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Due to the inability of immune system to identify certain proteins as self-antigens, rheumatoid arthritis (RA), a chronic, inflammatory, and autoimmune disorder that predominantly affects the joints, causes inflammation in the afflicted body parts. Both hereditary and environmental variables converge to cause RA. Anti-angiogenesis likely serves as a treatment approach as it is crucial to the maintenance of synovitis in RA. sFlt-1 is an angiogenic factor which functions by interacting with VEGF cytokines to compete with VEGF receptor to bind VEGF in order to obstruct cell signaling and hence halt angiogenesis. The absence of the transmembrane and cytoplasmic domains of sFlt-1, an alternatively spliced version of the VEGF receptor-1, ensures that binding will not cause inflammation. Decreased production of new blood vessels results in less joint inflammation and pannus development. That is what the therapy aims to treat so sFlt-1 is appropriate for use in anti-angiogenic therapy. In addition to the pathogenesis of the RA and the workings mechanism of sFlt-1, this article also mentions the detailed manufacturing process of sFlt-1: vector selected with specific HaloTag® tag, transformation by heat shock, transfection in A549 cells, extraction from culture and purification through HaloTag® protein purification and SEC method. Although the entire production process seems seamless, it can become very challenging in practice. Although challenging, the circumstances in which the biological reagents are maintained and cultured cells must be tightly managed. Besides, other social, ethical and economic concerns should also be taken into account. The system used specifically is the vesicular drug delivery system. Additionally, difficult therapeutic testing of sFLit-1is inevitable. sFlt-1 is still of significant research interest and has the potential to develop into a novel commercial treatment, even though there is not enough experimental evidence to demonstrate how successful it is in treating RA as a disease.
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