The most significant previous example of SL biosynthesis inhibition as a drug target was reported in fungi. Aureobasidin A (AbA), a depsipeptide, was first reported by Ikai et al. (1991) and soon after its antifungal properties were highlighted (Takesako et al. 1993). The target gene was further characterized (Hashidaokado et al. 1995) revealing its identity to be the IPC synthase (AUR1p). AbA is a specific and potent (low nanomolar) inhibitor of the fungal IPC synthase. This ushered in a new era in the search for anti-fungal chemotherapeutics, positioning IPC synthase as a promising, broad spectrum, anti-fungal drug target (Sugimoto et al. 2004). Other specific inhibitors were later added to the arsenal of fungal IPC synthase inhibitors: khafrefungin (Mandala et al. 1997), rustmicin (Harris et al. 1998; Mandala et al. 1998) and others (Ohnuki et al. 2009). Unfortunately, further development of these inhibitors stalled, either due to physical properties, e.g. aureobasidin A is very sparingly soluble in water (Georgopapadakou, 2000; Sugimoto et al. 2004), or because their highly complex chemical structures rendered chemical synthesis challenging, with the few synthetic efforts reported resulting in compounds with either reduced or no activity (Sugimoto et al. 2004; Aeed et al. 2009). However, recent works have highlighted that semi-synthetic strategies may overcome these barriers (Wuts et al. 2015).