It’s rare for a single drug to show promise against two very different illnesses. Researchers at the Keck School of Medicine of USC and the Cleveland Clinic Florida Research and Innovation Center have found a compound that, in early lab and animal studies, slowed both the virus that causes COVID-19 and certain hard-to-treat cancer cells. The common thread is a protein called GRP78.
What is GRP78?
GRP78 is a “chaperone” protein. Its normal job is to help other proteins fold into the right shape inside our cells, especially when cells are under stress. But some viruses and cancers take advantage of it:
- In COVID-19, GRP78 works alongside other receptors to help the SARS-CoV-2 virus get into cells and make copies of itself.
- In cancer, high levels of GRP78 can help tumor cells survive and resist treatment.
That shared role makes GRP78 an appealing target. If a drug could block it, it might slow down both problems.
What the COVID-19 research found
The work, published in Nature Communications, unfolded in several steps:
- Infected cells made more GRP78. In human lung cells, levels of the protein rose as the infection grew stronger.
- Less GRP78 meant less virus. When the researchers reduced GRP78 in lung cells, infected cells produced less of the virus’s spike protein and released far fewer new virus particles.
- A drug had the same effect. A compound called HA15, which binds to GRP78 and blocks its activity, reduced viral spread in lung cells at doses that didn’t harm healthy cells.
- It worked in mice. In mice engineered to carry the human receptor the virus uses, HA15 significantly lowered the amount of virus in the lungs.
The researchers described this as direct evidence that the virus depends on GRP78 to replicate.
The cancer connection
In a separate study with researchers at the University of Michigan, the USC team tested HA15 and a second GRP78 blocker, YUM70, against cancer cells carrying mutations in a gene called KRAS. KRAS mutations are common in pancreatic, lung and colorectal cancers and are notoriously difficult to treat. Both compounds reduced the mutant KRAS protein and lowered the number of cancer cells carrying it.
Why this is still early
These results come from cells grown in the lab and from mice. Many promising compounds never make it past these stages because they turn out to be unsafe or less effective in people. HA15 still needs to go through clinical trials in humans, which typically take years. It is not available as a treatment, and it isn’t something anyone should seek out.
What makes the research exciting is the idea itself: targeting a protein in our own cells that viruses depend on, rather than the virus directly. Because viruses mutate quickly but our proteins don’t, this approach could, in theory, hold up better against new variants.
What this means for you
- Rely on proven protection today. Recommended vaccines, prompt testing when you’re sick, and antiviral treatment for people at higher risk remain the best-supported tools against severe COVID-19.
- Keep up with cancer screening. Screenings for colorectal, lung (for eligible smokers and former smokers) and other cancers help catch disease early, when it’s most treatable.
- Be cautious about “wonder drug” headlines. Early lab results are an important step, but they aren’t the same as a proven treatment. Look for human trial results before drawing conclusions.
The bottom line
By blocking a protein that both the COVID-19 virus and certain cancer cells rely on, an experimental drug called HA15 showed promise in lab and mouse studies. It’s an intriguing new approach, but it’s years away from being tested and approved for people.
This article is for general information and isn’t medical advice. Talk with your healthcare provider about your individual needs.
