Objective: To investigate the inhibitory effect of rapamycin on growth of pancreatic cancer in vivo, as well as its influence on cell derived factor 1α (SDF-1α). Methods: Twenty nude mice, after pancreatic injection of pancreatic cancer SW1990 cells, were equally randomized into experimental group and control group. Mice in experimental group underwent daily intraperitoneal injection of rapamycin (1.5 mg/kg), and those in control group were given the vehicle of the same volume instead in the same fashion. The tumors were harvested 3 weeks later, the growth of the tumor between the two groups were compared, immunohistochemistry was performed to detect the infiltration of monoclemacrophages and tumor-associated macrophages (TAMs) and the expression of p-mTOR, HIF-1α and SDF-1α in the tumor tissues, and Western blot and qRT-PCR were also performed to determine the mRNA and protein expression of p-mTOR, HIF-1α and SDF-1α in the tumor tissues. Results: In experimental group compared with control group, both tumor weight (0.3340 g vs. 1.7790 g) and volume (0.2375 mm3 vs. 1.2662 mm3) were significantly reduced (both P<0.05). Results of immunohistochemical staining showed that in experimental group versus control group, the count of monocyte-macrophages and TAMs was significantly lowered (both P<0.05), the expression rates of p-mTOR, HIF-1α and SDF-1α were all significantly decreased (all P<0.05), and there was a positive correlation between score of the SDF-1α expression score and TAM count in the tumor tissue (r=0.52, P<0.05). Results of Western blot and qRT-PCR showed that both protein and mRNA expressions of p-mTOR, HIF-1α and SDF-1α in experimental group were lower than those in control group, and except for the HIF-1α mRNA (P>0.05), all differences had statistical difference (all P>0.05). Conclusion: Rapamycin can suppress growth of pancreatic cancer in vivo, and the mechanism is probably associated with its inhibiting the activity of mTOR pathway which thereby down-regulates SDF-1α expression, and then reduces TAMs within the tumor microenvironment.