Tiopronin is a small-molecular weight thiol drug used clinically to treat cystinuria and rheumatoid arthritis. Its thiol moiety confers antioxidant properties, enabling it to scavenge free radicals as well as reduce and chelate transition metal ions, and undergo thiol-disulfide exchange, which can serve to spare or restore levels of endogenous thiols, including GSH. Its primary metabolite, thiolactic acid (TLA) retains these properties. In addition, experiments conducted in our lab suggest that both the DPPH radical scavenging and CUPRAC reducing power of tiopronin and TLA exceed that of the well-known and widely used N-acetylcysteine (NAC). Thus, tiopronin possesses several characteristics that make it an attractive candidate for development as a treatment for oxidative stress-related conditions, such as cataracts. However, its labile thiol group represents a double-edged sword for implementation in living systems and ultimately the clinic because thiol drugs are often oxidized before they reach the proposed site of action, rendering them ineffective or even detrimental. Therefore, drug delivery strategies can be employed to safeguard and mediate sustained release of tiopronin. For this purpose, nanodiamonds represent a nearly ideal platform, as they are inert and biocompatible, with highly tailorable surface chemistry and extremely favorable surface area-to-mass ratio. Moreover, preliminary results in our laboratory suggest that detonation nanodiamonds synergistically increase the radical scavenging ability of tiopronin. Comparisons between nanodiamonds with different surface functionalization and specific current and potential applications will be discussed.