Our Technology

Our current drug development technology is based around (a) the experimental anti-cancer drug, idronoxil, and (b) the proprietary LIPROSE drug delivery technology, designed to greatly enhance the drug-like properties of idronoxil.


A. Anti-cancer effects

  • The main anti-cancer effects of idronoxil are:
  • block cancer cells from dividing (cytostatic)
  • kill cancer cells (cytotoxic)
  • enhance the killing effect of radiotherapy on cancer cells
  • enhance the killing effect of cytotoxic chemotherapies on cancer cells
  • enhance the ability of immune cells to kill cancer cells.

Idronoxil shows anti-cancer activity in the laboratory against all common forms of cancer as well as many uncommon and rare forms of cancer.

B. Idronoxil target

The anti-cancer effects of idronoxil stem from its ability to interfere with the normal function of the cancer cell’s various membranes (plasma, mitochondrial, nuclear). Idronoxil is a first-in-class inhibitor of protons across these membranes, particularly the external plasma membrane, the interface between the cancer cell and its environment.

Cell membranes are vital structures that actively receive and pass thousands of signals within the cell. Processing signals requires energy, and one of the key sources of energy for membranes is a battery-like charge known as the transmembrane electron potential – a positive-negative differential created by pumping protons, or hydrogen ions (H+), from one side of the membrane to the other side.

This movement of protons is regulated by a pump mechanism located within each membrane and known as the proton pump. The proton pump, in turn, is driven by an enzyme known as NADH oxidase (or NOX). Each type of membrane has its own particular form of NADH oxidase. The form of NADH oxidase present on the external plasma membrane of all human cells is known as external NADH oxidase (or ENOX), and this is the target for idronoxil.

Humans make 2 forms of ENOX known as ENOX1 and its splice variant form, ENOX2. The key difference between the two forms lies in the speed at which they cycle protons across the membrane, with ENOX2 being slightly faster than ENOX1.

Healthy human cells conducting normal levels of activity (metabolism, differentiation, growth etc) only express ENOX1; the gene responsible for producing ENOX2 is off-line. The ENOX2 gene appears to come on-line in response to extra-normal cell activity, supposedly in response to the need to higher levels of protons being generated through increased metabolic activity, requiring a more powerful proton pump action. Cancer is associated with increased metabolic activity, explaining why ENOX2 replaces ENOX1 in all cancer cells.

Idronoxil specifically binds to and inhibits the activity of ENOX2. Idronoxil has no binding affinity to ENOX1.

C. Mechanism of action

Inhibition of ENOX2

Build-up of protons in the external cell membrane

Disruption of sphingomyelin pathway in external cell membrane

Inhibition of sphingosine kinase

Inhibition of pro-survival signalling (sphingosine-1-phosphate) and activation of pro-death signalling (ceramide)

Loss of activity of PI3 kinase

Loss of phosphorylation of key pro-survival switches, Akt and mTOR and enzymes involved in DNA repair (PARP 1 and topoisomerases 1 and 2)

Activation of caspases, 3, 8 and 9 leading to apoptosis.



LIPROSE is a fatty acid shield designed to protect and enhance the drug-like action of idronoxil.

Idronoxil given to a patient in an unprotected state is subject to 2 outcomes, both of which detract from its anti-cancer abilities.

The first outcome is that the great majority of administered idronoxil ends up being inactivated by the body:

Idronoxil is insoluble in water, rendering it highly susceptible to Phase 2 metabolism. Phase 2 metabolism takes place in the lining of the gut and liver and is designed to convert any water-insoluble chemicals entering the body into a water-soluble form that enables them to be excreted in the urine. Phase 2 metabolism involves attaching a sugar (glucuronic acid) or a sulfate group onto the foreign chemical.

Between 95-99% of idronoxil in the body following oral or intravenous dosing occurs in this modified form, stripping the drug of its anti-cancer activities.

The second outcome is that the little amount of idronoxil that manages to avoid Phase 2 metabolism has a very short half-life in the body:

Free idronoxil has a half-life in human blood of about 45 minutes. This means that there is virtually no detectable drug left in an active form about 1 hour after dosing.

The problem that this presents is that the anti-cancer effect of idronoxil requires the drug to be present on a continual basis, with the DNA repair process resuming in the absence of idronoxil.

LIPROSE serves three functions:

1. It protects idronoxil from Phase 2 metabolism
2. It extends the half-life of idronoxil from 45 minutes to > 10 hours.
3. It allows idronoxil to cross the blood-brain barrier.