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BACKGROUND INFORMATION: T-20 FACT SHEET |
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Posted: 27-Sep-99
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| DRUG NAME: |
T-20 |
| CLASS OF DRUG: |
HIV fusion inhibitor |
| MECHANISM OF ACTION: |
HIV replicates via CD4+ 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 cell�s 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. |
| DEVELOPMENT: |
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 program by the United States Food and Drug Administration.
A large-scale pivotal Phase III clinical trial evaluating
T-20�s safety and efficacy is scheduled to begin in 2000. |
| ADMINISTRATION: |
Twice daily, self-administered subcutaneous injection. |
| ADVERSE EVENTS: |
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.
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