Leronlimab can reduce plasma viral load and help restore the immune system of COVID-19 patients, revealed a small observational study.
CytoDyn’s Leronlimab was found to be a promising candidate for COVID-19 treatment, said GlobalData. Leronlimab is said to have global peak sales of $747m in 2026 - putting it in second place after remdesivir, according to the current GlobalData sales forecast for COVID-19. Leronlimab is behind remdesivir in GlobalData's estimates as remdesivir has emergency use authorization, is already marketed in Japan and currently being developed by Gilead, one of the top 10 US biotech’s and a market leader in antivirals.
Johanna Swanson, Product Manager at GlobalData, comments: “Leronlimab Is currently in Phase III development for COVID-19, making it one of the leading COVID-19 drugs by development stage. Leronlimab is being investigated in two COVID-19 clinical trials - one study plans to recruit 75 subjects and the other 390 subjects.”
According to IncellDx, critically ill patients saw dramatic immune restoration and extubation within seven days of treatment.
Swanson continues: “While these results are promising, they are based on a small sample size of ten patients. Larger placebo-controlled clinical trials will need to be done to confirm these initial results.”
Leronlimab is an investigational humanized immunoglobulin (Ig)G4 monoclonal antibody drug that was originally developed as a treatment for human immunodeficiency virus (HIV). Leronlimab is directed against CCR5, a molecular portal that HIV uses to enter cells. The drug has recently reached a milestone in securing fast track designation from the FDA for the treatment of HIV.
Swanson added: “Leronlimab is currently undergoing two COVID-19 clinical trials based on the drug’s ability to mitigate the COVID-19 cytokine storm. The cytokine storm can lead to an increased risk of leakage of fluid and proteins from blood vessels to the interstitial space, multiorgan failure, and eventually death if high cytokine concentrations are not reduced.”
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