Mechanism of Action

Chemical Structure of IAD

IAD differs physio-chemically from its individual components and has pharmacokinetic and pharmacodynamic characteristics distinct from the characteristics of the individual components. IAD has been licensed since 1971 for the treatment of cell mediated immune deficiencies.

Mechanism of Action

On the basis of our current knowledge of mechanism of action for the drug we believe that:

The compound has a dual effect both as a T cell promoter and an antiviral agent; not solely as an immune promoting agent.
IAD induces cell cycle progression in activated T lymphocytes upregulating the cell mediated immune response (CMI) and enhancing downstream events from the CMI including NK cell/macrophage activation response and proliferation of activated B cells.
The drug interferes with viral replication within the cell nucleus allowing virally infected cells to proliferate as normal.

Further to this we envisage the compound to be most effective under the following conditions:

In patients where a depressed Th1 cell mediated immune response exists such as the elderly or other immune compromised patients.
In persistent latent viruses infection possibly owing to an increase in endogenous IFN production which has a key role in the eradication of virus residing in non labile cells.
When administered during days 1- 5 post viral outbreak during the window of activation of CMI.
As an adjunct therapy to existing antiviral treatments particularly in immune compromised patients.

The complete elucidation and understanding of the mechanism of the drug will underpin its basis for future development.

Pharmacokinetics

Following a single oral dose of IAD, peak plasma conditions of inosine occur within two hours. However two hours after administration, plasma concentrations decrease to undetectable amounts. IAD has a very short plasma half life of 50 minutes following an oral dose. The major excretion product of the inosine moiety is uric acid, while the p-acetamidobenzoic acid and N,N-dimethylamino-2-propanol components are excreted in the urine as glucuronidated and oxidised prioducts, respectively, as well as being excreted unchanged.