Latest research on Indinavir

A potent and specific HIV protease inhibitor that appears to have good oral bioavailability. [PubChem]

Latest findings

Furthermore, Ethanol exposure significantly decreased the IC50 values of Amprenavir, Darunavir, and nelfinavir but robustly elevated the IC50 of Indinavir and Ritonavir [12, 13], suggesting a differential impact of Ethanol on the binding and bio-transformation of protease inhibitors. [source, 2016]
For example, Ritonavir, Indinavir, and saquinavir inhibit CYP3A4 at the IC50 values of 0.034, 0.43, and 2.14 μM [36]. [source, 2016]
Similar to these findings we have previously reported that Ethanol significantly alters the IC50 for the protease inhibitors Indinavir and Ritonavir by perhaps facilitating the CYP3A4 and protease inhibitors interaction through hydrogen bonding and hydrophobic interactions [39]. [source, 2016]
To verify the accuracy of the employed docking methods, we first selected four known inhibitors for these enzymes (Physostigmine, Indinavir, epalrestat and Celecoxib, Fig. 1) as reference molecules. [source, 2016]
We also examined the effect of Methamphetamine on spectral binding of two type II PIs (Ritonavir and Indinavir) with CYP3A4. [source, 2016]
Methamphetamine significantly decreased the δAmax of Ritonavir (0.0038 ± 0.0003 vs. 0.0055 ± 0.0003) but didn’t affect Indinavir (0.0039 ± 0.0002 vs. 0.0044 ± 0.0002) (Fig 6, Table 2). [source, 2016]
However, Methamphetamine significantly decreased the KD values of both Ritonavir and Indinavir by approximately 33% and 50%, respectively (0.043 ± 0.0001 vs. 0.065 ± 0.001 for Ritonavir and 0.086 ± 0.01 vs. 0.174 ± 0.03 μM for Indinavir) (Table 2). [source, 2016]
Indinavir docking into CYP3A4 showed a slight decrease in the average score of major cluster in the presence of Methamphetamine both binding modes (Table 3). [source, 2016]
It is likely that Methamphetamine binding causes a conformation change in the active site of CYP3A4 that leads to increased affinity with Ritonavir and Indinavir. [source, 2016]
This is possibly because our participants were just on first-line therapy including NRTI’s and NNRTI’s with no PI while participants of the former study were on antiretroviral therapy including a PI (Indinavir). [source, 2016]