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TH-237A was investigated for effectiveness in protecting neurons against several toxic stimuli and its interaction with the microtubule network. In vitro studies using bovine brain microvessel endothelial cells experiments and in situ brain perfusion studies suggested that TH-237A can readily cross the blood-brain barrier in a passive manner. Chronic treatment of P301L mutant Tau mice with TH-237A led to a reduction of abnormal Tau in brain and spinal cord. The results suggest that this small, brain permeable compound may provide a lead structure for development of new therapeutic approaches to neurofibrillary pathology. Exposure of neuronal cultures to Aβ peptide in the presence of 5 nM TH-237A resulted in a 50% increase in survival. Neuronal cultures treated with other toxic stimuli such as staurosporine, thapsigargin, paraquat and H2O2 showed significantly enhanced survival in the presence of TH-237A. Microtubule binding and tubulin assembly studies revealed differences compared to paclitaxel, but confirmed the interaction of TH-237A with microtubules. Furthermore, in vitro studies using bovine brain microvessel endothelial cells experiments suggest that TH-237A can readily cross the blood-brain barrier in a passive manner.
| Molecular Weight | 333.33 |
| Formula | C18H17F2NO3 |
| CAS Number | 935467-97-3 |
| Solubility (25°C) | DMSO 45 mg/mL |
| Storage |
Powder -20°C 3 years ; 4°C 2 years In solvent -80°C 6 months ; -20°C 1 month |
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