- The researchers believe that a promising treatment for coronavirus is 30 times more potent than remdesivir and may work against the new highly infectious mutations.
- The cancer drug plitidepsin can accelerate patients’ recovery and, according to one study, a few months ago.
- A team led by UCSF has two studies, indicating that the drug is more efficient than remdesivir and can kill the mutation in the UK.
- Plitidepsin does not target the virus directly, but rather a human protein that the virus needs to replicate.
The first drug to be approved for therapy with COVID-19 was remdesivir, but it did not prove to be the key drug that would help doctors save lives or defeat the pandemic. The drug works in some patients, but it is not the definitive cure that the world needs, in addition to vaccines, to end the pandemic. Several teams of researchers are looking for new therapies to prevent the coronavirus from killing so many lives, with a group led by UCSF having now identified a cancer drug that appears to be almost 30 times more potent than remedying it.
The drug is called Aplidine (plitidepsin), and we heard about it several months ago, when researchers from Spain showed that the drug was able to block the virus from replicating. Plitidepsin helped patients recover much faster than others who received standard treatment, and 81% returned home within 15 days, a significant improvement over the typical 47% rate of return. Now, more recent studies also show another important advantage that the drug can have over other COVID-19 therapies: it works against the new highly infectious SARS-CoV-2 mutations. That’s because, instead of attacking the virus itself, the drug impacts 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 marine sea water called Aplidium albicans. The drug was approved in 2018 to treat multiple myeloma, but only after Pharma Mar handled some controversy at home. The European Union blocked the approval of plitidepsin in 2017, saying the risks outweighed the benefits – but Pharma Mar managed to overturn 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 thing we’ve seen.”
Researchers at the Quantitative Biosciences Institute at UCSF (the QCRG group) worked with Mount Sinai and the Institut Pasteur in Paris. QCRG researchers studied the coronavirus last year, trying to understand how it works at a microscopic level after infecting the human cell. The aim of the project was to find a way to block the virus. Of the thousands of drugs and experimental compounds tested in laboratories, 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 the mice with the coronavirus and treated them with plitidepsin, discovering that the drug removed the virus from their bodies. Plitidepsin did not attack the virus directly like remdesivir or other drugs and vaccines. Instead, the virus blocks the activity of a specific protein within cells (eEF1A), without which the virus cannot replicate.
The full study was published in Science.
The researchers did not stop there, however. They partnered with a laboratory in the UK to test plitidepsin against variant B.1.1.7 of the virus, the UK mutation that is now dominant in the country. They found that the drug can kill this strain as well and was more potent than remdesivir. This study was also published 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 and not depend on it,” said Krogan.
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Although the EU has concerns about the side effects of plitidepsin in cancer patients, Pharma Mar said The Chronicle that patients with COVID-19 would require substantially lower doses than patients with cancer. They would also need to take it for just three days, instead of months. Side effects in patients with COVID-19 have been minimal so far.
Although plitidepsin looks promising and could prove to be a drug that further reduces deaths from COVID-19, strict tests on humans will have to be carried out before the drug can be approved for therapy with COVID-19. Phase 3 tests are planned in Spain and the USA, according to Pharma Mar.
Chris Smith started writing about gadgets as a hobby and, before he knew it, was already sharing his views on technology with readers around the world. Whenever he’s not writing about gadgets, he miserably fails to stay away from them, although he tries desperately. But this is not necessarily a bad thing.