The thread title is part of a quote from the following paper (which was found by other HC users) and relates to the Hepatitis C virus:
https://www.biorxiv.org/content/10.1101/374793v3.full
The latest version of the paper was updated as of October 7, 2019.
The authors of the paper include scientists from:
- the University of Leeds in the UK
- the National Yang-Ming University, Taipei, Taiwan
- the University of Nottingham, Queen’s Medical Centre in the UK
- University of Minnesota Twin Cities in the US
The full quote is as follows (my emphasis):
“Finally, we compared JK3/32 with an amiloride derivative that has been progressed into early phase human trials in Asia. BIT225 was identified as an inhibitor of genotype 1a p7 using a bacterial screen and has been reported to display activity versus Bovine viral diarrhoea virus (BVDV) (36), and more recently HCV in cell culture (37). However, in our hands BIT225 showed no antiviral activity discernible from effects upon cellular viability (Fig S5); notably, no assessment of cellular toxicity was undertaken during previously reported HCV studies (37), which used a concentration higher (30 μM) than the observed Huh7 CC50 herein (18.6 μM) during short timescale assays (6-24 h).”
Given that Biotron spent over 15 years continually raising capital from investors (including me) based in part on their Hepatitis C program, I think investors have a right to an explanation for the findings outlined in this paper.
If Biotron is confident in their science, then an explanation should be quite easy to provide and they should have no qualms in doing so.
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- “…BIT225 showed no antiviral activity…”
“…BIT225 showed no antiviral activity…”
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