From Sun Tzu The Art of War: If you know the enemy and you know yourself, you need not fear the result of a hundred battles.
The following is my interpretation of Dr DeGrado's engagement with the University of Arizona research team and why the pre-print Brilacidin, a COVID-19 Drug Candidate, demonstrates broad-spectrum antiviral activity against human coronaviruses OC43, 229E and NL63 through targeting both the virus and the host cell is important, positive news.
In August Jun Wang published Targeting Viral Proteins and Host Factors for Discovery and Development of Antivirals Against Influenza, Enterovirus, and Coronavirus (full text: https://repository.arizona.edu/handle/10150/6...show=full) In this paper Jun Wang described the observed inhibitory action of heparin on the efficacy of Brilacidin. I theorize that upon reading Wang's findings Dr DeGrado engaged with Jun Wang and others at UoA to fully investigate the finding. What Dr DeGrado and his co-authors discovered was that heparin does indeed inhibit Brilacidin's ability to limit SARS-COV-2 replication . The beauty of the confirmation is in the WHY .
Heparin prevents Brilacidin binding to Host cells. It is the binding of Brilacidin to host cells that prevents viral attachment to host cells. It is the binding and blocking of viral attachment that is Brilacidin's second antiviral MOA.
Jun Wang's observation enabled Dr. DeGrado and UoA researchers to reveal and demonstrate an additional antiviral MOA of Brilacidin . This is a huge discovery. Do not mistake the discovery that Brilacidin efficacy is inhibited by heparin for bad news. The discovery validates a powerful antiviral MOA and describes an important counter-productive drug synergy.
It is never to your disadvantage to have learned more about how to combat your enemy. Innovation Pharmaceuticals just announced that they have a greater understanding of how Brilacidin defeats a virus.
From Sun Tzu The Art of War: If you know the enemy and you know yourself, you need not fear the result of a hundred battles.
From Brilacidin, a COVID-19 Drug Candidate, demonstrates broad-spectrum antiviral activity against human coronaviruses OC43, 229E and NL63 through targeting both the virus and the host cell : Our findings include: 1) Brilacidin has broad-spectrum antiviral activity against HCoV-OC43, HCoV-NL63, and HCoV-229E viruses in cell culture; 2) Brilacidin inhibits SARS-CoV-2 pseudovirus entry into multiple cell lines, indicating that the inhibition is not cell type dependent *; 3) Brilacidin has dual antiviral mechanisms of action which involves* targeting both the virus and the host cell. Brilacidin has virucidal
activity and blocks viral attachment to host cells by binding to HSPGs*; 4) Brilacidin has strong synergistic antiviral effect with the FDA-approved SARS-CoV-2 antiviral*
(Full text: https://www.biorxiv.org/content/10.1101/2021.11.04.467344v1
The following is my interpretation of Dr DeGrado's engagement with the University of Arizona research team and why the pre-print Brilacidin, a COVID-19 Drug Candidate, demonstrates broad-spectrum antiviral activity against human coronaviruses OC43, 229E and NL63 through targeting both the virus and the host cell is important, positive news.
In August Jun Wang published Targeting Viral Proteins and Host Factors for Discovery and Development of Antivirals Against Influenza, Enterovirus, and Coronavirus (full text: https://repository.arizona.edu/handle/10150/6...show=full) In this paper Jun Wang described the observed inhibitory action of heparin on the efficacy of Brilacidin. I theorize that upon reading Wang's findings Dr DeGrado engaged with Jun Wang and others at UoA to fully investigate the finding. What Dr DeGrado and his co-authors discovered was that heparin does indeed inhibit Brilacidin's ability to limit SARS-COV-2 replication . The beauty of the confirmation is in the WHY .
Heparin prevents Brilacidin binding to Host cells. It is the binding of Brilacidin to host cells that prevents viral attachment to host cells. It is the binding and blocking of viral attachment that is Brilacidin's second antiviral MOA.
Jun Wang's observation enabled Dr. DeGrado and UoA researchers to reveal and demonstrate an additional antiviral MOA of Brilacidin . This is a huge discovery. Do not mistake the discovery that Brilacidin efficacy is inhibited by heparin for bad news. The discovery validates a powerful antiviral MOA and describes an important counter-productive drug synergy.
It is never to your disadvantage to have learned more about how to combat your enemy. Innovation Pharmaceuticals just announced that they have a greater understanding of how Brilacidin defeats a virus.
From Sun Tzu The Art of War: If you know the enemy and you know yourself, you need not fear the result of a hundred battles.
From Brilacidin, a COVID-19 Drug Candidate, demonstrates broad-spectrum antiviral activity against human coronaviruses OC43, 229E and NL63 through targeting both the virus and the host cell : Our findings include: 1) Brilacidin has broad-spectrum antiviral activity against HCoV-OC43, HCoV-NL63, and HCoV-229E viruses in cell culture; 2) Brilacidin inhibits SARS-CoV-2 pseudovirus entry into multiple cell lines, indicating that the inhibition is not cell type dependent *; 3) Brilacidin has dual antiviral mechanisms of action which involves* targeting both the virus and the host cell. Brilacidin has virucidal
activity and blocks viral attachment to host cells by binding to HSPGs*; 4) Brilacidin has strong synergistic antiviral effect with the FDA-approved SARS-CoV-2 antiviral*
(Full text: https://www.biorxiv.org/content/10.1101/2021.11.04.467344v1
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