There is test tube evidence that abacavir (Ziagen) enhances the effects of the protease inhibitor amprenavir (Agenerase), although this may not translate into a more effective combination in people^[1].

A drug called mycophenolic acid (Myfortic) enhances the antiviral effectiveness of abacavir in test tube studies^[2]. Although clinical trials are ongoing to determine whether mycophenolic acid can improve the anti-HIV effects of abacavir without inducing high-level toxicity, a small safety study therapy found no significant benefit of the combination^[3]. At this stage, combining abacavir with mycophenolic acid is experimental and not recommended as standard treatment.

Clearance of methadone hydrochloride (Methadose) is increased by 22% when combined with abacavir, but no dose modification of methadone hydrochloride is required. However, patients taking both drugs should be monitored for methadone hydrochloride withdrawal symptoms.

Interactions are also possible with alcohol, which is known to increase blood levels of abacavir. Individuals with moderate to severe liver disease are most likely to be adversely affected by this interaction, although abacavir is not recommended for this group of patients. Dose adjustments are not required^[4].

The lack of an interaction between abacavir and the tuberculosis drug rifampicin (Rifadin / Rimactane) has led to suggestions that triple nucleoside reverse transcriptase inhibitor (NRTI) combinations including abacavir might be useful during anti-tuberculosis therapy. The drawback in this strategy is that abacavir hypersensitivity cannot be distinguished from immune restoration inflammatory syndrome that can occur when people with tuberculosis begin antiretroviral therapy. This condition is caused when the immune system begins to recover and mounts a new or stronger response to the organisms that cause tuberculosis. The outcome is a temporary worsening of symptoms, which often includes fever, and may be mistaken for a hypersensitivity reaction.