We don’t really understand how NSAIDs reduce pain, as a concrete example. In contrast we have a pretty good understanding of the pharmacology of caffeine.

It’s not like magnets, some things really are gaps.

Some medications are designed for one purpose, then other effects are discovered in practice. Gabapentin, for example, was designed as an anti-seizure medication structurally similar to the inhibitory neurotransmitter GABA.

Now it is primarily used to treat neuropathic pain, and the mechanism for that is not well understood. The GABA receptor is not involved. This effect is just a happy accident, and nobody really understands why it works.