| Indication | For the treatment of HIV-1 infection in combination with appropriate antiretroviral agents when therapy is warranted |
| Pharmacodynamics | Delavirdine is a non-nucleoside reverse transcriptase inhibitor (nNRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Delavirdine binds directly to reverse transcriptase (RT) and blocks the RNA-dependent and DNA-dependent DNA polymerase activities by causing a disruption of the enzyme's catalytic site. The activity of Delavirdine does not compete with template or nucleoside triphosphates. HIV-2 RT and eukaryotic DNA polymerases (such as human DNA polymerases alpha, beta, or sigma) are not inhibited by Delavirdine. |
| Mechanism of action | Delavirdine binds directly to viral reverse transcriptase (RT) and blocks the RNA-dependent and DNA-dependent DNA polymerase activities by disrupting the enzyme's catalytic site. |
| Absorption | Rapidly absorbed |
| Volume of distribution | Not Available |
| Protein binding | 98% |
| Metabolism | Hepatic |
| Route of elimination | Delavirdine is extensively converted to several inactive metabolites by cytochrome P450 3A (CYP3A). Delavirdine was excreted in the milk of lactating rats at a concentration three to five times that of rat plasma. |
| Half life | 5.8 hours |
| Clearance | Not Available |
| Toxicity | Major toxicity of delavirdine is rash and should be advised to promptly notify their physician should rash occur. The majority of rashes associated with delavirdine occur within 1 to 3 weeks after initiating treatment with delavirdine. The rash normally resolves in 3 to 14 days and may be treated symptomatically while therapy with delavirdine is continued. Any patient experiencing severe rash or rash accompanied by symptoms such as fever, blistering, oral lesions, conjunctivitis, swelling, muscle or joint aches should discontinue medication and consult a physician. |