inducing Its Deubiquitylation by USP22

Aidong Zhou, Kangyu Lin, Sicong Zhang, Yaohui Chen, Nu Zhang, Jianfei Xue, Zhongyong Wang, Kenneth D Aldape, Keping Xie, James R Woodgett, Suyun Huang

Nat Cell Biol. 2016 Sep;18(9):954-966.

PMID: 27501329

Regulation of the Nrf2 Pathway by Glycogen Synthase Kinase-3β in MPP⁺-Induced Cell Damage

Güliz Armagan, Elvin Sevgili, Fulya Tuzcu Gürkan, Fadime Aydın Köse, Tuğçe Bilgiç, Taner Dagcı, Luciano Saso

Molecules. 2019 Apr 8;24(7):1377.

PMID: 30965670

Tideglusib Rescues Neurite Pathology of SPG11 iPSC Derived Cortical Neurons

Tatyana Pozner, Annika Schray, Martin Regensburger, Dieter Chichung Lie, Ursula Schlötzer-Schrehardt, Jürgen Winkler, Soeren Turan, Beate Winner

Front Neurosci. 2018 Dec 6;12:914.

PMID: 30574063

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Case Study

Tideglusib Attenuates Hypoxic-Ischemic Brain Injury in Neonatal Mice

Wang, Haitao, et al. Biochimica et Biophysica Acta (BBA)-General Subjects 1860.10 (2016): 2076-2085.

Hypoxic-ischemic (HI) conditions are significant causes of neonatal brain injury and neurological disorders. Following neonatal stroke, the activity of glycogen synthase kinase-3β (GSK-3β) is upregulated. Tideglusib, a GSK-3β inhibitor, has shown neuroprotective effects in clinical trials for neurodegenerative diseases. However, the effects of tideglusib on neonatal hypoxic-ischemic brain injury remain unknown.
This study investigates the effects of tideglusib on neonatal hypoxic-ischemic (HI) brain injury.
Methods: Postnatal day 7 (P7) mouse pups underwent unilateral common carotid artery ligation followed by 1 hour of hypoxia or sham surgery. HI animals received intraperitoneal injections of tideglusib (5 mg/kg) or vehicle 20 minutes before the onset of ischemia. Brain infarct volumes and whole-brain images combined with Nissl staining were used to assess the protective effects of tideglusib. Protein levels of glial fibrillary acidic protein (GFAP), Notch1, cleaved caspase-3/9, phosphorylated signal transducer and activator of transcription 3 (STAT3), GSK-3β, and protein kinase B (Akt) were measured to identify potential molecular pathways involved.
Results: Tideglusib significantly reduced brain infarct volume at both 24 hours and 7 days post-HI injury. Tideglusib also increased the phosphorylation of GSK-3β (Ser9) and Akt (Ser473), while reducing the expression of GFAP and p-STAT3 (Tyr705). Additionally, tideglusib pretreatment elevated Notch1 protein levels and reduced the cleavage of pro-apoptotic caspase proteins, including caspase-3 and caspase-9, following HI injury. These findings suggest that tideglusib provides neuroprotection against hypoxic-ischemic brain injury in neonatal mice.

Preparation of Tideglusib (TDg)-Loaded Nanoparticles

Osorio, Raquel, et al. Dental Materials 40.10 (2024): 1591-1601.

Tideglusib (TDg)-loaded nanoparticles (NPs) can alleviate lipopolysaccharide-induced damage in human molar stem cells, enhancing osteogenic differentiation and mineralization.
Nanoparticle Preparation: The process of obtaining NPs was carried out using a polymerization precipitation method, which controls precipitation through thermodynamic methods. The framework monomer for the NP design was 2-hydroxyethyl methacrylate, methacrylic acid was used as the functional monomer, and ethylene glycol dimethacrylate as the crosslinker. Subsequently, half of the produced NPs were loaded with the peptide TDg. For the NP loading process, 100 mg of NPs were immersed in 1 mL of a 0.0017 mg/mL TDg solution and shaken at room temperature (12 rpm) for 2 hours. The NPs were then left until the solvent completely evaporated, ensuring all TDg remained on the NPs.

Tideglusib Induces Apoptosis in Human Neuroblastoma IMR32 Cells

Mathuram, Theodore Lemuel, et al. Environmental toxicology and pharmacology 46 (2016): 194-205.

Neuroblastoma is the most common tumor in children, accounting for nearly 15% of cancer-related deaths. Tideglusib was designed as an "orphan drug" for the treatment of neurodegenerative Alzheimer's disease and has shown significant progress in clinical trials.
Several researchers have reported that treating human IMR32 neuroblastoma cells with different concentrations of Tideglusib reduces cell viability. We investigated the effects of varying concentrations of Tideglusib and lithium chloride on IMR32 cells. Lithium, a known GSK-3 inhibitor, was used as a standard to compare Tideglusib's efficacy in a dose-dependent manner. Tideglusib was reported to significantly increase pro-apoptotic proteins (PARP, Caspase-9, Caspase-7, Caspase-3) and tumor-related genes (FasL, TNF-α, Cox-2, IL-8, Caspase-3) in a dose-dependent manner. When cells were exposed to Tideglusib and lithium chloride, protein levels of anti-GSK3 β, pGSK3 β, Bcl-2, Akt-1, and p-Akt1 were observed. No significant dose-dependent changes were noted in the mRNA expression of collagenase MMP-2, tumor suppressor p53, or cell cycle protein p21. The study also reported that Tideglusib reduced colony formation in IMR32 cells and increased the levels of the sub-G0/G1 population. These findings highlight the potential of Tideglusib as a promising apoptosis-inducing agent in human neuroblastoma IMR32 cells.