Bioxytran has reported positive results from its completed phase 2 trial of ProLectin‑M, showing rapid and sustained viral clearance in subjects with laboratory‑confirmed acute viral infection. The company said the study demonstrated complete elimination of viral load in all treated patients by day seven, compared with placebo.
The randomized, double‑blind, placebo‑controlled, dose‑optimisation study enrolled 38 subjects, all of whom completed the seven‑day treatment period. Participants received one of three dose levels of orally administered ProLectin‑M or a matching placebo. Viral shedding was assessed using RT‑PCR analysis of nasopharyngeal swabs, with clearance defined as non‑detection of viral RNA.
According to Bioxytran, the trial confirmed and expanded on findings from an earlier phase 2 study, which had shown statistically significant reductions in viral load by day seven, early clearance as soon as day three and no viral rebounds during a 14‑day post‑treatment observation period. The latest trial refined dose selection to four tablets per day and evaluated the reproducibility of rapid viral clearance.
Following database lock and unblinding, Bioxytran reported complete elimination of viral load in 100% of treated subjects by day 7, with no viral rebounds observed during the 14‑day follow‑up. Across the full study population, one subject showed non‑detection by day three, 16 by day five and all 38 by day seven.
Dr Leslie Ajayi, Chief Medical Officer of Bioxytran, said: “The study design of seven days reflects real-world applications for treating acute viral diseases, with the objective of demonstrating a statistically meaningful reduction in viral load by day seven. The results demonstrate that viral clearance occurred more rapidly than anticipated, with a significant proportion of treated subjects achieving viral non-detection by day three and complete clearance by day seven.”
Dr Platt added: “What continues to distinguish ProLectin-M as a broad-range antiviral drug is its novel mechanism of action. Rather than targeting viral replication inside the cell, our galectin antagonist is designed to interfere with viral entry at the cell surface.”
