"The main motivation behind my research is that classic antibiotics all of us and our children have used, like Penicillin, Amoxicillin and Augmentin, are becoming less effective."

-Jeffrey Toney

Physicians have come to depend on antibiotics to treat illnesses brought on by bacteria that for centuries were a major source of disease and death. However, the effectiveness of several antibiotics has begun to decline at an alarming rate. When bacteria develop resistance, antibiotics no longer kill them, making the antibiotic ineffective in treating or curing the disease.

Jeffrey Toney, the new Margaret and Herman Sokol chair in Chemistry, recognizes that protecting public health relies heavily on the use of antibiotics, so he is waging a war against resistant strains of bacteria by conducting research he hopes will result in inhibitors that will target antibiotic resistance.

It seems fitting that Toney is engaged in research involving antibiotics. The Sokol position, funded by a $1.25-million donation from alumna Margaret McCormack Sokol '38, is in memory of her husband Herman '37, who was instrumental in discovering the antibiotic tetracycline and the process for its manufacture. A research chemist, teacher and industrialist, Dr. Sokol was president of Bristol-Meyers Company from 1976 until he retired in 1981.

Toney said it was intellectual freedom that prompted him to leave his position as senior research fellow at Merck Research Laboratories to become the University's second Sokol chair. He looks forward, he said, to driving his own research program without the limitations put upon researchers in the industry.

Q. Tell us more about your research.
A. The main motivation behind my research is that classic antibiotics all of us and our children have used, like penicillin, amoxicillin and augmentin, are becoming less effective. The response to penicillin, which was 100-percent effective in the 1950s, is now down to 20 percent and getting lower. That phenomenon, coupled with people who are allergic to certain types of antibiotics, points to a strong need for industry to come up with something that will work against these microbes that have become resistant. They can outlive all sorts of mechanisms that scientists never could have predicted back when Alexander Fleming discovered penicillin in 1929.

At Merck we worked on ways to counter those resistance mechanisms using a new generation of Penicillin. That went out of favor a few years ago in industry and I sense that interest in it is coming back.

Q. How do bacteria become resistant to antibiotics?
A. Bacteria take genes already present in their genome and mutate them so gene products are no longer sensitive to the original antibiotic. Bacteria can divide into two only if they make a new cell wall, doubling their cell line and genomic information. Penicillin blocks that wall-building system until bacteria work out a way to mutate key genes that break down the medicines before they can work. Now the cell line can keep dividing, even with Penicillin.

Q. Why did industry step away from this research?
A. All programs in pharmaceuticals are evaluated from both clinical and marketing points of view. When this program was getting ready to go into a more broad scale application it was decided that the clinical and marketing need wasn't high enough to warrant the huge investment that it takes to bring these things into clinical trials. It costs anywhere from $100-$200 million to take one small molecule through all the steps to get approval from the Food and Drug Administration. So before you take that leap, you want to be sure that in the end you'll have something that has a strong clinical need and will have a good market.

Q. So what can be done?
A. Physicians need to be more judicious in prescribing antibiotics. Over-prescribing is the main cause for resistance. The scientific community keeps reminding physicians and clinics that they should be careful in administering, especially the most potent antibiotics. The most common mistake is prescribing an antibiotic to people who have a virus with all the symptoms typical of an infection, but if it's just a virus the antibiotic is useless. It actually can make patients even sicker because not only are physicians not treating them for what they have, but those physicians are actually setting those patients up to be resistant the next time they get a bacterial infection.

Q. How will you utilize the endowment?
A. Thanks to President [Susan A.] Cole, the University is renovating an existing 400-square-foot lab in Richardson Hall. The grant money from Margaret Sokol will help equip and maintain the lab and allow me to bring in a full-time research associate. I also plan to use the Sokol funds to support companies like Merck to bring back that program, which hopefully will lead to a clinical candidate. That's my dream outcome.

Q. How has adding the teaching aspect affected your research?
A. I've always had strong academic interests and the desire to work with students. While I was at Merck I hosted several summer interns from universities, and working one-on-one with those students was so much fun. During that time I imagined that it would be nice to do that full time rather than just on the side.

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