ANTIVIRAL DRUGS

We develop Proprietary Antiviral Drugs

COVID-19 Treatment

  • On May 22, 2020, we filed a patent application in the United States for a new treatment for Coronavirus infections. Our patent application covers composition subject matter pertaining to small molecules for inhibition of Coronavirus protease. The treatment is anticipated to be in a tablet form which can be taken at home.

  • In August 2020, we completed the synthesis of four different potential inhibitors of Coronavirus protease. These compounds are based on the technology described in our patent application filed on May 22, 2020.

  • In September 2020, we completed the screening of our four compounds and subsequently identified a lead Anti-Coronavirus drug candidate (SBFM-PL4).  The screening which pinpointed the lead compound was performed at the University of Georgia, College of Pharmacy under the leadership of Dr. Scott D. Pegan, Director of the Center for Drug Discovery and Interim Associate Head of Pharmaceutical and Biomedical Sciences.

  • In October 2020, we expanded our collaboration with Dr. Scott Pegan by entering into a research agreement with the University of Georgia to further develop our Anti-Coronavirus lead compound, SBFM-PL4. 

  • On February 1, 2021, we entered into an exclusive license agreement with the University of Georgia for two Anti-Coronavirus compounds which the University of Georgia had previously developed and patented.

  • Currently, we are advancing the development of these two compounds in parallel with our SBFM-PL4 by conducting a transgenic mice study in collaboration with the University of Georgia. The mice being used in the study have been genetically engineered to express the human angiotensin-converting enzyme 2 (hACE2) transmembrane protein in their lungs making them susceptible to lethal infection by SARS-CoV-2, the causative agent of COVID-19. The SARSCoV-2 virus uses the hACE2 receptor to gain entry into human cells to replicate. The goal of the study is to determine if our protease inhibitors will protect the hACE2-transgenic mice from disease progression and death following infection with SARS-CoV-2 virus. Should these mice studies prove successful, we plan to submit the results to the FDA for authorization to conduct testing on actual COVID-19 patient volunteers in a Phase I clinical trial setting. The implications of a COVID-19 treatment becoming available are vast. This is particularly the case in view of the fact that some of the variants emerging around the world are more virulent and may escape neutralization by the current vaccines.

Coronavirus, a highly aggressive pathogen!

Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) is the causative agent of COVID-19, the current ongoing pandemic that has claimed the lives of over 2.8 million people worldwide since it first appeared in December 2019. SARS-CoV-2 is a Betacoronaviruses, one of four genera of Coronaviruses belonging to the family, Coronaviridae.  The remaining three genera are Alpha, Gamma and Delta Coronavirus.  Gamma and Delta Coronaviruses do not infect humans while the Alphacoronaviruses are responsible for approximately 30% of the annual common cold cases.

The Betacoronaviruses are comprised of three highly virulent starins including: (i) SARS-CoV which appeared in 2002 having an associated mortality rate of 10 to 15 percent, (ii) MERS-CoV which came on the seen in 2015 wielding a case-fatality rate of 34 to 37 percent, and (iii) SARS-CoV-2, the causative agent of the current pandemic (COVID-19) with a mortality rate of 3 to 5 percent.

In addition to the main protease (Mpro), which is shared among coronaviruses, Betacoronaviruses have a second virus-encoded protease called papain-like protease (PLpro).  These two proteases are responsible for cleaving the initial expression products of the viral genome (polyproteins 1a and 1ab) at 15 different sites to produce 16 different mature virus proteins essential for viral replication.  While Mpro cleaves the viral polyproteins 1a and 1ab at 12 different locations, PLpro cleaves polyprotein 1a at only 3 sites.  PLpro, however, is also involved in cleaving certain host proteins (various ubiquitinated proteins and ISG15), resulting in suppression of the host’s innate immune response.  It is believed that PLpro is responsible for the enhanced pathogenicity of Betacoronaviruses.  Our COVID-19 Treatment is an inhibitor of PLpro.