Patients
Autoimmune Diseases
Autoimmune Diseases
Autoimmune diseases arise from an overactive immune response of the body against substances and tissues normally present in the body. In other words, the body actually attacks its own cells. The immune system mistakes some part of the body as a pathogen and attacks it. Coronado Biosciences is currently focused on the following autoimmune diseases but many other autoimmune diseases may be amendable to treatment with CNDO-201.
Crohn's Disease is a chronic autoimmune disease that can affect any area of the gastrointestinal tract, from the mouth to the anus, but most commonly affects the lower part of the small intestine, the ileum and has the characteristic of relapsing inflammatory processes. In Crohn’s disease, inflammation may be patchy and segmental, typically transmural and is usually limited to only the rectum and colon. Mucosal inflammation generates large amounts of IFNy and TNFa suggesting that excess production of Thl-type cytokines is one common mechanism underlying the pathogenesis of disease. Immune response to helminths promotes Th2-response and exposure to TSO may prevent an exuberant Thl inflammation at mucosal surfaces like that seen in Crohn's disease.
While the disease can present itself at any age in a patient, initial incidence is often in the teens and twenties, with another peak incidence in the fifties to seventies. There is evidence of a genetic link to Crohn's disease, putting individuals with siblings afflicted with the disease at higher risk. It is thought to have a large environmental component as evidenced by a higher incidence in western industrialized nations compared to other parts of the world, although the hygiene hypothesis might explain the industrialized nations distribution. Males and females are equally affected, while smokers are two times more likely to develop Crohn's disease than nonsmokers. There is no known pharmacological or surgical cure for Crohn’s disease; treatment options are limited to the control of symptoms, maintenance of remission, and prevention of relapse.
The pathophysiology is characterized by a chronic occurrence of inflammations in the intestine where acute attacks are followed by periods of remission. Since the etiology of the disease is not completely understood, curative therapies have not yet been developed. Current therapeutic options in the management of patients are symptomatic only. Therapeutic approaches concentrate on suppression of acute flare-ups combined with induction and maintenance of remission to prevent further recurrences. Standard therapy for the symptomatic treatment of Crohn’s disease may include sulfasalazine, mesalazine, systemic and topical glucocorticoids, immunosuppressants like azathioprine or 6-mercaptopurine, and in severe cases also treatment with anti-TNF-alpha therapy, methotrexate, or cyclosporine as monotherapy or in combination with other agents.
Ulcerative colitis is an inflammatory bowel disease that causes chronic inflammation of the digestive tract, is characterized by abdominal pain and diarrhea. Ulcers form where inflammation has killed the cells that usually line the colon, then bleed and produce pus. Inflammation in the colon also causes the colon to empty frequently, causing diarrhea. When the inflammation occurs in the rectum and lower part of the colon it is called ulcerative proctitis. If the entire colon is affected it is called pancolitis. If only the left side of the colon is affected it is called limited or distal colitis.
Ulcerative colitis can occur in people of any age, but it usually starts between the ages of 15 and 30, and less frequently between 50 and 70 years of age. It affects men and women equally and appears to run in families, with reports of up to 20 percent of people with ulcerative colitis having a family member or relative with ulcerative colitis or Crohn's disease.
Multiple Sclerosis is an autoimmune inflammatory disease of the central nervous system that is characterized by progressive neuronal loss that manifests clinically as worsening physical disability. The key pathophysiological hallmark of MS is the loss of myelin, a layer of lipids and proteins produced by cells called oligodendrocytes that wrap around the neuron and act like an insulating sheath to facilitate electrical conduction along the nerve. Destruction of myelin by an inflammatory cascade leads to neuronal degeneration. As a result, we believe that there is a substantial unmet need for effective treatments for chronic progressive MS as well as a need for therapies that are more conveniently delivered (e.g., oral agents, less frequently administered injectable drugs).