Fig. 1: Stimulator of interferon gene (STING)-activating liposomal vesicles (SAProsomes) for potentiating anticancer immunity.

a, b Rational design of MSA-2–derived STING pro-drugs 1–4 via hydrolytic ester bond for optimization of in vivo liposomal delivery. The pro-drugs were designed to be hydrolyzed by esterase to spontaneously release active MSA-2 in the target cells. Unlike free MSA-2, these pro-drugs can be stably assembled into lipid constituents to form liposomal vesicles. c Schematic illustration of esterase-responsive activation of MSA-2 as a STING-activating molecule followed by antitumor immune stimulation in the tumor-bearing mice. d Drug activation kinetics from pro-drugs 1–4 in the presence or absence of porcine liver esterase (PLE, 50 unit/mL) in phosphate-buffered saline (PBS) at 37 °C. Data are presented as ± s.d. of the mean, n = 3. e, f Extrapolation of pseudo-first-order rate constants from the curves in (e) when the pro-drugs were incubated in PLE-containing PBS. Data are presented as ± s.d. of the mean, n = 3. g Representative transmission electron microscopy (TEM) and Cryo-TEM images of SAProsome-3. Each experiment was independently repeated in triplicates, yielding similar results. h, i Stability of SAProsomes. Particle sizes (h) and polydisperse index (PDI) (i) were monitored via dynamic light scattering analysis over 72 h. Data are presented as ± s.d. of the mean, n = 3. Source data are provided as a Source data file.