In a new study, researchers found that three decades-old antibiotics administered together can block a type of pain triggered by nerve damage.
These drugs—demeclocycline, chlortetracycline, and minocycline—have a long history of safe use and minimal side effects.
The finding could offer an alternative to opioid-based painkillers, addictive prescription medications that are responsible for an epidemic of abuse in the U.S.
The research was conducted by a team at UT Southwestern and elsewhere.
Over 100 million Americans are affected by chronic pain, and a quarter of these experience pain on a daily basis, a burden that costs an estimated $600 billion in lost wages and medical expenses each year.
For many of these patients—those with cancer, diabetes, or trauma, for example—their pain is neuropathic, meaning it’s caused by damage to pain-sensing nerves.
To treat chronic pain, prescriptions for opioid painkillers have increased exponentially since the late 1990s, leading to a rise in abuse and overdoses.
Despite the desperate need for safer pain medications, the development of a new prescription drug typically takes over a decade.
In the study, the team explored the potential of drugs already approved by the Food and Drug Administration (FDA).
They focused on EphB1, a protein found on the surface of nerve cells. Research has shown that this protein is key for producing neuropathic pain.
The researchers scanned a library of FDA-approved drugs, and they found three tetracyclines, members of a family of antibiotics used since the 1970s.
These drugs—demeclocycline, chlortetracycline, and minocycline—have a long history of safe use and minimal side effects.
They found each of these drugs inhibited the protein at relatively low doses.
In three different mouse models of neuropathic pain, injections of these three drugs in combination strongly blunted reactions to painful stimuli such as heat or pressure, with the triplet achieving a greater effect at lower doses than each drug individually.
When the researchers examined the brains and spinal cords of these animals, they confirmed that EphB1 on the cells of these tissues had been inactivated, the probable cause for their pain resistance.
The team says a combination of these drugs might be able to blunt pain in humans too, the next stage for this research.
One author of the study is Hesham A. Sadek, M.D., Ph.D.
The study is published in PNAS.
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