Maraviroc (UK-427,857), a Potent, Orally Bioavailable, and Selective Small-Molecule Inhibitor of Chemokine Receptor CCR5 with Broad-Spectrum Anti-Human Immunodeficiency Virus Type 1 Activity
By P. Dorr, M. Westby, Susan Dobbs, P. Griffin, B. Irvine, M. Macartney, J. Mori, G. Rickett, C. Smith-Burchnell, C. Napier and 6 more. Antimicrobial Agents and Chemotherapy, 2005
1,170 citations recorded by the source corpus.
Subfields: Immunology, Infectious Diseases, Virology
View Paper: https://www.semanticscholar.org/paper/fafec5fef3a404060fb31f274c587b4b87d090af
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Citations in the corpus
- Staphylococcus aureus Leukocidin LukED and HIV-1 gp120 Target Different Sequence Determinants on CCR5 (2016, background): “MVC, the small-molecule entry inhibitor of CCR5-tropic HIV-1, was demonstrated to block both HIV infection (22) and LukED intoxication (5).”
- International Union of Basic and Clinical Pharmacology. LXXXIX. Update on the Extended Family of Chemokine Receptors and Introducing a New Nomenclature for Atypical Chemokine Receptors (2014, neutral): “Maraviroc is potent against all known CCR5-tropic HIV-1 strains, with a mean IC90 value of 2 nM in antiviral assays (Dorr et al., 2005), and acts by an allosteric mechanism, suggesting that the transmembrane cavity remains accessible for maraviroc in CCL3-bound and gp120-bound CCR5 (Garcia-Perez”
- HIV-1 antiretroviral drug therapy. (2012, background): “Thus far, three antagonists (VCV, MVC, and Aplaviroc) have been shown to inhibit virus replication in humans (Dorr et al. 2005).”
- Role of the CXCL8-CXCR1/2 Axis in Cancer and Inflammatory Diseases (2017, neutral): “Currently, Maraviroc, a CCR5 antagonist used for HIV-1 infection, and Plerixafor, a CXCR4 antagonist, used as a hematopoietic stem cell mobilizer in patients with non-Hodgkin lymphoma and multiple myeloma, are the only two FDA approved chemokine receptor inhibitors [7].”
- HIV: cell binding and entry. (2012, background): “Maraviroc is a small-molecule allosteric inhibitor that binds within the CCR5 transmembrane cavity resulting in conformational changes in the extracellular loop domains of the chemokine receptor that interact with Env (Dorr et al. 2005).”