The　binding　between　the　immune　checkpoints,　programmed　cell　death　ligand　1　(PD-L1)　and　programmed　cell　death　1　(PD-1),　compromises　T-cell-mediated　immune　surveillance.　Immune　checkpoint　therapy　using　immune　checkpoint　inhibitors　(ICIs)　to　block　PD-L1　on　cancer　cell　membrane　or　PD-1　on　activated　T　cell　membrane　can　restore　antitumor　function　of　T　cell.　However,　the　intracellular　expression　of　PD-L1　and　its　active　redistribution　to　cancer　cell　membrane　may　impair　the　therapeutic　benefits　of　ICIs.　To　address　this　issue,　herein　we　develop　a　nanodrug　(MS　NPs)　capable　of　reducing　PD-L1　expression　and　enhancing　antitumor　effects.　Methods:　The　nanodrug　was　self-assembled　from　immunoadjuvant　metformin　(Met,　an　old　drug)　and　anticancer　agent　7-ethyl-10-hydroxycamptothecin　(SN38)　via　hydrogen　bonds　and　electrostatic　interactions.　A　series　of　experiments,　including　the　characterization　of　MS　NPs,　the　validation　of　MS　NPs-mediated　down-regulation　of　PD-L1　expression　and　in　vitro　therapeutic　effect,　the　MS　NPs-mediated　in　vivo　chemo-immunotherapy　and　tumor　metastasis　inhibition　were　carried　out.　Results:　Different　from　ICIs　that　conformationally　block　PD-L1　on　cancer　cell　membrane,　MS　NPs　directly　reduced　the　PD-L1　level　via　metformin　to　achieve　immunotherapy.　Therefore,　MS　NPs　showed　enhanced　chemo-immunotherapy　effect　than　its　counterparts.　MS　NPs　were　also　effective　in　inhibiting　tumor　metastasis　by　remodeling　the　extracellular　matrix　and　restoring　immune　surveillance.　Additionally,　no　obvious　toxicity　was　observed　in　major　organs　from　MS　NPs-treated　mice　and　a　high　survival　rate　of　mice　was　obtained　after　MS　NPs　treatment.　Conclusion:　We　have　designed　nanodrug　MS　NPs　by　self-assembly　of　the　immunoadjuvant　Met　and　the　anticancer　agent　SN38　for　combined　immunotherapy　and　chemotherapy.　MS　NPs　might　break　the　deadlock　of　antibody-based　ICIs　in　immunotherapy,　and　repurposing　old　drug　might　provide　a　new　perspective　on　the　development　of　novel　ICIs.