How does evolution help?

One of the questions Dennis Prager continually brings up in his attempts to dispense with evolution is, "how does it help a researcher develop a new antibiotic"" or "...treat cancer?" And in Forbes Magazine:

“The essence of the theory of evolution is the hypothesis that historical diversity is the consequence of natural selection acting on variations. Regardless of the verity it holds for explaining biohistory, it offers no help to the experimenter–who is concerned, for example, with the goal of finding or synthesizing a new antibiotic, or how it can disable a disease-producing organism, what dosages are required and which individuals will not tolerate it. Studying biohistory is, at best, an entertaining distraction from the goals of a working biologist.”

Arthur Hunt at The Panda's Thumb writes:

This essay summarizes one such example. I have chosen this one because it refutes, specifically, the claim that an understanding of the evolutionary history of an organism “offers no help to the experimenter–who is concerned, for example, with the goal of finding or synthesizing a new antibiotic, or how it can disable a disease-producing organism”.

In the 1990’s, two parallel, seemingly unrelated areas of research came together in a most remarkable way; moreover, they were tied together by explicit evolutionary connections and reasoning. One field concerned the nature of the Apicomplexa, a group of protists that includes some of the most serious and problematic of parasites of humans. For example, the malaria parasite Plasmodium falciparum is a member of this group of organisms. The Apicomplexa possess (and require for survival) a novel organelle, the apicoplast. In the ‘90’s, it was discovered that the apicoplast is related to another organelle, the chloroplast.
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In the meantime, scientists working in a different field were discovering interesting things about chloroplasts, and especially about the unique metabolic capabilities these organelles bring to the plant cell. Specifically, it was discovered that plastids possess a prokaryotic pathway for the biosynthesis of isoprenoids, the precursors of sterols and myriads of secondary metabolites in plants. This is in addition to the more usual pathway known in humans, a pathway also found in plants. These pathways are, respectively, the non-mevalonate and mevalonate pathways.

The apicoplast, which is needed by the parasite, became an obvious new target for therapies. This is where the two lines of research summarized in preceding paragraphs came together, linked through decidedly evolutionary reasoning. Briefly, several groups followed an obvious line of thought - since the parasite has an organelle that is evolutionarily-related to plastids, see if it has plant-like metabolic pathways or other targets that plant (and chloroplast)-specific drugs would act upon. And indeed, what was found that the Apicomplexa possess a non-MVA pathway for isoprenoid biosynthesis, that this pathway is apicoplast-associated, and that drugs that inhibit the non-MVA pathway inhibit the growth of parasites such as P. falciparum.
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It must be emphasized that, without the evolutionary connection, people would likely not have thought of looking for non-mevalonate isoprenoid pathways in Plasmodium. This pathway is chloroplast-localized in higher plants and is not known in animals. Without the evolutionary link, there is little chance of pulling this pathway “out of the hat”, as opposed to any of the hundreds of other pathways one has to choose from.