Oncolyze

www.oncolyze.com

Oncolyze is developing a disruptive technology for the treatment of cancer. Our novel approach uses a simple mechanism of action to selectively kill cancer cells and cancer stem cells while sparing normal cells. This provides a highly effective treatment with little to no side effects. Our lead drug candidate, OM-301, has two parts; the first attaches to a molecule that is present on the cell surface of more than 80% of cancer types we have assessed, but not on normal cells. When our drug attaches to this target, it uses it as an anchor; the second part then pokes holes in the cell membrane, causing extracellular liquid to rapidly enter, which in turn causes the cancer cell to burst. No known cancer drug uses such a mechanism, although many antibiotics kill bacteria in a similar way. Our initial therapeutic target is acute myelogenous leukemia (AML). Most AML patients relapse within 1 year of standard therapy, because it does not destroy cancer stem cells. As a result, AML has only a 25% 5-year survival rate. In contrast, OM-301 does destroy cancer stem cells, which has the potential to disrupt current medical treatment and fully cure AML. Recently, we showed that mice injected with AML cells taken directly from patients lived twice as long after receiving our drug. Following our proof of concept in AML, we expect to pursue development for patients with Multiple Myeloma and other blood and solid cancers.

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Oncolyze is developing a disruptive technology for the treatment of cancer. Our novel approach uses a simple mechanism of action to selectively kill cancer cells and cancer stem cells while sparing normal cells. This provides a highly effective treatment with little to no side effects. Our lead drug candidate, OM-301, has two parts; the first attaches to a molecule that is present on the cell surface of more than 80% of cancer types we have assessed, but not on normal cells. When our drug attaches to this target, it uses it as an anchor; the second part then pokes holes in the cell membrane, causing extracellular liquid to rapidly enter, which in turn causes the cancer cell to burst. No known cancer drug uses such a mechanism, although many antibiotics kill bacteria in a similar way. Our initial therapeutic target is acute myelogenous leukemia (AML). Most AML patients relapse within 1 year of standard therapy, because it does not destroy cancer stem cells. As a result, AML has only a 25% 5-year survival rate. In contrast, OM-301 does destroy cancer stem cells, which has the potential to disrupt current medical treatment and fully cure AML. Recently, we showed that mice injected with AML cells taken directly from patients lived twice as long after receiving our drug. Following our proof of concept in AML, we expect to pursue development for patients with Multiple Myeloma and other blood and solid cancers.

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New York

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New York City

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