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When knowledge fails to provide answers to important questions such as how to improve the bioavailability of vital medications, “Imagination is more important than knowledge,” as Albert Einstein once said. Ingenuity in the design of effective prodrugs has been lacking in quantity and quality. The reasons behind the low quality of ingenuity could be related to the fact that medicinal chemists have expertise in organic and organometalic chemistry not in biochemistry and biology. On the other hand, pharmaceutical chemists, biologists, and biochemists do not have the expertise to make sophisticated chemical devices. Therefore, in order for a prodrug strategy to work, a team consisting of all this expertise is necessary. A prodrug is a pharmacologically inactive chemical derivative that can be utilized to temporarily alter the physicochemical properties of a specific drug to increase its usefulness and minimize its toxicity. Prodrugs have gained attention as an approach for improving drug therapy since the early seventies. Examples of prodrugs include the antirheumatic agent oxindole succinicate, the anticonvulsant agent progabide, the anti-inflammatory drugs valdecoxib, prednisolone and fluocinolone acetonide, and the anti-glaucoma agent (dipivefrin) [1]. Ideally, the prodrug should be cleaved to the parental drug as soon as its purpose is achieved, followed by rapid elimination of the released linker moiety [2,3]. Prodrugs are designed so that they undergo cleavage in physiologic environments via enzyme catalysis and/or via in vivo chemical reactions. In both cases, the rate of prodrug cleavage from its parental drug is not controlled by the chemist but by the dosage route environment and the abundance of certain enzymes in the route.