Objective To explore the efficacy and mechanism of a new monoclonal antibody (ranibizumab) to inhibit the hemangioma of the subcutaneous connective tissue of nude mice, and to study the optimal ratio of drug use. Methods The animal experiment model was successfully set up by hemangioma cells injections. According to the corresponding use without medication, injection of 0.25, 0.50 and 0.75 mg/cm3 ranibizumab, 1 mg/cm3 pingyangmycin, 0.75 mg/cm3 ranibizumab + 10 ng/cm3 insulin-like growth factors-1 (IGF-1), 0.75 mg/cm3 ranibizumab + 30 ng/cm3 propylene glycol monomethyl ether acetate (PMA), divided into group A (basis control group), group B, C, D, group E (drug control group), group F (rezumumab+ IGF-1) and group G (rezumumab+ PMA). Using histocytological and molecular biological detection methods to verify the efficacy and mechanism. Results After 2 weeks of treatment, the volume of hemangioma was reduced [group A: (171.76±52.46) mm3, B: (70.85±8.73) mm3, C: (69.84±16.33) mm3, D: (41.83±18.65) mm3, E: (61.52±8.12) mm3, F: (103.41±19.33) mm3 and G group: (101.19±57.51) mm3,P=0.001]. The expression of CD34 and Ki-67 in nude mice was significantly decreased. Except ranibizumab with IGF-1 group, lung injuries appeared in all others drug treatment groups, while of ranibizumab treatment groups were lighter than pingyangmycin group. Ranibizumab significantly inhibited the expression of vascular endothelial growth factor A (VEGF-A) protein in nude mice, leading to tissue cell apoptosis. The use of ranibizumab with IGF-1 can maintain phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) signaling pathway, so that can protect lung tissue cells. Conclusion The expression of VEGF-A protein in tumor tissue was inhibited by ranibizumab by blocking the PI3K/Akt signaling pathway, leading to the proliferation of hemangioma cells. While, ranibizumab combined with IGF-1 can reduce the lung damage. Key words: Hemangioma; Vascular endothelial growth factor; Ranibizumab; Insulin-like growth factors-1