- Researchers think a promising coronavirus treatment is 30 times more powerful than remdesivir and could work against the highly contagious new mutations.
- Cancer drug plitidepsin can speed up patients’ recovery, a study said a few months ago.
- A team led by UCSF has conducted two studies, indicating that the drug is more efficient than remdesivir and can kill the British mutation.
- Plitidepsin does not target the virus directly, but rather a human protein that the virus needs to replicate.
The first drug approved for COVID-19 therapy was remdesivir, but it turned out not to be the primary drug that would help doctors save lives or beat the pandemic. The drug works in some patients, but it is not the definitive cure the world needs in addition to vaccines to end the pandemic. Multiple teams of researchers are looking for new therapies to prevent the coronavirus from taking so many lives, with a UCSF-led group now identifying a cancer drug that appears to be nearly 30 times more potent than remdesivir.
The drug is called Aplidin (plitidepsin), and we heard about it several months ago when researchers from Spain showed that the drug could block replication of the virus. Plitidepsin helped patients recover much more quickly than others who received standard care, and 81% returned home within 15 days, a significant improvement from the typical return rate of 47%. Now, newer studies are also showing another important advantage the drug could have over other COVID-19 therapies: it works against the new, highly contagious SARS-CoV-2 mutations. That’s because instead of attacking the virus itself, the drug affects a specific protein in human cells that the new coronavirus needs to replicate.
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The Spanish company Pharma Mar developed plitidepsin, which was extracted from a sea syringe called Ecology Albicans. The drug was approved in 2018 to treat multiple myeloma, but only after Pharma Mar addressed some controversy at home. The European Union blocked the approval of plitidepsin in 2017, saying the risks outweighed the benefits, but Pharma Mar was able to reverse that decision.
“We need some new weapons in the arsenal,” said UCSF molecular biologist Nevan Krogan SF Chronicle about plitidepsin. “This is by far the best we’ve seen.”
Researchers from UCSF’s Quantitative Biosciences Institute (the QCRG group) collaborated with Mount Sinai and the Institut Pasteur in Paris. The QCRG researchers studied the coronavirus last year to understand how it works at a microscopic level after it infects the human cell. The goal of the project was to find a way to block the virus. Of the thousands of drugs and experimental compounds tested in labs, plitidepsin stood out.
The scientists used extremely low concentrations of the drug to kill the virus in lung cells developed from human and monkey tissue. They then infected mice with the coronavirus and treated them with plitidepsin, finding that the drug cleared the virus from their bodies. Plitidepsin did not directly attack the virus like remdesivir or other drugs and vaccines. Instead, the virus blocks the activity of a specific protein in the cells (eEF1A), without which the virus cannot replicate.
The full study is published in Science.
However, the researchers didn’t stop there. They teamed up with a lab in the UK to test plitidepsin against the B.1.1.7 variant of the virus, the UK mutation that is now dominant in the country. They found that the drug can kill that strain as well and was more potent than remdesivir. That research has also been posted online, but in a non-peer-reviewed format.
The team thinks the drug would continue to work against other mutations because of the eEF1A protein it targets. “If you get a drug that targets a human protein, it would be incredibly difficult for the virus to mutate so that it doesn’t depend,” said Krogan.
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While the EU was concerned about the side effects of plitidepsin in cancer patients, Pharma Mar said The Chronicle that COVID-19 patients would require significantly lower doses than cancer patients. They would also only need it for three days instead of months. Side effects in COVID-19 patients have been minimal so far.
While plitidepsin sounds promising and could prove to be a drug that further reduces deaths from COVID-19, strict human testing will need to be done before the drug can be approved for COVID-19 therapy. Phase 3 trials are planned in Spain and the US, according to Pharma Mar.
Chris Smith started writing about gadgets as a hobby and before he knew it, he shared his thoughts on tech matters with readers around the world. If he doesn’t write about gadgets, he sadly fails to stay away from them, although he desperately tries. But that’s not necessarily a bad thing.