Because there already are too many drug-resistant infections to show superiority

Because they do not really have clear advantages over current treatments

Because there are not enough drug-resistant infections yet to prove superiority

Because it is easier to design a non-inferiority trial

Clindamycin

Linezolid

Chloramphenicol

Cycloserine

Increased antibiotic degradation

Reduced antibiotic uptake

Increased antibiotic efflux

Altered antibiotic target

The acquisition of horizontally acquired resistance genes leads to the production of peptidoglycan with D-Ala-D-Lac terminal residues that are insensitive to vancomycin

The altered expression of intrinsic genes leads to the production of a thicker cell wall that reduces the effectiveness of vancomycin

The acquisition of horizontally acquired resistance genes leads to a reduction in overall peptidoglycan production, which reduces the effectiveness of vancomycin

The altered expression of intrinsic genes leads to the production of peptidoglycan with D-Ala-D-Lac terminal residues that reduce the effectiveness of vancomycin

Avibactam is a suicide inhibitor of β-lactamase enzymes, so it saves the amoxycillin, which is a suicide inhibitor of penicillin binding proteins

Both of these compounds are β-lactams and inhibit penicillin binding proteins, but by binding at different sites, so they act synergistically

Amoxycillin is a β-lactam antibiotic while avibactam is a protein synthesis inhibitor, so they act synergistically

Amoxycillin is a suicide inhibitor of β-lactamase enzymes, so it saves the avibactam which is a suicide inhibitor of penicillin binding protein

The mutation in PmrB would lead to increased activity of the PmrB protein, which in turn increases expression of the phosphoethanolamine transferase PmrA

The mutation in PmrB would inactivate the phosphoethanolamine transferase PmrB, which would result in loss of lipopolysaccharide production

The mutation in PmrB would lead to increased activity of the PmrB protein, which in turn increases expression of the phosphoethanolamine transferase PmrC

The mutation in PmrB would lead to increased expression of the phosphoethanolamine transferase PmrB and production of lipopolysaccharide with reduced negative charge

High chemotherapeutic index, low solubility, low membrane permeability

Low chemotherapeutic index, high solubility, high membrane permeability

Low chemotherapeutic index, low solubility, high membrane permeability

High chemotherapeutic index, high solubility, high membrane permeability

Swap to vancomycin

Use the carbapenem at increased concentration

Use the carbapenem plus an aminoglycoside

Use the carbapenem at the same concentration but add clavulanic acid

PD-1 binds to its ligand PD-1L and leads to T cell activation

PD-1 binds to its ligand CTLA4 and leads to T cell activation

PD-1 binds to its ligand PD-L1 and induces T cell division and expansion

The PD-1/PD-1L interaction leads to downregulation of the PI3-K / m-TOR/ RAS/Ras/MAPK/Erk pathways and T cell exhaustion 

Antibodies in which the majority of the sequence is of human origin except for the complementarity determining regions (CDR), which are mouse sequence

Antibodies in which the entire constant and variable regions are human sequence

Antibodies in which the entire constant and variable regions are mouse sequence

Fab fragments that are entirely of human sequence