Indication

Target/marker/pathway

Summary

Licensing status

Publication and contact information

Various

Atherosclerosis; periodontitis

Caspase recruitment domain family member 15 (CARD15; NOD2)

Mouse studies suggest stimulating NOD2 could help treat atherosclerosis and periodontal bone loss. In an apolipoprotein E (ApoE) knockout model of inflammation, deletion of Nod2 increased Porphyromonas gingivalis-induced atherosclerosis, periodontal bone loss and inflammatory serum cytokine levels compared with no Nod2 alteration. In ApoE-/- mice, a NOD2 stimulator decreased serum cytokine levels, atherosclerosis and bone loss compared with vehicle. Next steps could include testing NOD2 stimulators in additional models of periodontal bone loss and atherosclerosis.
Takeda Pharmaceutical Co. Ltd. markets the NOD2-targeting biologic Junovan mifamurtide to treat bone cancer.
At least two other companies have NOD2-activating compounds in Phase I or earlier development to treat cancer or infectious diseases.

SciBX 7(2); doi:10.1038/scibx.2014.64
Published online Jan. 16, 2014

Patent and licensing status unavailable

Yuan, H. et al. Proc. Natl. Acad. Sci. USA; published online
Dec. 9, 2013;
doi:10.1073/pnas.1320862110
Contact: Salomon Amar, Boston University, Boston, Mass.
e-mail:
samar@bu.edu

Contact: Susan E. Leeman, same affiliation as above
e-mail:
sleeman@bu.edu