HCV infection is a major cause of mortality worldwide. HCV-related deaths also represent a leading cause of mortality in HIV-coinfected individuals. Telaprevir is an NS3/4A protease inhibitor approved for the treatment of chronic HCV genotype 1 infection in adults in combination with pegylated interferon and ribavirin. Telaprevir-based treatment has been shown to increase rates of sustained viral response in HCV genotype-1-monoinfected patients, and studies in HCV-HIV-coinfected patients are ongoing. Drug-drug interactions of telaprevir with antiretroviral drugs were investigated in a series of studies in healthy subjects. This review summarizes the results of interaction studies with low-dose ritonavir, ritonavir-boosted HIV protease inhibitors (atazanavir, darunavir, fosamprenavir and lopinavir), efavirenz, etravirine, rilpivirine, tenofovir disoproxil fumarate and raltegravir.
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http://dx.doi.org/10.3851/IMP2527 | DOI Listing |
Arch Biochem Biophys
January 2025
Department of Laboratory Medicine, The Third Xiangya Hospital of Central South University, Changsha, 410013, China. Electronic address:
Iron overload-dependent ferroptosis is believed to contribute to the brain injury of ischemia/reperfusion (I/R), whereas toll-like receptor 4 (TLR4) can exert pro-ferroptosis effect via inhibiting the glutathione peroxidase 4 (GPX4) level, but the mechanisms behind these phenomenon are not fully elucidated. Tumor necrosis factor receptor correlated factor 3-interaction Jun amino-terminal kinase [JNK]-activating modulator (T3JAM) can activate specific molecule and its downstream signaling pathways, including TLR4. This study aims to explore whether targeting T3JAM can reduce I/R-induced ferroptosis in brain via downregulating TLR4.
View Article and Find Full Text PDFInt Immunopharmacol
November 2024
Department of Gastroenterology, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou City, Gansu Province, China; Key Laboratory of Digestive Diseases, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou City, Gansu Province, China. Electronic address:
ACS Chem Neurosci
September 2023
Department of Laboratory Medicine, The Third Xiangya Hospital of Central South University, Changsha 410013, China.
Mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) has been confirmed to contribute to brain injury in ischemic stroke via promoting excitotoxicity and necroptosis. Telaprevir, a hepatitis C virus protease inhibitor, is predicted to be a potential MALT1 inhibitor. Here, we showed that telaprevir protected against cerebral ischemic injury via inhibiting MALT1, thereby preventing glutamate receptor ionotropic NMDA 2B (GluN2B) activation, limiting calcium overload, and suppressing necroptosis.
View Article and Find Full Text PDFComput Biol Med
January 2023
Department of Botany, University of Calcutta, Kolkata, West Bengal, India. Electronic address:
Background: The main protease is an important structural protein of SARS-CoV-2, essential for its survivability inside a human host. Considering current vaccines' limitations and the absence of approved therapeutic targets, M may be regarded as the potential candidate drug target. Novel fungal phytocompound Astrakurkurone may be studied as the potential M inhibitor, considering its medicinal properties reported elsewhere.
View Article and Find Full Text PDFMol Oncol
October 2022
Department of Sciences, Section Biomedical Sciences and Technology, University Roma TRE, Italy.
Previously, we found that telaprevir (Tel), the inhibitor of hepatitis C virus NS3/4A serine protease, reduces estrogen receptor α (ERα) content at the transcriptional level without binding to the receptor, prevents ERα transcriptional activity, and inhibits basal and 17β-estradiol (E2)-dependent cell proliferation in different breast cancer (BC) cell lines. Here, we further characterize the Tel action mechanisms on ERα levels and function, identify a possible molecular target of Tel in BC cells, and evaluate Tel as an antiproliferative agent for BC treatment. Tel-dependent reduction in ERα levels and function depends on a Tel-dependent decrease in FOXA1 levels and activity.
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