Fig. 6 Autophagy inhibitors signi fi cantly enhanced anti-cancer ef fi cacy of TNP-1-mediated PTT in the 4T1 model. a, b The body weight ( a ) and tumor volume ( b ) changes of mice in the various treatment groups during the 15-day therapeutic period. Dosing used: TNP-1 or TNP-2, 1.5 mg kg − 1 ; CQ, 25 mg kg − 1 ; 3-MA, 100 μ mol kg − 1 . Mean ± s.e.m. n = 5. *** p < 0.001. Student ’ s t -test. c Photographs of the tumors excised on day 15. d Tumor weight of mice on day 15 in the various treatment groups. Mean ± s.e.m. n = 5. ** p < 0.01, *** p < 0.001. Student ’ s t -test. e Tumor weight of mice in the various treatment groups after a 7-day PTT treatment regimen in a different study. Mean ± s.e.m. n = 6. *** p < 0.001. Student ’ s t -test. f TUNEL staining (red) of sections from tumor in ( e ) was performed to show apoptotic cells. Nucleus were stained with DAPI (blue). Scale bar, 50 μ treatment regimen, the tumors were harvested and photographed either TNP-2 or TNP-1. In contrast, dramatically reduced tumor (Supplementary Fig 20). Dox was ineffective in this drug-resistant size was observed with the combination of TNP-1, NIR and 3- tumor model, with the mice exhibiting similar size as the control MA, with the tumor weight decreased by 93% as compared to the groups (PBS + NIR and 3-MA + NIR). PTT treatments control group (PBS + NIR). In comparison, only 64% decrease in (TNP-2 + NIR and TNP-1 + NIR) signi fi cantly reduced tumor tumor weight was observed for the combination of TNP-2, NIR weight, with no statistical difference between the two PTT groups and 3-MA. The TUNEL assay revealed the number of apoptotic (Fig. 7f). Adding Dox did not further enhance PTT ef fi cacy for cells in opposite correlation with the tumor volume, with the