Researchers in Denmark testing if senicapoc drug can reduce lung damage in COVID-19 patients

pharmafile | May 13, 2020 | News story | Research and Development COVID-19, Sars, coronavirus 

Scientists are studying if senicapoc, a treatment for sickle cell anemia, can be repurposed to mitigate damage to a COVID-19 patient’s lungs.

The Danish government has given a grant to a research team at Aarhus University to launch a clinical trial which will investigate if the treatment can prevent the lung damage seen in COVID-19 and SARS, to reduce the need for a patient to be on a ventilator.

The trial will evaluate 46 patients with low blood oxygen saturation levels and will have the treatment shipped from a manufacturing facility in China.

Ulf Simonsen, Professor and Doctor of Medical Science at Aarhus Univerisity, commented on the trial and said: “It has surprised me how fast things can move globally with the attempt to combatting coronavirus and how supportive people are when you have an idea how to do it.

“When a person is infected with COVID-19, the worst-case scenario is that they will suffer severe lung disease that could lead to death. This is the situation where the need for treatment with a ventilator occurs. It’s also here that we hope the senicapoc treatment can make a difference, if only so that the patients require a shorter period on a ventilator.”

Senicapoc had previously been found to be safe in clinical trials but was not effective in reducing the number of sickle-cell crises. The drug had been repurposed to treat Alzheimer’s, and a 2019 trial showed that the treatment reduced neuroinflammation by suppressing microglia which in turn reduced Alzheimer’s disease-like deficits in mice.

This evidence made researchers at Azheimer’s Association and the Alzheimer’s Drug Discovery Foundation test the treatment at a Phase 2 clinical trial level.

The team at Aarhus University previously found that senicapoc binds to calcium-activated potassium channels involved in fluid secretion on the surface of the airway in the lungs. The drug also binds to potassium channels in macrophages and T-cells that are involved in immune responses.

Conor Kavanagh

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