Targeting tie-2 receptor with rebastinib (DCC-2036) for angiogenesis Inhibition in early-stage arthritis : enhanced efficacy through liposomal sustained release.

The prevalence of arthritis continues to increase, which has driven research on new therapeutic approaches. However, existing treatments often have limitations. Angiogenesis and pathological changes in the synovium are the key contributors to the early development of arthritis. Rebastinib, a tie-2 receptor inhibitor, blocks the activation of tie2-expressing macrophages, which are involved in angiogenesis. Although previous studies have highlighted the importance of angiogenesis in early arthritis, few have focused on targeting the tie-2 receptor to slow disease progression. In this study, we evaluated the effects of rebastinib encapsulated in pH-dependent liposomes in a rabbit model of surgically induced arthritis. Additionally, we investigated the efficacy of a pH-dependent liposomal formulation, developed using microfluidic technology for sustained drug release. The results demonstrated that rebastinib-loaded pH-dependent liposomes were stable and provided controlled release and rebastinib effectively inhibited the progression of early stage arthritis in this model. Statistical analyses were performed using SPSS software (IBM Corp., Armonk, NY, USA), and significance was assessed using one-way ANOVA. In conclusion, rebastinib encapsulated in pH-dependent liposomes holds promise as a potential therapeutic strategy for the treatment of early arthritis, offering both stability and efficacy in disease suppression.