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Technology


IGF is very closely linked to cancer. The defining feature of a cancer cell is that the cell divides uncontrollably, and the natural biological role of the hormone IGF is to cause cells to divide. So perhaps it should not be surprising that one study found the IGF receptor is 43-times more abundant on breast cancer cells than on normal breast tissue. IGF has also been linked to most other types of cancer. The concept for the technology platform is supported by an abundance of scientific literature.


The company’s first candidate drug is a conjugate in which the standard cancer chemotherapy drug methotrexate is attached to an engineered form of IGF. Our testing shows the IGF-methotrexate conjugate, even at 6-fold lower concentration, is more effective than unconjugated methotrexate against a prostate cancer model in mice. http://www.ncbi.nlm.nih.gov/pubmed/19446281 That is, IGF-methotrexate is more effective than methotrexate even at 1/6 of the dose of methotrexate.


By targeting much more specifically to cancer cells, the company’s drugs largely spare non-cancerous cells and have greatly reduced side effects compared to conventional chemotherapy drugs.


Not only do malignant cells have more IGF-1 receptors than healthy cells, but the most dangerous and aggressive cancer cells have been found to have the most IGF-1 receptors. Thus, not only does the company’s technology target cancer cells over healthy cells, but it targets the most aggressive cancer cells more than the less important cancer cells.

  1. McTavish H, Griffin RJ, Terai K, Dudek AZ. 2009. Novel insulin-like growth factor-methotrexate covalent conjugate inhibits tumor growth in vivo at lower dosage than methotrexate alone. Translational Research 153:275-82
  2. Peyrat JP, Bonneterre J. 1992. Type 1 IGF receptor in human breast diseases. Breast Cancer Research and Treatment 22:59-67.
  3. Stewart CE, Rotwein P. 1996. Growth, differentiation, and survival: multiple physiological functions for insulin-like growth factors. Physiol. Revs. 76:1005-1026.
  4. Papa, V. et al. 1990. J. Clin. Invest. 86:1503-1510.
  5. Jammes, H. et al. 1992. Br. J. Cancer 66:248-253
  6. Resnicoff M, Burgaud JL, Rotman HL, Abraham D, Baserga R. 1995. Correlation between apoptosis, tumorigenesis, and levels of insulin-like growth factor I receptors. Cancer Res. 55:3739-41.
  7. Surmacz, E. 2000. Function of the IGF-I receptor in breast cancer. J. Mammary Gland Biol. Neoplaisa 5:95-105.