By Maayan Jaffe-Hoffman (Jerusalem Post)
“If it does not completely annihilate the cancer, the remaining cells can start to get mutations again, and then the cancer comes back, but this time it is drug resistant,” Morad said.
He explained that because cancer cells are born out of mutations that occur in cancer stem cells, most of the over-expressed proteins which are targeted on the cancer cell exist in the cancer stem cells. MuTaTo’s multiple-target attack ensures that they will be destroyed as well.
Finally, some cancer tumors erect shields which create access problems to large molecules, such as antibodies. MuTaTo acts like an octopus or a piece of spaghetti and can sneak into places where other large molecules cannot reach. Morad said the peptide parts of MuTaTo are very small (12 amino acids long) and lack a rigid structure.
“This should make the whole molecule non-immunogenic in most cases and would enable repeated administration of the drug,” he said.
Morad said their discovery could also reduce the sickening side-effects of most cancer treatments, which stem from drug treatments interacting with the wrong or additional targets, or the correct targets but on non-cancerous cells. He said MuTaTo’s having a combination of several highly specific cancer-targeting peptides on one scaffold for each type of cancer cell would increase the specificity to the cancer cell due to the avidity effect. In addition, in most cases, the non-cancer cells that have a protein in common with the cancer cells do not over-express it.
“This makes a great difference between the two kinds of cells and should decrease the side effects dramatically,” Morad said.
He equated the concept of MuTaTo to the triple drug cocktail that has helped change AIDS from being an automatic death sentence to a chronic – but often manageable – disease.
Today, AIDS patients take protease inhibitors in combination with two other drugs called reverse transcriptase inhibitors. The drug combination disrupts HIV at different stages in its replication, restrains an enzyme crucial to an early stage of HIV duplication and holds back another enzyme that functions near the end of the HIV replication process.
“We used to give AIDS patients several drugs, but we would administer them one at a time,” Morad explained. “During the course of treatment, the virus mutated, and the AIDS started attacking again. Only when patients started using a cocktail, were they able to stop the disease.” Now, he said, people with AIDS are HIV carriers, but they are not sick anymore.
The MuTaTo cancer treatment will eventually be personalized. Each patient will provide a piece of his biopsy to the lab, which would then analyze it to know which receptors are overexpressed. The individual would then be administered exactly the molecule cocktail needed to cure his disease.
The company is now writing patents on specific peptides, which will be a large bank of targeting toxin peptides wholly owned and hard to break, said Aridor.
Morad said that so far, the company has concluded its first exploratory mice experiment, which inhibited human cancer cell growth and had no effect at all on healthy mice cells, in addition to several in-vitro trials. AEBi is on the cusp of beginning a round of clinical trials which could be completed within a few years and would make the treatment available in specific cases.