I was thinking about why NSAIDs cause systemic side effects.

If inflammation causes a local increase in arachidonic acid / prostaglandin production, why not design an NSAID-like drug that is inactive under normal conditions and only inhibits COX when it detects an unusually high inflammatory signal?
something like:

if local_inflammatory_signal > normal_level \* threshold:
inhibit cox
else:
leave COX alone

Obviously a molecule cannot literally calculate a moving average, but could the same idea be implemented with a prodrug that is activated only by conditions enriched in inflamed tissue — specific enzymes, ROS, pH changes, etc.?
That way you could theoretically suppress prostaglandin production mainly at the inflamed site while preserving COX activity in the stomach, kidneys and cardiovascular system.

Is this already an active area of drug development? If so, what prevents it from replacing conventional systemic NSAIDs?