|CLASS OF DRUG:
||HIV fusion inhibitor
|MECHANISM OF ACTION:
||HIV replicates viaCD4+ cells. This process
starts when the virus attaches to the host cell surface and subsequently fuses with the
membrane of a host cell. For this process to occur, the HIV virus attaches to a cell using
a viral protein known as gp120. Gp120 is then stripped away exposing two regions of
another protein called gp41. These then bind to each other to form a coil-like structure.
This coil allows the HIV virus to draw closer to the cells membrane and gain entry
into the cell.
Fusion inhibition works by binding to one of these peptide sections of
the gp41 protein and blocking the structural rearrangement necessary to make a functional
coil. This results in the inability of the HIV virus to fuse with the cells and thereby
prevents the virus from infecting the cell.
||T-20 is currently in Phase II clinical
trials. Results from clinical trials evaluating the safety and efficacy of T-20 in
combination with other antiretrovirals have shown T-20 has a potent effect out to week 16
in suppressing the HIV virus in treatment-experienced patients.
In February 1999, T-20
was granted designation as a fast-track programby the United States Food and Drug
A large-scale pivotal Phase III clinical trial evaluating T-20s safety and
efficacy is scheduled to begin in 2000.
||Twice daily, self-administered subcutaneous
||In all clinical studies to date, most adverse
events reported on T-20 were mild or moderate in severity. The most frequent adverse
events included fever, headache and lymph node abnormalities, in addition to local
irritation resulting from the subcutaneous injection.