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.