CDP323

CDP323 is an experimental drug that was developed by Biogen Idec and UCB for the treatment of multiple sclerosis. It is a small molecule VLA-4 antagonist that inhibits the binding of Very Late Antigen-4 (VLA-4) to vascular cell adhesion molecule-1 (VCAM-1), thereby preventing the adhesion and migration of white blood cells into the central nervous system. This mechanism of action is thought to reduce the inflammation and nerve damage associated with multiple sclerosis.

Development and Clinical Trials

CDP323 was first synthesized in the early 2000s and entered clinical trials in 2006. The drug was tested in a Phase II, randomized, double-blind, placebo-controlled study involving patients with relapsing-remitting multiple sclerosis. However, the development of CDP323 was discontinued in 2010 due to lack of efficacy in the Phase II study.

Mechanism of Action

CDP323 is a small molecule that binds to the alpha4 subunit of VLA-4, a protein on the surface of white blood cells. This binding prevents VLA-4 from adhering to VCAM-1, a protein on the endothelial cells that line the blood vessels in the brain and spinal cord. By blocking this interaction, CDP323 inhibits the migration of white blood cells into the central nervous system, reducing inflammation and potentially slowing the progression of multiple sclerosis.

Potential Applications

While CDP323 was not successful in treating multiple sclerosis, research into VLA-4 antagonists continues. These drugs may have potential applications in other autoimmune diseases, such as rheumatoid arthritis and inflammatory bowel disease, where the migration of white blood cells into tissues contributes to inflammation and tissue damage.

See Also

• Multiple sclerosis
• VLA-4 antagonist
• Biogen Idec
• UCB