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BIT036 as an anitirul for COVID-19

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    Biotron’s Compound BIT036 as an antiviral for COVID-19

    Biotron’s expertise is to do with viroporin proteins, which create “gateways” – ion channels - in cell membranes that allow viruses to cross cell membranes, resulting in increased host infection. Biotron was first to demonstrate that the E Protein within SARS is a viroporin, and has since developed compounds that inhibit viroporin activity.

    Since Biotron’s initial work with SARS and their unique discovery of the E protein and ion channel relationship, they have gone on to develop compounds effective against other RNA viruses, most notably their main HIV drug candidate, BIT225.

    Very recently (26/12/2019), Biotron had a US Patent published regarding their compound technology. Furthermore, since the recent outbreak of SARS-CoV-2, they have begun testing their compounds against the new corona virus in conjunction with the Peter Doherty Institute, who cloned the new virus from an infected person in Australia.

    All corona viruses have four essential proteins: S; M; N; and E that make up the majority of the virus particle.

    SARS-CoV-2 and the original SARS virus (2013) share 94.7% of their respective E Protein genome, as seen in the table below.


    https://hotcopper.com.au/data/attachments/2028/2028802-59404c2b8e09f01f1da399b5748aef25.jpg

    https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.mdpi.com/1999-4915/12/3/254/pdf&ved=2ahUKEwjX14mH5oXoAhXWgUsFHUg5BdsQFjAJegQIAhAB&usg=AOvVaw1dU3e2hIyhmNCks61LhF-L&cshid=1583495962758

    This is an excellent start for any possibility of Biotron’s compounds being effective against SARS-CoV-2, because having a significant genome similarity between the two closely related viruses, especially within the E Protein, may result in Bioton’s compounds having the same effectiveness on SARS-C0V-2 as it had on SARS. This is critical because it has been demonstrated by many researchers that the coronavirus E Protein is significant in viral replication. https://virologyj.biomedcentral.com/articles/10.1186/s12985-019-1182-0/tables/1.

    From their Patent we can read:
    https://hotcopper.com.au/data/attachments/2028/2028819-c744b152bacdb3a27da2306230ace237.jpg
    Page 18.

    BIT036 isthe compound, Cinnamoylguaginine, and has shown to positively effect ionchannel activity in the original virus that caused SARS.

    https://hotcopper.com.au/data/attachments/2028/2028810-a5c1137279489a8d5b222425769ac7ec.jpg

    http://www.freepatentsonline.com/20190389816.pdf. Page30.

    It is myview, the likelihood of Biotron’s compounds being successful in suppressing or eradicatingCOVID-19 is good to highly likely. This is because genomic research on SARS-CoV-2has shown that the E Protein is only slightly different from that of theoriginal SARS in which Biotron’s compounds, notably, BIT036, has been effectiveon ion channel activity that is essential to viral replication. Most notably,the first amino acids of the E Protein are identical, and these are crucial tothe activity under discussion.

    On a sidenote, Biotron is presenting their latest HIV Phase 2 test results next week inBoston. They have boldly described in past announcements that their main HIVdrug candidate, BIT225, has shown “vaccine-like” results.

    This isbecause their results on the ion channels prevents viral replication, which ofcourse has the same final result of vaccines, although by a different method.

    With regardto SARS-CoV-19, readers will be aware that the S – spike - protein is thetarget of vaccine research. This is because it causes the virus to latch and penetrateinto host cells, and vaccines will prevent this from occurring by creating a proper immunological response.

    Biotron’s compoundsas antivirals act differently by preventing viral replication from the EProtein. Whether or not their technology is adapted to vaccine development, ispresently unknown, or at least not public.

    But regardless, I’ve placed my trade on theirtechnology becoming a successful antiviral in the near term.
 
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