Antibiotics vs. Artilysin®

Antibiotics vs. Artilysin®

While classic antibiotics require non-resistant cells, hours to work and only kill cells that are metabolically active, fast-acting Artilysin®s destroy resistant and persistent bacterial cells within minutes.

ANTIBIOTICS ARTILYSIN®S
Resistance Low resistance potential
Damage the microbiome Kill only targeted bacteria
Weaken the immune system No impact on the immune system
Accumulate in the environment Rapidly biodegradable and do not accumulate
Slow-acting Fast-acting
Ineffective against persistent cells Treatment of chronic bacterial infections
Limited activity in biofilm Work in biofilm
Cause numerous side-effects Very limited potential for side-effects
Often toxic Non-toxic

Mechanism of Action

Artilysin® molecules selectively attack the cell wall of bacterial cells leading to cell death caused by high osmotic pressure. β-lactam antibiotics (penicillins, cephalosporins and carbapenems) represent the most important and widely used group of antibiotics. These antibiotics also target the bacterial cell wall. However, they inhibit the assembly of a functional peptidoglycan by specific binding to enzymes of dividing cells.

 

Figure 1: Comparison of the Gram-negative (left) and Gram-positive (right) bacterial cell wall.

The cell wall is composed of a peptidoglycan layer which surrounds the plasma membrane. Additionally, the peptidoglycan of Gram-negative bacteria is covered by an outer membrane mainly consisting of phospholipids and lipopolysaccharides (LPS) which are stabilised by divalent cations like Ca2+ or Mg2+.

Figure 2: Translocation of β-lactam antibiotics (left) and Artilysin®s (right) through the outer membrane of Gram-negative bacteria.

Due to the positive charges and hydrophobic properties of the targeting peptides, Artilysin®s destabilize the outer membrane of Gram-negative bacteria and can reach the peptidoglycan. In the case of Gram-positive bacteria, the peptide moieties of Artilysin®s increase the affinity of the molecules to the bacterial cell wall. In contrast to Artilysin®s, β-lactam antibiotics are translocated through the outer membrane via porins into the periplasmic space.

 

Figure 3: β-lactam antibiotics bind to enzymes involved in cell division. Therefore, they are limited to dividing cells and are prone to resistance development.

Subsequently, β-lactam antibiotics bind to enzymes called peptidoglycan transpeptidases and thus inhibit the crosslinking of peptidoglycan precursors to build the functional cell wall of metabolically active and dividing cells. This leads to the death of the bacteria. Unlike antibiotics, Artilysin®s do not require an active metabolism because they work directly on the cell envelope by combining electrostatic and hydrophobic peptides with a muralytic moiety. Under high osmotic pressure, the inner membrane blebs out and finally the bacterial cell bursts.

 

Figure 4: The unique mode of action enables Artilysin®s to overcome limitations of conventional antimicrobial technologies.

In summary, while classic antibiotics require hours to kill only metabolically active cells that are not resistant to the drug being used, their fast mode of action allows Artilysin®s to kill all bacterial cells within minutes or even seconds

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