PROTACs are a completely different class of drug from traditional inhibitors. Traditional inhibitors work like a cork in a bottle. They block a protein's function while the drug is present, but wear off when the drug leaves the body. PROTACs work differently: they're Y-shaped molecules that simultaneously attach to the target protein AND to the cell's waste-disposal system (the proteasome). The cell then destroys the target protein entirely. It's like replacing the cork with a "self-destruct button". Instead of just blocking the protein, you're telling the cell to eat it.
Why PROTACs could matter for MCHS: If a CDK2-targeting PROTAC were developed for neuroinflammation, it could potentially provide longer-lasting effects than traditional inhibitors with fewer doses. However, they're much harder to develop (the Y-shaped molecule has to hit two targets simultaneously) and are still in early research stages for CDK2.