Hyundai Bioscience announced on Thursday that its U.S. subsidiary, Hyundai Bio USA, has proposed to the World Health Organization (WHO) and local health authorities to provide their broad-spectrum antiviral candidate XAFTY (CP-COV03) free of charge to patients in Ebola-affected countries.
This proposal came in response to a suggestion from Professor David Smith in San Diego, who recommended the urgent deployment of XAFTY to combat the spread of Ebola.
If requested by the WHO and health authorities in affected countries, Hyundai Bio USA plans to offer its stored clinical supplies of XAFTY at no cost. The company is also prepared to cover expenses for local clinical trials if necessary.
According to Hyundai Bio, XAFTY has demonstrated safety through COVID-19 clinical trials in South Korea. In cell experiments, it showed inhibitory efficacy (IC50) against the Ebola virus at lower concentrations compared to those required for the COVID-19 virus.
Bae Byung-jun, Chief Executive Officer (CEO) of Hyundai Bioscience , stated that it believes XAFTY could be a significant treatment candidate for high-risk infectious diseases like Ebola. It hopes the WHO and global health authorities will conduct swift scientific reviews and make timely decisions.
Kim Taek-sung, representative of Hyundai Bio USA, emphasized that it can’t afford to miss treatment opportunities for high-mortality diseases like Ebola due to procedural or cost barriers. The decision to provide the drug for free and fund clinical trials themselves is driven by the urgency to save lives. The rapid spread of mutant viruses presents a critical and time-sensitive crisis that demands this action.
In related news, Hyundai Bioscience ‘s cancer treatment candidate, Phenitrium, began its first clinical trial involving cancer patients at Seoul National University Hospital on June 5.
The Phase 1 trial, led by Professor Jung Chang-wook from the Department of Urology at Seoul National University Hospital, aims to assess Phenitrium’s safety in humans and, for the first time, confirm its mechanism for normalizing the tumor microenvironment.
