FTDCAG NPs accumulate in tumor tissues through EPR effects, bind specifically to cells overexpressing the folate receptor (FA) to release CA4 to specifically disrupt angiogenesis, then release CA4 through receptor-mediated endocytosis into tumor cells, degraded in a high-GSH and low-pH environment, and rapidly release DOX and CPT for synergistic multidrug therapy. Here, CA4 is linked to neoplasm.