Tosk uses two proprietary discovery methods to identify potential CompanionTM drugs. Together, we call these methods OMDTM for Optimizing Marketed DrugsTM because they allow us to efficiently screen compounds for their potential to block adverse side effects or make certain drugs effective in patients who currently do not benefit from therapy.
The OMD technology we employ to eliminate toxic effects of standard cancer drugs -- what we call the Side EffectTM Fly model -- uses the common fruit fly (Drosophila melanogaster), a surprisingly complex animal species with some 65 to 75 percent of human gene analogs. The life cycle of a fruit fly is approximately two weeks, so preliminary tests can be done on them in rapid succession and at reasonable cost.
The first step in the process that Tosk's scientists take is to measure the toxic effect the parent drug has on the fruit flies. We then test thousands of compounds looking to identify those that have the potential to eliminate or reduce the toxicity. These tests are conducted within assay vials, where flies are given the parent drug and a compound simultaneously in assembly line fashion. Compounds that increase survival of the flies' eggs and result in larva or mature fruit flies are considered "hits." The hits are tested in cell culture models using human cancer cells to select "leads" that do not block the cancer killing efficacy of the parent compound. Our researchers then use traditional rodent models to confirm safety, adverse effect reduction and non-interference with the beneficial effects of the parent compound. This is the process used to design our first drug, TK-90, which recently completed a successful human trial, as well as TK-39 and TK-88. It's an arduous process requiring immense skill and patience, but our scientist believe it is the most comprehensive method to eventually design highly effective therapies.
In our other proprietary screening method, the Genetically Modified Fruit Fly ModelTM our goal is to identify compounds that block the cancer causing effect of mutated human kRAS genes. We implant a mutated gene into the fly's genome, causing their wings to crimp, then screen for compounds that reverse the crimping by blocking the activity of the mutated gene. Confirmed "hits" are optimized using molecular modeling, then in cell culture, followed by tests in rodent models. Mutated kRAS genes cause 90 percent of pancreatic cancer, 45 percent of colon cancer, 35 percent of lung cancer, and a portion of most other cancers, and there is no approved therapy that target oncogenic kRAS. Some 40 percent of cancer patients carry the mutated kRAS gene, which blocks the efficacy of a class of widely-used cancer drugs known as EGFR inhibitors such as Erbitux. We're also using genetic modificaltions of the flies to identify promising compounds to block the activity of other mutant cancer-causing genes.Others have tried to block the toxic effects of existing drugs, but have generally failed. Tosk's scientists believe that's because their high throughput methods using cell culture, biochemical screens and molecular modeling techniques were insufficient, as compared to the non-mammalian animal species methodolgy we discovered and patented. This OMDTM technology in itself is extremely valuable now, and, we believe, for optimizing cancer treatment in the future.
The Common Fruit Fly – Drosophila melanogaster
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