Work stemming from Biomedcode’s Board of Directors in 1991 validated TNF as a target for the treatment of Rheumatoid Arthritis (Keffer et al. 1991). Today, anti-TNF biologics constitute a multi-billion market as they have proven to be a great success in the clinical treatment of inflammatory conditions. 

Additional research work from Biomedcode’s Board of  Directors has shown that uncoupling the TNFR1-mediated pro-inflammatory effects of TNF from its TNFR2-mediated immunosuppressive propertieswould be an advantageous approach for the treatment of inflammatory diseases (Kassiotis and Kollias, 2001).

For efficacy evaluation of anti-human TNFR1 therapeutics Biomedcode offers a unique humanized TNFR1 mouse model where the human TNFR1 has functionally replaced the mouse counterpart. This unique proprietary mouse is successfully used by the pharmaceutical industry for the efficient evaluation of anti-human TNFR1 therapeutics in disease models of Arthritis, Multiple Sclerosis and Inflammatory Bowel Disease.

The hTNFR1KI mice have normal phenotype and can be used in combination to other genetic models (e.g. Tg197hTNFR1KI) or with a variety of induced disease models in order to test the efficacy of anti-human TNFR1 therapeutics.

Bibliography

1.  Keffer J., Probert L., Cazlaris H., Georgopoulos S., Kaslaris E., Kioussis D., Kollias G., 1991, "Transgenic mice expressing human tumour necrosis factor: a predictive genetic model of arthritis", EMBO J., 10, 4025-4031.

2. Kassiotis G, Kollias G. 2001 "Uncoupling the proinflammatory from the immunosuppressive properties of tumor necrosis factor (TNF) at the p55 TNF receptor level: implications for pathogenesis and therapy of autoimmune demyelination", J Exp Med. 193, 427-34.