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Our science

Our goal is to progress the clinical development of our discoveries,

substantially increase their values, and to ultimately market or out-license.

Cancer metabolism

Cancer cell has unique metabolic characteristics that is quite different from a normal cell metabolism. Cancer cell takes up large amount of glucose and converts to lactic acid continuously to produce energy instead of TCA cycle in normal cell, which was named as Warburg effect. OMT-110 is a promising first in class anticancer drug candidate modulating cancer cell metabolism from the suppressed glycolysis to activation of citric acid cycle in mitochondria.

OMT-110 anticancer mechanism

When OMT-110 is treated to cancer cells, OMT-110 induces its own target protein in the cancer cell, which activates pyruvate dehydrogenase kinase (PDH), the main gate for activating the citric acid cycle of mitochondria (Figure 1).
(Figure 1) Activation of PDH by OMT-110 in cancer cells.
The mitochondrial metabolism leads to the degradation of Hypoxia inducible factor (HIF)-1α, which is responsible for malignancy of cancer by linking (Figure 2).
(Figure 2) Degradation of HIF-1α proteins by remodeling of cancer-specific metabolism after OMT-110 treatment in cancer cells.
HIF-1α is a transcription factor for various oncogenes including glucose transport channel (GLUT-1), hexokinase (HK2), vascular growth factor (VEGF) and PDH kinase (PDH inactivation inducible enzyme; PDK-1) (Figure 3 & 4).
(Figure 3) Suppression of GLUT-1, HK2 and PDK-1 expression by OMT-110 in cancer cells.
(Figure 4) Suppression of expression of VEGF protein and mRNA and inhibition of angiogenesis using human vein endothelial cells (HUVEC) by OMT-110 in cancer cells.

OMT-110 anticancer effect

Since the Warburg effect, a cancer-specific metabolism, is well known as a common metabolism of solid tumors, OMT-110 is a promising anticancer drug candidate that might be applied to the treatment of all known solid tumors in the world, regardless of the type of cancer or the mutation of various cancer genes (Figure 4-7).
(Figure 4) Subcutaneous transplant the human-derived colorectal cancer cells into the experimental rats and confirmation of the anticancer effect by the administration of OMT-110.
(Figure 5) Subcutaneous transplant the human-derived epidermal growth factor receptor (EGFR) mutant-resistant lung cancer cells into the experimental rats and confirmation of the anticancer effect by the administration of OMT-110.
(Figure 6) Subcutaneous transplant the human-derived triple-negative breast cancer cells into the experimental rats and confirmation of the anticancer effect by the administration of OMT-110.
(Figure 7) Subcutaneous transplant the human-derived pancreatic cancer cells into the experimental rats and confirmation of the anticancer effect by the administration of OMT-110.
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