Rheumatoid arthritis (RA) is a chronic inflammatory systemic autoimmune disease that has a global distribution with an estimated prevalence of 0.5% to 2%. RA is characterized by symmetric arthritis of arthrodial joints, leading to progressive erosion of cartilage and bone.

Current RA treatment aims at limiting joint damage, preventing loss of function, and decreasing pain. In RA, the transcription factors NF-κB and NFAT have been recognized as important factors in regulating the inflammatory processes and progression of the disease. In vivo studies suggest that IKKβ inhibition, a factor that regulates the activity of NF-κB, is an effective therapeutic approach to treat both inflammation and bone/cartilage destruction of RA.

IB-RA: exerts its anti-inflammatory effects by inhibiting NF-κB binding to DNA and thus reducing IL-2. IB-RA reduce nuclear factor of activated T cell (NFAT)

Target Indication:
Rheumatoid Arthritis

Route of Administration:
Oral and Injectable

Mechanism of Action:
In-vitro research had shown IB-RA to inhibit NFkB and NFAT; reduce IL-2, COX-2 and PGE2; stimulates osteoblasts and calcium deposists.

Clinical Results:
• Human Clinical showed IB-RA to reduce number of swollen joints, total grade of swollen joint and tender joints

• Reduction of rheumatoid factor, CRP Protein, and IgA

• IB-RA inhibits NF-κB and NFAT, important factors in regulating the inflammatory processes and progression of RA.

• IB-RA inhibits COX-2 and reduce PGE2, one of the main mechanisms for the control of inflammation and pain in RA.

• IB-RA decreases Rheumatoid Factor via reduction in TNF-α production

• IB-RA reduces IgA and IgM, which is beneficial as there is positive correlation between the grade of cartilage damage in active RA

• IB-RA inhibits NFAT activity, a transcription factor linked with bone erosion

• IB-RA induces osteoblast mineralization on the bones via COX-2 expression, could be of useful in osteoporosis.