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The fully humanized monoclonal antibody is licensed to Bristol-Myers Squibb.
Innate Pharma announced on Sept. 17, 2015 that it expects data on its first-in-class investigational monoclonal antibody (mAb) lirilumab-now in Phase I clinical trials-by 2016.
According to Innate's website, lirilumab works by blocking interaction between killer-cell immunoglobulin-like receptors (KIR) on natural killer (NK) cells with their ligands. Blocking the binding of KIR on NK cells facilitates a boost in immune response characterized by enhanced activation of NK cells and is thought to improve the tumor cell destruction capabilities of these cells.
Lirilumab and all related compounds blocking KIR receptors are licensed to Bristol-Myers Squibb through an agreement from July 2011. The efficacy of the monoclonal antibody (mAb) is being tested in a total of seven distinct clinical trials-as a monotherapy in one trial and in combination with other products in the remaining six trials. The therapy is being investigated as a treatment option for select solid tumors, select hematological tumors, multiple myeloma, acute myeloid leukemia, and chronic lymphocytic leukemia.
Innate is also developing another immune-oncology target-IPH2201-with AstraZeneca. This deal, which was announced in April 2015, allows Innate to co-develop, co-promote, and co-commercialize IPH2201, a strategy which Innate's CEO Hervé Brailly said in a press release will allow Innate to further mature the company's "capabilities in late-stage development". Additional Phase II clinical trials for IPH2201 will be opened in the second half of 2015, Reuters reports.
IPH2201 is a first-in-class humanized mAb targeting NKG2A receptors expressed on tumor infiltrating cytotoxic NK and CD8 T lymphocytes. By expressing HLA-E, Cancer cells can protect themselves from killing by NKG2A+ immune cells by expressing HLA-E on their surfaces. The overexpression of HLA-E in several cancer types is thought to protect abnormal cancer cells from attack by the immune system, allowing the cancer cells to evade destruction via a "cloaking" mechanism. IPH2201 works by blocking the binding of NKG2A receptors on immune cells to HLA-E, freeing up the NKG2A receptors, thereby allowing activation of NK and cytotoxic T-cell responses.
Innate asserts that IPH2201 is the “only checkpoint inhibitor developed to date that is capable of acting simultaneously on T and NK cells, which could provide a more effective immune response.”
Sources: Innate Pharma, Reuters