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. 2019 Mar 16;20(6):1332. doi: 10.3390/ijms20061332

Table 2.

Summary of potential targets for RA.

Drug or Compound Target Potential Mechanism Immune-Modulation
Developing inhibitor of miR-155 miR-155 regulatory functions on the expression of genes by modulating the cell transcriptome directly Inhibit TLR/cytokine receptor pathways and suppress the production of TNF, IL-1β, IL-6, and chemokines CCR7
Developing inhibitor of visfatin Visfatin Upregulation of miR-199a-5p expression through modulation of the ERK, p38, and JNK pathways Decrease the production of IL-6 and TNF-α
Developing inhibitor of PI3Kγ PI3Kγ modulation of chemokine-induced migration Control enrollment of inflammatory cells (i.e., neutrophils, monocytes, and macrophages)
andclozapine
tJNJ77777120 (JNJ)
Histamine 4 receptor (H4R) Block H4R in synovial tissue to prevent the destruction cartilage and bone Immune-modulatory effect and repression of chemotaxic potentials by influencing the secretion of MMP-3
the pan HDAC inhibitors: ITF 2357 and SAHA
HDAC6 inhibitors: Tubastatin A, Tubacin, and CKD-L
histone deacetylase (HDAC) repress the production of IL-6 in RA FLS and macrophages by promoting mRNA decay CKD-L increased CTLA-4 expression in Foxp3+ T cells and inhibited the T cells proliferation in the suppression assay. CKD-L significantly increased IL-10, and inhibited TNF-α and IL-1β
a monoclonal antibody against cadherin-11 cadherin-11 Block the reaction of engagement with a recombinant soluble form of the cadherin-11 extracellular binding domain linked to immunoglobulin Fc tail induced MAPK and NF-κB activation in SFL Suppression the production of IL-6, chemokines, and MMP expression in SFL
GnRH-antagonism—cetrorelix LHRH (luteinizing hormone-releasing hormone) rapid anti-inflammatory effects decreased TNF-α, IL-1β, IL-10, and CRP
knock-down model of SOX5 Block the MMP-9 Inhibit high expression of transcription factor SOX5 in RA-FLS repressed IL-17 through interacting with the macrophages
anti-CX3CL1 monoclonal antibody CX3CL1 Block monocyte chemotaxis and angiogenesis Decreased MMP-2
NI-0101, a TLR4 antagonism TLR4 block the HMGB1-dependent upregulation of HIF-1α mRNA expression amend cytokines release including IL1, IL-6, IL-8 and TNF-α.
Hydroxychloroquine (complex formation
of the inflammasome)
TLR overexpression Inflammasome priming mechanism Potential decreased TNF-α
VX 740 Caspace-1 Inhibit CARD8 overexpression Decrease NLRP-3 and dwonstream cytokines