Current Stage of Development

 


 

 

ALD518

ALD518 is a humanized monoclonal antibody, designed to block a pro-inflammatory molecule called interleukin-6 (IL-6), which plays a key role in the inflammatory cascade leading to the inflammation, swelling, pain, and destruction of large and small joints associated with rheumatoid arthritis. IL-6 acts as a central early mediator in the inflammation cascade and impacts multiple signaling pathways as well as cell types. Targeting of the IL-6 pathway is a clinically validated mechanism for the treatment of rheumatoid arthritis.

ALD518 may also have relevance in the treatment of cancer through modulating the immune response, which plays a key role in the disease. Targeting the IL-6 pathway affects tumor cells that overproduce IL-6, which goes on to stimulate inflammation-related conditions such as cancer-related fatigue, cachexia, and anemia. In a Phase I oncology clinical study presented at ASCO 2009, ALD518 given to patients with advanced cancer was shown to be safe and well tolerated. In this study, ALD518 reversed fatigue, and increased hemoglobin and albumin. ALD518 had a median elimination half-life of 25 days, suggesting a long duration of action.

View results of the ALD518 Phase I cancer study (400k PDF)


ALD806

ALD806 is a humanized monoclonal antibody designed to block the interaction between a potent cell growth factor and its cell surface receptor known to be involved in tumor growth and proliferation. If successful in clinical studies, ALD806 may have potential for the treatment of a variety of cancerous conditions.

ALD901

ALD901 is a humanized monoclonal antibody designed to block a key factor involved in the generation of severe pain. The pathway has recently been established to play a central role in human pain sensation. ALD901 neutralizes the central regulator of this pathway, which is not targeted by pain medications approved for use today. It is envisioned that this product may one day present a novel and efficacious approach to pain management.