The content: Leronlimab, a CCR5-blocking monocl
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Posted On: 03/27/2022 7:53:34 AM
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Leronlimab, a CCR5-blocking monoclonal antibody, binds to the external domains of CCR5 and through a competitive mechanism prevents HIV and SIV from binding to the CCR5 coreceptor, entering the cell and replication (199, 200). Beside the CCR5 masking from SIV/HIV, leronlimab CCR5 binding does not downregulate CCR5 expression or deplete CCR5-expressing cells (199), but prevents CCL-5-induced activation and migration of inflammatory CCR5-expressing monocytes and T lymphocytes along a chemical gradient (199). In this context, leronlimab appears a an excellent prospect for treatment of diseases, in which the CCL5-CCR5 pathway is involved in the pathogenesis. Given the role of CCR5 in immune cell migration and inflammation, CCR5 blockade with leronlimab was applied in critical COVID-19 patients, and led to the reduction of the IL-6 levels, restoration of CD4/CD8 ratio, and resolution of SARS-CoV-2 burden, thus implicating CCR5 as a potential therapeutic target for COVID-19 (201).
Leronlimab, a CCR5-blocking monoclonal antibody, binds to the external domains of CCR5 and through a competitive mechanism prevents HIV and SIV from binding to the CCR5 coreceptor, entering the cell and replication (199, 200). Beside the CCR5 masking from SIV/HIV, leronlimab CCR5 binding does not downregulate CCR5 expression or deplete CCR5-expressing cells (199), but prevents CCL-5-induced activation and migration of inflammatory CCR5-expressing monocytes and T lymphocytes along a chemical gradient (199). In this context, leronlimab appears a an excellent prospect for treatment of diseases, in which the CCL5-CCR5 pathway is involved in the pathogenesis. Given the role of CCR5 in immune cell migration and inflammation, CCR5 blockade with leronlimab was applied in critical COVID-19 patients, and led to the reduction of the IL-6 levels, restoration of CD4/CD8 ratio, and resolution of SARS-CoV-2 burden, thus implicating CCR5 as a potential therapeutic target for COVID-19 (201).
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