Xeophin’s foundational IP is the cornerstone of our business, and central to everything that we do, and we take this very seriously. Our IP has been developed by the Founders Molloy and Neilson, and Xeophin has full worldwide exclusivity to exploit the IP. Along with this, patents are produced by FB Rice, and a full “Freedom to Operate” search has also been undertaken by FB Rice to ensure no unforeseen IP issues will arise, giving us a clear pathway ahead to market exclusivity for up to 32 years
Xeophin is currently undertaking genetic engineering to create a modified version of our XeRA-1 sequence, derived from the Tanapox virus. This therapeutic will be a powerful Anti-TNF agent, acting on both TNF-a and TNFR1/R2, and is highly suitable for the treatment of Rheumatoid Arthritis (RA). This however is step one of an integrated four step plan for the use of XeRA-1, the remaining steps being:
Genetic Engineering – Master the potential of XeRA-1
protein as an immunotherapeutic;
Oligonucleotide Interruption of Immune Response – Forecast and overcome any long-term immunogenic response to XeRA-1
(a problem shared by all current Anti-TNF therapies);
Gene Therapy – Integrate XeRA-1 into the patient’s genome to create permanent, patient mediated TNF management;
Therapeutic Gene Discovery Platform - Therapeutic Gene Discovery Platform – Continue to feed the pipeline with other XeRA-1 like genes
The combination of these four factors will result in ‘Mastery of TNF Modulated Inflammation’ and a sustainable means to dominate the RA mark
our gene therapy approach
Antisense therapy through oligonucleotide interruption
what we’re treating
A debilitating condition…
Rheumatoid arthritis is the most common type of immune mediated inflammatory disease which is triggered by a faulty immune system and mostly affects the wrist and small joints of the hand including the knuckles and the middle joints of the fingers. In this disorder, the body’s immune system, which normally protects the health of the individual, starts attacking foreign substances, like bacteria and viruses and mistakenly it attacks its own joints as well.
In cases where the inflammation goes unchecked, it can damage the cartilage and the elastic tissue that covers the end of bones in a joint as well as the bones themselves. Treatments have improved greatly and help many of those who are affected. For most people inflicted with rheumatoid arthritis, early treatment can control the joint pain and swelling, and lessen joint damage.
About 1.5 Million people in the United States have rheumatoid arthritis (RA). The occurrence of rheumatoid arthritis in women is nearly three times more prevalent than in men. In women, rheumatoid arthritis most commonly begins between 30yrs to 60yrs of age. In men, it often occurs later in life. Having a family member with rheumatoid arthritis increases the odds of you suffering from rheumatoid arthritis; however, the majority of people with rheumatoid arthritis have no family history of the disease.
Tumor Necrosis factor in rheumatoid arthritis
The symptoms of rheumatoid arthritis include joint pain, swollen joints, fever, limping, loss of range of motion, tender joints, loss of joint function, stiff joints, joints infirmity and many more.
It is well established that pro-inflammatory cytokines such as IL-6 and TNF-α, are involved in the pathogenesis of rheumatoid arthritis. Both TNF- α and IL-6 play dominant roles in the pathobiology of rheumatoid arthritis. TNF is a key mediator of cell migration and inflammation in rheumatoid arthritis.
Anti-TNF therapy induces a shift in the cytokine equilibrium producing less anti-inflammatory cytokines. Studies have demonstrated the improvement in the synovial inflammation in rheumatoid arthritis patients using Anti-TNF therapy.