A prodrug is a compound that is pharmacologically inactive as administered and must be metabolically converted in the body into the active species.

Aspirin is the classic example. Chemically it is acetylsalicylic acid, and in the body esterases hydrolyse it to release salicylic acid, which is the active anti-inflammatory agent.

The reason for making the acetyl ester is instructive. Salicylic acid itself is strongly acidic and severely irritating to the gastric mucosa. Acetylating the phenolic -OH masks that acidity, giving a compound that is far better tolerated by mouth. This is exactly what prodrug design sets out to achieve — improving palatability, absorption, stability or targeting while leaving the active molecule unchanged once released.

There is a subtlety worth noting: aspirin is not only a prodrug. The intact acetyl group is what irreversibly acetylates serine-530 of cyclooxygenase, and that is the basis of its unique, permanent inhibition of platelet COX-1 — the reason low-dose aspirin works as an antiplatelet agent for the whole 8-10 day life of the platelet.

The other three are active as given. Vancomycin is a glycopeptide that binds D-Ala-D-Ala directly to block cell-wall cross-linking. Amphotericin B is a polyene that binds ergosterol and forms membrane pores. Penicillin G acts directly through its strained β-lactam ring, which acylates the transpeptidase — and although it is unstable in gastric acid, that is degradation rather than activation.

Hence the prodrug among the options is aspirin.