- 23ME-01473 (‘1473) seeks to treat cancer by restoring anti-tumor immunity through NK and T cells
- ‘1473 has dual mechanisms of blocking the immunosuppressive effects of soluble ULBP6, and inducing Fc receptor-mediated killing of ULBP6-expressing cancer cells through enhanced effector function
- Phase 1 clinical study in patients with solid tumors to commence in H1 2024
- The target for ‘1473 was discovered through 23andMe’s proprietary research platform, the world's largest recontactable database of de-identified human genetic and phenotypic information
‘1473 targets ULBP6 to restore anti-tumor immunity through NK and T cells. ULBPs are stress-induced ligands found on the surface of cancer cells that bind to their receptor, NKG2D, on NK and T cells. Cancers escape immune cell recognition by shedding ULBP ligands from their cell surface, which act as immunosuppressive molecular decoys.
Blocking the binding of soluble ULBP6 to NKG2D may restore immune cell recognition and killing of cancers. Further, ‘1473 is Fc-effector enhanced, which provides an additional mechanism for NK cells to induce cell death of ULBP6-expressing cancer cells.
'1473 also has the potential to address a major unmet need in cancer treatment: patients who may have or may develop tumor resistance to checkpoint inhibitors. By combining NK and T cell activation, '1473 may initiate a broader and deeper response of the immune system to kill cancer cells, and delay tumor resistance seen in treatment with traditional checkpoint inhibitors.
“This program further validates the 23andMe database as a proven resource for identifying novel therapeutic targets,” said
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23andMe is a genetics-led consumer healthcare and biopharmaceutical company empowering a healthier future. For more information, please visit www.23andMe.com.
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