Molecular Formula | C20H21FN6O5 |
Molar Mass | 444.42 |
Density | 1.46±0.1 g/cm3(Predicted) |
Melting Point | 216 °C(Solv: isopropanol (67-63-0)) |
Solubility | DMSO 89 mg/mL Water <1 mg/mL Ethanol <1 mg/mL |
Appearance | Solid |
Color | White to Light Beige |
pKa | 4.50±1.00(Predicted) |
Storage Condition | -20°C Freezer |
Refractive Index | 1.65 |
Use | A potent integrase strand transfer inhibitor for (PFV) IN. |
In vitro study | PFV integration carries IN replaced by S217H, and then the sensitivity to Raltegravir is reduced by 10 times, and the IC50 is 900 nM. PFV IN has 10% WT activity and is inhibited by Raltegravir, IC50 is 200 nM, indicating that compared with WT IN, it is more effective than integrase (IN) chain transfer inhibitor (INSTI) the sensitivity is reduced by about 2 times. The sensitivity of S217Q PFV IN to Raltegravir is at least similar to that of the WT enzyme. Raltegravir is metabolized by glucuronidation, not by the liver. Raltegravir was effective at HIV-1 in vitro on human T-lymphocyte cultures, inhibiting up to 95% at a concentration of 31±20 nM. Raltegravir acts on CEMx174 cells and is also effective on HIV-2, with an IC 95 of 6 nM. Raltegravir is metabolized mainly by glucuronidation. The strong inducer of glucuronidase, UGT1A1, significantly reduced Raltegravir concentrations. Raltegravir weakly inhibits hepatic cytochrome P450. Raltegravir did not induce CYP3A4 RNA expression or cyp3a4-dependent testosterone 6-β-hydroxylase activity. In the presence of magnesium and calcium, the proliferation of Raltegravir cells decreased. Raltegravir and the related HIV-1 integrase (IN) strand transfer inhibitor (INTIS) efficiently block viral replication. Effect of Raltegravir on human lymphoid CD4 in acute infection |
In vivo study | Raltegravir acts on non-human primates carrying SIVmac251 infection to enhance viral-immunity. When Raltegravir was administered alone to non-human primates, viral loads were undetectable. |