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NK Cell Activator
(CNDO102)
Background
We believe that cancer cannot be cured without participation of the patient’s immune system. This is particularly important in the elimination of minimal residual disease (MRD), the cancer that remains after completion of chemotherapy and radiation treatment.
Natural killer (NK) cells (CD56+CD3-), are part of the innate immune system and primarily responsible for eliminating MRD. When activated, NK cells specifically identify and kill cancer cells by a process known as granzyme mediated lysis.
In many ways, our CNDO102 NK cell activator functions similarly to targeted therapy with anti-cancer antibodies. In general, targeted monoclonal antibodies do not directly destroy cancer pathogens. Rather, the antibody binds to a target on the cancer cell membrane that allows the patient’s immune system to see the previously invisible cancer cell. The patient’s innate immune system then attacks the antibody-labeled cancer cell; NK cells are largely responsible for its elimination.
Application
MRD may be the cause of cancer relapse. Chemotherapy and radiation therapy may remove up to 99% of cancer cells and result in a complete response (CR), however cancer cells remain left behind. This persistent disease (MRD) may continue to proliferate, generating new cancer cells and ultimately cause relapse. Immunotherapy such as targeted antibody therapy and CNDO102, are most effective in eliminating MRD in patients that have responded to their initial chemotherapy and radiation therapy. CNDO102 is proposed as a final step in the cancer treatment algorithm, eliminating residual disease and minimizing risk of relapse. From the oncologist’s perspective, CNDO102 should allow a patient to be converted from a complete response to a molecular cure.
Pre-clinical in vitro studies using human NK cells and primary tumor specimens from patients have shown that CNDO102 is active against hematologic and epithelial malignancies, including leukemia (acute myelogenous leukemia [AML]), breast, and ovarian cancers.
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