Prospective evaluation of the efficacy, safety, and the optimal biomarker enrichment strategy for nangibotide, a TREM-1 inhibitor, in patients with septic shock: a double-blind, randomized, controlled, phase 2b trial. The Lancet Respiratory Medicine
Evaluation of the efficacy and safety of TREM-1 inhibition with nangibotide in patients with COVID19 receiving respiratory support: results of the ESSENTIAL randomized, double-blind trial. eClinicalMedicine
Increased sTREM-1 plasma concentrations are associated with poor clinical outcomes in patients with COVID-19. Bioscience Reports
sTREM-1 is a specific biomarker of TREM-1 pathway activation
Rationale and protocol for the efficacy, safety and tolerability of nangibotide in patients with septic shock (ASTONISH) phase IIb randomised controlled trial. BMJ Open
Potentiation of NETs release is novel characteristic of TREM-1 activation and the pharmacological inhibition of TREM-1 could prevent from the deleterious consequences of NETs release in sepsis. Cellular and Molecular Immunology
Nangibotide in patients with septic shock: a Phase 2a randomized controlled clinical trial. Intensive Care Medicine.
High STREM-1 levels and low monocyte HLA-DR expression are associated with nosocomial infections and mortality in septic shock patients. Critical Care
The SOFA score—development, utility and challenges of accurate assessment in clinical trials. Critical Care
Safety and pharmacodynamic activity of a novel TREM-1 pathway inhibitory peptide in septic shock patients: phase IIa clinical trial results. Intensive Care Medicine Experimental.
A first-in-man safety and pharmacokinetics study of nangibotide, a new modulator of innate immune response through TREM-1 receptor inhibition. British Journal of Clinical Pharmacology.
Review : TREM-1; Is It a Pivotal Target for Cardiovascular Diseases? Journal of Cardiovascular Development and Disease
TREM-1 multimerization is essential for its activation on monocytes and neutrophils. Cellular and Molecular Immunology.
Roche Sees « New Front in Critical Care Medicine » With CDx Deal Aimed at Septic Shock. GenomeWeb.
Targeted endothelial gene deletion of Triggering Receptor Expressed on Myeloid cells-1 protects mice during septic shock. Cardiovasc Res.
TREM-1 SNP rs2234246 regulates TREM-1 protein and mRNA levels and is associated with plasma levels of L-selectin. PLoS ONE.
Triggering Receptor Expressed on Myeloid cells-1: a new player in platelet aggregation. Thrombosis and Haemostasis.
LR12-peptide quantitation in whole blood by RP-HPLC and intrinsic fluorescence detection: Validation and pharmacokinetic study. Biomedical Chromatography.
TREM-1 and its potential ligands in non-infectious diseases: from biology to clinical perspectives. Pharmacological Research
Genetic and Pharmacological Inhibition of TREM-1 Limits the Development of Experimental Atherosclerosis. Journal of the American College of Cardiology. Inotrem collaborated in this study with Pr Hafid Ait Oufella from team 5 of the the Paris Cardiovascular Research Center (PARCC) to demonstrate the role of TREM-1 in the development of atherosclerosis.
The Triggering Receptor Expressed on Myeloid cells-1: A new player during acute myocardial infarction. Pharmacological Research
Pharmacological inhibition of the triggering receptor expressed on myeloid cells-1 limits reperfusion injury in a porcine model of myocardial infarction. ESC Heart Failure.
TREM-1 Mediates Inflammatory Injury and Cardiac Remodeling Following Myocardial Infarction. Circulation Research. Inotrem published here new results demonstrating the role of TREM-1 during the pathophysiology of acute myocardial infarction. We are really proud of this disruptive paper showing for the first time the role of TREM-1 in cardiovascular setting
Attenuation of responses to endotoxin by the triggering receptor expressed on myeloid cells-1 inhibitor LR12 in nonhuman primate. Anesthesiology
Effects of a TREM-like transcript 1-derived peptide during hypodynamic septic shock in pigs. Shock.
Soluble TREM-like transcript-1 regulates leukocyte activation and controls microbial sepsis. The Journal of Immunology.
Triggering receptor expressed on myeloid cells-1 as a new therapeutic target during inflammatory diseases. Self/Non-Self.