Use of these agents has been studied across a variety of indications and populations, and at different stages in the disease course. Failure to respond or loss of response can result from different causes, and can be medically managed in many cases. More research on the pleiotropic

Fer-1 research buy effects, safety of biological agents and biomarkers in the prediction of response will provide a sounder basis for individually directing therapy. Adverse events such as opportunistic infection and malignancy can occur, and screening prior to therapy and discussion on risk-benefit of the various management options are important. Cost of these medications especially with maintenance therapy remains an important issue in many Asia-Pacific countries. New and more specific agents will better target therapy and minimize adverse events. Biological agents” describe a class of substances manufactured from a living organism

or by recombinant technology that includes peptides, monoclonal antibodies, fusion proteins and antisense oligonucleotides that bind to nucleic acids.1 In inflammatory bowel diseases (IBD), this group of drugs manipulates key molecules that are involved in the induction and maintenance of intestinal inflammation. They are expensive and risk adverse effects, but this is counterpoised by their superiority to conventional immunosuppressive agents in their efficacy to decrease refractory inflammation, induce mucosal healing, and reduce rates of surgical intervention and long-term complications. Romidepsin concentration Molecules MCE and targets.  An evolving understanding of the pathogenesis of IBD has identified several immunomodulatory therapeutic targets. In Crohn’s disease (CD), T helper 1 (Th1) and the distinctively different T helper 17 (Th17) cells mediate proinflammatory cytokines.2 Both Th1 and Th17 pathways lead to increases in circulatory and tissue

tumor necrosis factor (TNF)-α, the target of anti-TNF-α therapy in both CD and ulcerative colitis (UC).1 Three anti-TNF agents are used in the treatment of IBD. Infliximab is a murine-human chimeric monoclonal antibody, adalimumab is a humanized monoclonal antibody, and certolizumab pegol is a pegylated monoclonal antigen binding fragment (Fab’) to TNF-α. Other anti-TNF-α biological agents currently in clinical trial include golimumab, and this may offer an additional therapeutic option. The alternative Th17 pathway involves interleukin (IL)-23, liberating IL-17A, IL-17F, IL-22 and TNF-α. IL-23 receptor polymorphism is known to protect against the development of CD, and other polymorphisms of the pathway are linked to the development of inflammatory diseases such as ankylosing spondylitis and Grave’s ophthalmopathy.3 Therapeutic neutralization of human IL-12/23 using ustekinumab and briakinumab, approved or are under trial for psoriasis, are currently under evaluation for IBD.