During the recent Analyst Day event in New York, Xencor highlighted its lead candidate to treat systemic lupus erythematosus (SLE), now in Phase 2 clinical testing, and other potential treatments advancing in development.
“We believe our flexible bispecific oncology platform has substantial potential. Our programs are built on a novel XmAb Fc domain, which allows for the rapid creation of drug candidates that maintain important full-length antibody properties, without the manufacturing and commercialization challenges that have historically blocked the viability of bispecific antibodies,” Bassil Dahiyat, PhD, president and chief executive officer of Xencor, said in a press release.
The company is also collaborating with Novartis to develop two lead bispecific oncology programs, XmAb14045 and XmAb13676, to treat neuroendocrine tumors and multiple cancers, respectively. Xencor will maintain commercialization rights for both candidates in the U.S.
“We are also pleased to report on the continued advancement of our pipeline of wholly-owned programs. We remain on track to … announce initial data from our ongoing Phase 2 trials of XmAb5871 in IgG4-Related Disease (IgG4-RD) and systemic lupus erythematosus (SLE) in 2017 and 2018, respectively,” Dahiyat said.
Currently, nine candidates engineered with Xencor’s XmAb technology are in clinical development, including XmAb5871, a first-in-class monoclonal antibody (i.e., antibodies that are made by identical immune cells and are able to recognize and attach to specific proteins). In this case, XmAb5871 specifically targets CD19, a protein linked to SLE pathogenesis.
The primary goal of the Phase 2 lupus clinical trial (NCT02725515), which is currently recruiting adult SLE patients at more than a dozen sites across the U.S., is to evaluate the ability of XmAb5871 to maintain improvements in SLE disease activity realized by a brief intramuscular injection of a disease-suppressing steroid therapy.
Initial data is expected in the first half of 2017, and the trial is set to conclude in December 2018. More information is available through this link.
Scientists at The Scripps Research Institute identified key mechanisms contributing to the generation of autoimmune B-cells that attack the body’s own tissues in diseases like systemic lupus eurythematosus. In a cluster of microRNA (miRNA) molecules, the research team found one factor with exaggerated presence that allows faulty cells to sneak past quality control checkpoints.