ArticleImmune network2015
The Anti-inflammatory Effect of GV1001 Mediated by the Downregulation of ENO1-induced Pro-inflammatory Cytokine Production.
Article in Immune network, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The trial behind it
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Who cites it
29 citing papers in PubMed, 36 citations in OpenAlex.
- Enolase-1 and Inflammation.Biomolecules · 2026Review
- ENO1 as an Immunoregulatory Hub in Cancer: Mechanisms and Translational Implications.Biomolecules · 2026Review
- Review
- Article
- Targeting Telomerase in Cancer: Vaccine-Based Strategies, Clinical Evidence, and Synergy with Immunotherapy.Diseases (Basel, Switzerland) · 2026Review
- Astragaloside IV Alleviates Ulcerative Colitis Progression by Inhibiting WDR5-Mediated ENO1 H3K4me3 Modification.The Kaohsiung journal of medical sciences · 2025Article
- Targeting Kupffer Cell Enolase 1 Attenuates Liver Inflammation and Injury in Hemorrhagic Shock.International journal of molecular sciences · 2025Article
- A randomized, active-controlled, multicenter, phase 3 clinical trial to evaluate the efficacy and safety of GV1001 in patients with benign prostatic hyperplasia.Prostate international · 2025Article
- hTERT Peptide Fragment GV1001 Prevents the Development ofInternational journal of molecular sciences · 2024Article
- The Impaired Wound Healing Process Is a Major Factor in Remodeling of the Corneal Epithelium in Adult and Adolescent Patients With Keratoconus.Investigative ophthalmology & visual science · 2023Article
- Article
- Retrospective Analysis of the Clinical Characteristics of Patients with Breast Cancer Treated with Telomerase Peptide Immunotherapy Combined with Cytotoxic Chemotherapy.Breast cancer (Dove Medical Press) · 2023Article
- Identification of Cancer Cells in the Human Body by Anti-Telomerase Peptide Antibody: Towards the Isolation of Circulating Tumor Cells.International journal of molecular sciences · 2022Article
- The essential roles of mJournal of experimental & clinical cancer research : CR · 2022Article
- Colorectal cancer cell intrinsic fibroblast activation protein alpha binds to Enolase1 and activates NF-κB pathway to promote metastasis.Cell death & disease · 2021Article
- Article
- Outcomes of Peptide Vaccine GV1001 Treatment in a Murine Model of Acute Noise-Induced Hearing Loss.Antioxidants (Basel, Switzerland) · 2020Article
- Telomerase Biology Associations Offer Keys to Cancer and Aging Therapeutics.Current aging science · 2020Review
- Article
- Telomerase-Targeted Cancer Immunotherapy.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GV1001 is a peptide derived from the human telomerase reverse transcriptase (hTERT) sequence that is reported to have anti-cancer and anti-inflammatory effects. Enolase1 (ENO1) is a glycolytic enzyme, and stimulation of this enzyme induces high levels of pro-inflammatory cytokines from concanavalin A (Con A)-activated peripheral blood mononuclear cells (PBMCs) and ENO1-expressing monocytes in healthy subjects, as well as from macrophages in rheumatoid arthritis (RA) patients. Therefore, this study investigated whether GV1001 downregulates ENO1-induced pro-inflammatory cytokines as an anti-inflammatory peptide. The results showed that GV1001 does not affect the expression of ENO1 in either Con A-activated PBMCs or RA PBMCs. However, ENO1 stimulation increased the production of pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6, and these cytokines were downregulated by pretreatment with GV1001. Moreover, p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB were activated when ENO1, on the surface of Con A-activated PBMCs and RA PBMCs, was stimulated, and they were successfully suppressed by pre-treatment with GV1001. These results suggest that GV1001 may be an effective anti-inflammatory peptide that downregulates the production of pro-inflammatory cytokines through the suppression of p38 MAPK and NF-κB activation following ENO1 stimulation.
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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.