Inh2-B1 serves as a therapeutically important “antibiotic-resistance-breaker,” which enhances the bactericidal activity of Ceftriaxone/Cefotaxime against highly pathogenic MDRSA infection.
Highly pathogenic and multidrug-resistant Staphylococcus aureus (MDRSA) encompasses methicillin-resistant strains of S. aureus that have developed resistance to multiple traditional antibiotics. Because of the recent emergence of antimicrobial resistance, MDRSA has been commonly incriminated in a variety of invasive infections of the bloodstream and surgical site at a much higher frequency.
The use of antibiotics in food has also resulted in faster mutations of S. aureus, exacerbating this burgeoning issue. Additionally, both small and large companion and livestock populations have been problematic for both the animals as well as immuno-deficient humans in contact with them.
Given the lag in development of newer antibiotics, emerging multidrug-resistant traits in the bacterial strains warrants a more urgent need to identify new agents for effective treatment of MDRSA infections. Recent findings suggest that S. aureus serine/threonine kinase STK1 may serve as a target for the development of a novel targeted therapeutic that permits physicians to use on the market antibiotics to treat antibitotic-resistant bacterial and disrupt MDRSA biofilms.
Researchers at The Ohio State University, led by Dr. Vijay Pancholi, have discovered novel small molecule quinazoline derivatives (Inh2-B1) that can be combined with cephalosporins such as Ceftriaxone (CFTX) and Cefotaxime (CFT) to inhibit MDRSA infection. Inh2-B1 inhibits the kinase activity by directly binding to the catalytic domain of Ser/Thr protein kinase (STK1). Inh2-B1 causes none to minimal cell-dependent toxicity to human cells and enhances the bactericidal activity of Ceftriaxone and Cefotaxime antibiotics against MDRSA both in vitro and in vivo. Inh2-B1 also disrupts MDRSA biofilms. Thus, combination therapy utilizing Inh2-B1 as an “antibiotic-resistance breaker” with Ceftriaxone/Cefotaxime results in a more effective treatment against MDRSA infections by disrupting biofilm and by augmenting the bactericidal activity of cephalosporins.
- Pharmaceutical development
- Drug-resistant disease treatment methodology
- New treatments for MDRSA
- MDRSA growth inhibited
- Minimal toxicity to normal cells
- Disrupts MDRSA biofilm formation
- Enhances efficiency of common antibiotic agents
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