Knockdown reduces FTO expression, while an FTO inhibitor binds to the catalytic pocket of the FTO protein so it cannot function. Imagine your mouth was FTO, your fist was Zantrene, and a piece of cake was m6A. If you put your fist (Zan) in your mouth (FTO) then you wont be able to bite into the cake (m6A).
Zantrene is always functioning primarily as an FTO inhibitor. It's just when all the FTO in a cell is bound by Zantrene, then it collects and loiters around in the cell possibly doing other things. Imagine a cell is a strip club, Zantrene are the strippers, and the patrons are FTO. The patrons come into the strip club and are available to the strippers. All of the strippers are very talented and bind to their patron. However, there are more strippers than patrons (more Zantrene is pumped into the cell), so they have the opportunity to loiter in the club and can act in other ways like getting drunk and/or chatting nonsense to their fellow workmates (their other functions). Sure, the strippers (Zan) could get drunk and chat nonsense, but they are much better at binding with their patron (FTO).
FTO overexpression (hyper-demethylation) is the issue. You therefore just need to inhibit the process of hyper-demethylation, which is by binding to the catalytic pocket of FTO with Zan.
We'll most likely see Zantrene replicate all FTO KD models.
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