ReviewDrugs2007
Maraviroc.
Review in Drugs, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 59 citations in OpenAlex.
- Deadbolt Drug Discovery: Locking the Door to Class 1 Viral Entry by Small Molecules.ACS infectious diseases · 2026Review
- Chemokine receptor type-5: a key regulator of immunity, disease pathogenesis, and emerging therapeutic target.Inflammopharmacology · 2025Review
- Single-cell transcriptomics unravels the early immune landscape of renal allograft rejection and nominates Ccl3-Ccr5 as a therapeutic target.Frontiers in immunology · 2025Article
- CXCR4 Is a Potential Target for Anti-HIV Gene Therapy.International journal of molecular sciences · 2024Review
- Osteoid cell-derived chemokines drive bone-metastatic prostate cancer.Frontiers in oncology · 2023Review
- Palladium-catalyzed difluoroalkylative carbonylation of styrenes toward difluoropentanedioates.Chemical science · 2022Article
- Exploring New Scaffolds for the Dual Inhibition of HIV-1 RT Polymerase and Ribonuclease Associated Functions.Molecules (Basel, Switzerland) · 2021Article
- Review
- Critical View of Novel Treatment Strategies for Glioblastoma: Failure and Success of Resistance Mechanisms by Glioblastoma Cells.Frontiers in cell and developmental biology · 2021Review
- Binding Characterization of GPCRs-Modulator by Molecular Complex Characterizing System (MCCS).ACS chemical neuroscience · 2020Article
- A High-Throughput HIV-1 Drug Screening Platform, Based on Lentiviral Vectors and Compatible with Biosafety Level-1.Viruses · 2020Article
- The dawn of precision medicine in HIV: state of the art of pharmacotherapy.Expert opinion on pharmacotherapy · 2018Review
- Maraviroc decreases CCL8-mediated migration of CCR5(+) regulatory T cells and reduces metastatic tumor growth in the lungs.Oncoimmunology · 2016Article
- Chemokine co-receptor usage in HIV-1-infected treatment-naïve voluntary counselling and testing clients in Southern Taiwan.BMJ open · 2015Article
- Placental transfer of maraviroc in an ex vivo human cotyledon perfusion model and influence of ABC transporter expression.Antimicrobial agents and chemotherapy · 2013Article
- Deep sequencing to infer HIV-1 co-receptor usage: application to three clinical trials of maraviroc in treatment-experienced patients.The Journal of infectious diseases · 2011Article
- Review
- Drug-class specific impact of antivirals on the reproductive capacity of HIV.PLoS computational biology · 2010Article
- [CCR5 antagonists and HIV-1 infection: Bases and consequences of this therapeutic approach].Antibiotiques (Paris, France : 1999) · 2010Article
- HIV entry inhibitors and their potential in HIV therapy.Medicinal research reviews · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maraviroc is a specific, slowly reversible, noncompetitive, small-molecule antagonist of the CCR5 chemokine receptor, which also serves as an HIV-1 coreceptor. By acting as an antagonist at the CCR5 coreceptor, maraviroc inhibits HIV-1 from entering host cells. Clinical data for maraviroc are available from two large, well designed, ongoing phase IIb/III trials (MOTIVATE-1 and MOTIVATE-2) conducted in patients infected with R5-tropic HIV-1 who had previously received at least one agent from three of the four classes of antiretroviral drugs and/or were triple-class resistant. According to 24-week interim results of the MOTIVATE-1 and -2 trials, a significantly greater reduction in viral load occurred in patients receiving maraviroc 150 or 300mg (depending on optimised background therapy [OBT]) twice daily plus OBT compared with placebo plus OBT. This significant difference was maintained at 48 weeks in MOTIVATE-1. In the MOTIVATE-1 and -2 trials, a significantly greater proportion of patients receiving maraviroc plus OBT achieved an HIV-1 RNA level <400 and <50 copies/mL compared with those receiving placebo plus OBT. In addition, the CD4+ cell count was increased to a significantly greater extent with maraviroc plus OBT compared with placebo plus OBT. The 48-week results of MOTIVATE-1 also report a significant difference in favour of maraviroc for all these endpoints. In general, maraviroc at dosages of up to 300mg twice daily was well tolerated in treatment-experienced patients infected with R5-tropic HIV-1.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.