ArticleInflammatory bowel diseases2018
Activation of LANCL2 by BT-11 Ameliorates IBD by Supporting Regulatory T Cell Stability Through Immunometabolic Mechanisms.
Article in Inflammatory bowel diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Safety, Tolerability, and Pharmacokinetics of NIM-1324 an Oral LANCL2 Agonist in a Randomized, Double-Blind, Placebo-Controlled Phase I Clinical Trial.Clinical and translational science · 2025Trial
- Six promising drug repurposing candidates for Alzheimer's disease and their sex-specific mechanisms and efficacy.Neural regeneration research · 2026Article
- Loss of LanC-like proteins delays post-injury regeneration of aging skeletal muscles.bioRxiv : the preprint server for biology · 2026Article
- BT-11 targets the LANCL2 pathway to attenuate cognitive deficits and hippocampal pathology in Alzheimer's transgenic rats.Scientific reports · 2025Article
- Recent advances in the therapeutics and modes of action of a range of agents used to treat ulcerative colitis and related inflammatory conditions.Inflammopharmacology · 2025Review
- Protective Effects of Octyl Gallate Against Deoxynivalenol-Induced Colon Inflammation: Insights from Proteomic and Metabolomic Analyses.Environment & health (Washington, D.C.) · 2025Article
- Nuclear transport of phosphorylated LanCL2 promotes invadopodia formation and tumor progression of glioblastoma by activating STAT3/Cortactin signaling.Journal of advanced research · 2025Article
- Abscisic acid signaling through LANCL2 and PPARγ induces activation of p38MAPK resulting in dormancy of prostate cancer metastatic cells.Oncology reports · 2024Article
- New Insights into the LANCL2-Pharmaceutics · 2023Article
- Chemistry and biology of enzymes in protein glutathionylation.Current opinion in chemical biology · 2023Review
- Computational modeling of complex bioenergetic mechanisms that modulate CD4+ T cell effector and regulatory functions.NPJ systems biology and applications · 2022Article
- First-in-class topical therapeutic omilancor ameliorates disease severity and inflammation through activation of LANCL2 pathway in psoriasis.Scientific reports · 2021Article
- Identification of prognostic values defined by copy number variation, mRNA and protein expression of LANCL2 and EGFR in glioblastoma patients.Journal of translational medicine · 2021Article
- Immunological Impact of Intestinal T Cells on Metabolic Diseases.Frontiers in immunology · 2021Review
- Phytohormone Abscisic Acid Improves Memory Impairment and Reduces Neuroinflammation in 5xFAD Mice by Upregulation of LanC-Like Protein 2.International journal of molecular sciences · 2020Article
- Goals in Nutrition Science 2020-2025.Frontiers in nutrition · 2020Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
backgroundInflammatory bowel disease (IBD) afflicts 5 million people and is increasing in prevalence. There is an unmet clinical need for safer and effective treatments for IBD. The BT-11 is a small molecule oral therapeutic that ameliorates IBD by targeting lanthionine synthetase C-like 2 (LANCL2) and has a benign safety profile in rats.
methodsMdr1a-/-, dextran sodium sulphate , and adoptive transfer mouse models of colitis were employed to validate therapeutic efficacy and characterize the mechanisms of therapeutic efficacy of BT-11. In vitro cultures of CD4+ T cell differentiation and human peripheral blood mononuclear cells from Crohn's disease patients were used to determine its potential for human translation.
resultsBT-11 reduces inflammation in multiple mouse models of IBD. Oral treatment with BT-11 increases the numbers of lamina propria regulatory T cells (Tregs) in a LANCL2-dependent manner. In vitro, BT-11 increases the differentiation in Treg phenotypes, the upregulation of genes implicated in Treg cell stability, and conditions Treg cells to elicit greater suppressive actions. These immunoregulatory effects are intertwined with the ability of BT-11 to regulate late stage glycolysis and tricarboxylic acid cycle. Immunometabolic mechanistic findings translate into human peripheral blood mononuclear cells from healthy individuals and Crohn's disease patients.
conclusionsBT-11 is a safe, efficacious oral therapeutic for IBD with a human translatable mechanism of action that involves activation of LANCL2, immunometabolic modulation of CD4+ T cell subsets leading to stable regulatory phenotypes in the colonic LP.
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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.