Synovium Targeting Delivery of TNFα Blocker for Rheumatoid Arthritis Therapy - A Mini Review

Riyona Desvy Pratiwi ,Muhammad Novrizal Abdi Sahid

doi:10.7324/japs.2018.81021

Abstract

Tumor necrosis factor α (TNFα) blockers are proven as potential suppressing agents on rheumatoid arthritis. Not only showing significant effects in clinical treatment, yet they are also known as top largest selling among the biological agents. However, several systemic side effects are shown after treatments with TNFα blockers which are related to infection and cancer. In order to reduce and overcome the side effects, a targeted delivery is then requested. Synovial membrane is considered as a promising delivery target because TNFα is highly accumulated therein. The current article reviewed a number of strategies that might be applied in the synovial membrane targeting for TNFα blocker.

Highlights

Tumor necrosis factor α (TNFα) blocker as a biological drug is recommended for patients with moderate and severe Rheumatoid arthritis (RA) when DMARD
Conclusion and future perspective TNFα blockers are known as strong inhibitors for inflammation diseases, like RA, but they might cause a systematic side effect
The systematic side effect of TNFα blockers can be reduced by specific delivery to a certain target

Summary

INTRODUCTION

Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation of synovial joints leading to cartilage destruction and bone erosion (Belluci et al, 2016; Chaudari et al, 2016). An anti-PDPN is considered in PDPN neutralization, but on the other hand, it can be fused with other RA therapy agents, such TNFα blocker, for the sake of a specific delivery Visfatin, another RA biomarker, is demonstrated as a potential therapeutic target. In mouse models and patients with RA, serum and synovial tissue level of visfatin were found to be significantly higher than in normal population (Busso et al, 2008; Mirfeizi et al, 2014; Lee et al, 2017) It induced secretion of pro-inflammatory cytokines and assumed to be facilitating joint damage via MMP secretion (Bao et al, 2009). Finding out the capacity of visfatin in the synovial tissue so as to accumulate anti-visfatin or other RA drugs in the local joint still requires more studies (Bao et al, 2009)

Conclusion and future perspective

Findings

CONFLICT OF INTEREST