Compounds discovered by FASgen selectively kill cancer cells by inhibiting fatty acid synthase. Since this enzyme is minimally present in normal body cells or not at all, our compounds do not affect them. This mechanism differs sharply from currently used cytotoxic agents that damage a variety of proliferating normal as well as cancerous cells. Thus, FAS inhibitors represent an entirely new approach to treat solid cancers without serious adverse effects.

FAS collects inside cancer cells and spills into the blood stream. Thus, the drug target attacked by our anticancer compounds can be easily detected in the tumor tissue and patient's blood prior to treatment. This offers a distinct advantage rarely available to oncologists while they are formulating their therapeutic plans.

Screening studies have revealed no major impediment to successful drug development. Programmed cell death (apoptosis) is initiated within 1 hour of exposure. Apoptosis is not initiated in non-transformed cells.

Anti-cancer efficacy is gauged using human tumor xenograft models in athymic mice, especially ovarian cancer Ovcar 3 and colon cancer HCT116. (Lead compound candidates are active when given by mouth or parenterally.) Cures have been obtained in ovarian, breast, colon and lung xenograft models at doses well below toxic levels. In fact, the sole dose limiting toxicity thus far identified is the profound weight loss first encountered with C-75, FASgen's index compound. This weight loss effect has been designed out of our new generation lead compound candidates.

In May 2006, JHU Oncology Center reported results to the Company of a remarkably successful in-vivo trial demonstrating FAS93 to be effective in elimination of tumor in a H460 human cancer xenograft model in nude mice by oral dosing for 10 days at 25 mg/k twice daily. This study was conducted and financed under an NCI Spore Grant.

Another exciting result has been obtained with two different FAS inhibitors in separate 18-month experiments in neu-N transgenic mice that invariably develop FAS over-expressing breast cancers during the last quarter of their first year. A short, 12 week course of FAS inhibitor beginning at 8 weeks of age completely prevented the development of cancer in one third of the mice and significantly delayed the onset of cancer in the remainder.