New monoclonal antibody treatment could be effective against COVID-19
CytoDyn, an American pharmaceutical company, has announced that it has made some progress in research into a therapy against COVID-19, a disease caused by the new SARS-CoV-2 coronavirus.
The treatment, known as Leronlimab is a humanised monoclonal antibody IgG4 that blocks the CCR5 cell receptor, which plays a crucial role in HIV infection, tumour growth (metastasis) and other diseases, including non-alcoholic steatohepatitis (NASH). Currently, the drug has completed nine clinical trials for more than 800 people, including reaching primary endpoints in a key phase III study in combination with antiretroviral drugs in HIV-infected patients with treatment experience.
It would appear that Leronlimab is able to help mitigate the ‘cytokine cascade’, where the body’s immune starts to attack the body itself – a phenomenon that is being observed in many COVD-19 patients.
Commenting on the first data on Leronlimab, the company's interim chief medical officer Jacob Lalezari, said:
“The preliminary results from patients who were seriously ill with COVID-19 and received Leronlimab are encouraging. Although the data set is still small, we observed fairly quick and positive laboratory responses in all four patients, and in three of them the laboratory results were associated with a favourable clinical outcome. We look forward to receiving additional results from patients undergoing treatment under the IND program, as well as the results of several randomized clinical trials that will begin soon.”
CytoDyn is expecting enrolment completion for its 75 patient, Phase-II double blinded, placebo controlled, randomized study by the end of May.
The company has also submitted a request to the FDA to grant expanded access, also known as “compassionate use,” to make Leronlimab available for patients not eligible for participation in two ongoing clinical trials for coronavirus infections. So far 54 INDs (Investigational New Drug) applications have been approved by the FDA.
