CEN-101: Difference between revisions

=Biofilm Physiology=

According to the CDC, of the estimated annual 2 million hospital-acquired infections in the US, approximately half are due to staph bacteria, including both methicillin-resistant as well as methicillin-sensitive S. aureus and S. epidermidis.

Until a little over one decade ago, bacteria were thought to act only as independent organisms, in a planktonic state. A bioflim is an aggregate of microbes with a distinct architecture. It is a “microscopic city” in which microbial cells bring nutrients, oxygen and other necessities through fluid filled channels to support life within the biofilm community. Bacteria growing within the biofilm are protected from antibiotic exposure and are up to 1,000 times more resistant than bacteria not growing inside a biofilm [1,2]. A growing body of peer reviewed publications supports the approach of attacking biofilm as an effective method to combat staph infections.

It is now well know that staph must have a sufficient population (quorum) to allow them to form biofilms, enabling much improved survival in the host. Molecules involved in quorum sensing (QS) by Staphylococci like S. aureus include RNAIII activating protein (RAP), target of RAP (TRAP) and proteins encoded by the accessory gene regulator locus (agr), which ultimately initiate the expression of a myriad of virulence factors such as proteases, hemolysins and various other toxins [2, 9]

StaphOff developed CEN-101 (also known as RIP or RNAIII Inhibiting Peptide), the first treatment for staph whose mechanism of action IS NOT to kill the bacteria. Rather, it eliminates the ability of these bacteria to form biofilms, to produce toxins and to survive. The molecule is a heptapeptide that can be delivered by a variety of dosing methods: (1) topical, (2) locally injectable, (3) intravenous administration, and (4) in solution as a medical device coating or in sterile locks.