This group of drug is designed to prevent the release of Caspsid, a key viral protein from its precursor protein. The drug in question, PA- 457, is a derivative of betulinic acid, and interferes with the production of the capsid conical shield which protects the genetic material of HIV inside it.
Around 80 per cent of people being treated for HIV show resistance to one or more of the current drugs available and this figure is likely to rise as rate of infection soars and treatment options become increasingly limited.
The article, published in the >Journal of Virology, concluded that PA-457 blocks release of Capsid only when Gag is in an assembled form, suggesting that the drug candidate's target has a specific three-dimensional conformation that is not present in unassembled Gag.
The study also indicated that no other viral proteins or human cellular components are required for PA-457 activity.
"These experimental results validate Gag as PA-457's molecular target and support the finding of a novel mechanism of action for this first-in-class HIV inhibitor," said Graham Allaway, Panacos' chief operating officer.
"This provides the basis for future studies that will be designed to provide a detailed understanding of the interaction between PA-457 and its target as well as insights into the design of new generations of maturation inhibitors."
Despite the success that these results represent, the researchers have stressed the importance of further testing. They anticipated that it would be at least 2009 before the drug is on the market.
Further research, due to commence this month; will test how PA-457 works in combination with other drugs. Combination treatments are most effective because of the high levels of drug resistance seen in HIV treatment.
Antiretroviral drugs disrupt the HIV enzyme's ability for genetic copying, or making virus that can infect other cells. In a person who takes antiretroviral drugs, most of the HIV are killed or prevented from multiplying further.
Protease Inhibitors (PIs) inhibit the digestive enzyme protease that is needed in the replication of HIV to generate new virus particles.
It breaks down proteins and enzymes in the infected cells, which can then go on to infect other cells. The protease inhibitors prevent this breakdown of proteins and therefore slow down the production of new virus particles.
A recent market report by Datamonitor's suggests that by 2012, global product sales could amount to just under $12 billion (€9.2 billion), approximately double the value recorded for 2003 ($5.76 billion).
Companies with no existing HIV market experience are currently developing more than half of the HIV pipeline with the greatest compound diversity.
Despite this, Datamonitor predicts that only 30 per cent of revenue ($3.5 billion) will be derived from these new players in 2012 should their clinical development plans be successful. Schering-Plough and Tibotec-Virco are the most noticeable new entrants