Sandbox Reserved 1105: Difference between revisions

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[[Image: Drugstructure.png | thumb | left | alt=Puzzle globe| Structures of thyroxine (T4), the natural ligand of TTR and other designed TTR fibril formation inhibitors| 200 px]]
[[Image: Drugstructure.png | thumb | left | alt=Puzzle globe| Structures of thyroxine (T4), the natural ligand of TTR and other designed TTR fibril formation inhibitors| 200 px]]


Drug research is basée on the inhibition of amyloidogenic TTR by stabilization of native tetrameric conformation, using binding ligands to prevent TTR dissociation.
Drug research is based on the inhibition of amyloidogenic TTR by stabilization of native tetrameric conformation, using binding ligands to prevent TTR dissociation.


The fibril formation inhibitors studied are ligands that resemble to the natural ligand T4 but more efficient in binding TTR, leading to a decrease of the amyloidogenic potential. The first potent amyloid inhibitors developed were non-steroidal anti-inflammatory drugs (NSAID), such as flufenamic acid ([[1bm7]]), diclofenac ([[1dvx]]), flurbiprofen ([[1dvt]]), indomethacin, diflunisal, meclofenamic acid, mefenamic acid, or fenoprofen.
The fibril formation inhibitors studied are ligands that resemble to the natural ligand T4 but more efficient in binding TTR, leading to a decrease of the amyloidogenic potential. The first potent amyloid inhibitors developed were non-steroidal anti-inflammatory drugs (NSAID), such as flufenamic acid ([[1bm7]]), diclofenac ([[1dvx]]), flurbiprofen ([[1dvt]]), indomethacin, diflunisal, meclofenamic acid, mefenamic acid, or fenoprofen.