The Process:  How Ryboquin™ works:

• In most cases, chemotherapy aims to promote the cell death (suicide or apoptosis) of cancer cells.
• Sufficient levels of a protein called p53 are required in the cancer cells to trigger cell death.  p53 is a tumour suppressant.
• However, in over 50% of tumours, p53 is deficient in the cancer cells (p53 null or p53 mutated) and chemotherapy fails to have the desired effect.
• Another protein from the same family – p73 – can act as a substitute trigger mechanism.
• But p73 exists only at low levels in cells, so it has to be boosted (up-regulated).
• This can be achieved by switching off an enzyme called Itch Ubiquitin Ligase (Itch for short) which controls p73 levels.
• Proteins within cells are broken up when they have 4 Ubiquitin molecules attached to themselves.
• Preventing the Ubiquitin molecules from performing – ie. degrading or down-regulating Itch – allows p73 to go on accumulating in cells.
• Higher levels of p73 mean the cancer cells are more susceptible to cell death as a result of sustaining DNA damage caused by chemotherapeutic agents.  In other words, the cells are less likely to be chemotherapy resistant.
• The technology which down-regulates Itch is based on small interfering RNA (siRNA) which prevents messenger RNA (mRNA) from creating the Ubiquitin Ligase enzyme.
• The challenge is how to deliver the ribonucleic acids (ie. siRNA) direct to the cancer cells because they rapidly break down before reaching the cells.
• The London School of Pharmacy has discovered a way of creating nano particles which are a combination of a dendrimer (a small polymer) and a DNA gene grown in bacteria (a plasmid gene).
• This nano particle – the Ryboquin™ product – is delivered into the body intravenously.  DNA separates when Ryboquin™ meets the cancer cells and siRNA is created which then blocks the Ubiquitin Ligase, so increasing the levels of the p73 protein.