Old news but still a nice read for a Sunday night.
VRSA treatment
CytoGenix
CytoGentix announces the results of a pre-clinical proof-of-concept study demonstrating that its antimicrobial compound CY401 is active against Vancomycin-resistant Staphylococcus aureus (VRSA). This laboratory study demonstrated that CytoGenix CY401 inhibits growth of VRSA, bacteria that are resistant to approved doses of all antibiotic products.
The National Institute of Allergy and Infectious Diseases (NIAID) reports, "In bacteria, antibiotic resistance evolves by mutations in their genes, by rearrangement of their genes, or by acquiring genes that provide antibiotic resistance from other bacteria. The strains of Staphylococcus aureus (SA) bacteria that have intermediate resistance to Vancomycin appear to be the result of mutations in their genes. However, scientists are concerned that SA might also acquire genes for full Vancomycin resistance from other bacteria, specifically, Vancomycin-resistant Enterococci (VRE).
As more and more strains of disease-causing bacteria become resistant to commonly used antibiotics, physicians must switch to other, often more expensive drugs. For example, switching from the penicillin to methicillin in the treatment of Staphylococcus aureus (SA) infections increased treatment costs about 10-fold.
It is difficult to assess the overall cost of antibiotic resistance. A report from the Government Accounting Office indicates that no federal agency adequately monitors antibiotic resistance or evaluates its social and financial costs. One estimate, however, places the annual cost of antibiotic resistance as high as $5 billion per year."
Dr. Malcolm Skolnick, CytoGenix president and CEO, commented, "We believe that the CY401 compound is highly effective against a wide range of human pathogenic bacteria strains including the most resistant. Results achieved to date support this premise. Planned additional experiments will further demonstrate that this compound effectively addresses a significant unmet medical need
