Table 1.

Various anti-persister approaches.

Approaches	Mechanisms
Addition of carbon source with antibiotics (Allison et al., 2011; Orman & Brynildsen, 2013; Taber et al., 1987)	Resuscitates persisters and allows cells to increase intake of conventional antibiotics
Addition of efflux pump inhibitors with antibiotics (phenylalanine arginyl β-naphthylamide (PAbN) or 1-(1-Naphthylmethyl) piperazine (NMP) (Pu et al., 2016)	Blocks efflux of conventional antibiotics
Acyldepsipeptide (ADEP 4 (Carney et al., 2014; Conlon et al., 2013; Lee et al., 2010; Li et al., 2010)	Activates ClpP to be a non-specific protease and kills persister cells by uncontrollable protein degradation
Defensins, cathelicidins (Defraine et al., 2018; Mohammad et al., 2015) HT61 (Hu et al., 2010; Hubbard et al., 2017a)	Disrupts bacterial cell membrane in a growth-independent manner
KCN (Respiration inhibitor) (Orman & Brynildsen, 2015)	Impairs stationary phase respiratory activity and prevents self-digestion of endogenous proteins and RNA, which yields bacteria that are more capable of translation, replication and concomitantly cell death when exposed to antibiotics
M64 (MvfR inhibitor) (Allegretta et al., 2017; Starkey et al., 2014; Vieira et al., 2022)	Targets quorum sensing regulator and inhibits persister formation
Relacin (Wexselblatt et al., 2012)	Affects entry into stationary phase in several Gram-positive bacteria, leading reduction in cell survival
Cis-2-decenoic acid (Marques et al., 2014)	Increases metabolic activity and reverts persisters into an antibiotic-susceptible state