A Double-Blind, Placebo-Controlled Phase I/II Study in Patients With Mild to Moderate Ulcerative Colitis Treated With GI-270384X, an Oral ICAM-1 and E-Selectin Inhibitor

The aim of this double blind, placebo controlled, study is to evaluate activity consistent with efficacy provided by 14 days administration of GI270384X, and to provide preliminary pharmacokinetics and safety/tolerability of 14 days administration of GI270384X in patients with mild to moderate active ulcerative colitis (UC).

Start Date01 Dec 2004

Sponsor / Collaborator

GSK Plc

100 Clinical Results associated with E-sel x ICAM-1

100 Translational Medicine associated with E-sel x ICAM-1

0 Patents (Medical) associated with E-sel x ICAM-1

3,578

Literatures (Medical) associated with E-sel x ICAM-1

31 Dec 2025·Renal Failure

Endothelial injury is one of the risk factors for the progression of vascular calcification in patients receiving maintenance dialysis

Article

Author: Yan, Xiao-Wei ; Qiu, Fang-Xin ; Li, Zuo-Lin ; Yao, Dan-Dan ; Zhou, Yan

BACKGROUNDVascular calcification is common and progressive in patients with chronic kidney disease. However, the risk factors associated with the progression of vascular calcification in patients receiving maintenance dialysis have not been fully elucidated. Here, we aimed to evaluate vascular calcification and identify the factors associated with its progression in patients receiving maintenance hemodialysis.METHODSThis is a prospective longitudinal study that included 374 patients receiving maintenance hemodialysis. The participants received assessments of coronary artery calcification (CAC) and abdominal aortic calcification (AAC), as measured by computed tomography. After the baseline investigation, a 2 years follow-up was performed. We also detected the markers of endothelial injury [E-selectin and soluble intercellular adhesion molecule-1 (sICAM-1)]. Finally, the risk factors affecting the CAC and AAC progression were examined by multivariate logistic regression analysis.RESULTSAmong 374 patients, the median [interquartile range (IQR)] age was 54.0 (40.0-62.0) years; 59.9% of patients were male. The median (IQR) follow-up time was 1.9 (1.8-2.0) years for all patients. By the end of 2-year follow-up, progression of vascular calcification (including CAC and AAC) was observed in 58.0% of patients. Further, compared with the patients without progression of vascular calcification, the endothelial injury (including E-selectin and sICAM-1) of patients with progression of vascular calcification was markedly enhanced. Moreover, after adjustment for the confounders, endothelial injury was a risk factor for the progression of vascular calcification.CONCLUSIONThe present study indicated that endothelial injury is one of the risk factors for the progression of vascular calcification in patients receiving maintenance hemodialysis.

01 Dec 2025·Inflammation Research

Endocan as a marker of endotheliitis in COVID-19 patients: modulation by veno-venous extracorporeal membrane oxygenation, arterial hypertension and previous treatment with renin–angiotensin–aldosterone system inhibitors

Article

Author: Teixeira-Santos, Luísa ; Morato, Manuela ; Sarmento, António ; Tavares, Margarida ; Bessa, João ; Silva-Pereira, Carolina ; Sousa, Teresa ; Paiva, José-Artur ; Albino-Teixeira, António ; Pereira-Terra, Patrícia ; Pinho, Dora ; Martins, Sandra ; Alves, David ; Dias, Cláudia Camila ; Reina-Couto, Marta ; Roncon-Albuquerque, Roberto ; Guimarães, João T

AbstractBackground and aimsEndocan has been scarcely explored in COVID-19, especially regarding its modulation by veno-venous extracorporeal membrane oxygenation (VV-ECMO), hypertension or previous renin–angiotensin–aldosterone system (RAAS) inhibitors treatment.We compared endocan and other endotheliitis markers in hospitalized COVID-19 patients and assessed their modulation by VV-ECMO, hypertension and previous RAAS inhibitors treatment.Material and methodsSerum endocan, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin were measured in “severe” (n = 27), “critically ill” (n = 17) and “critically ill on VV-ECMO” (n = 17) COVID-19 patients at admission, days 3–4, 5–8 and weekly thereafter, and in controls (n = 23) at a single time point.ResultsAdmission endocan and VCAM-1 were increased in all patients, but “critically ill on VV-ECMO” patients had higher endocan and E-Selectin. Endocan remained elevated throughout hospitalization in all groups. “Severe” and “critically ill” hypertensive patients or previously treated with RAAS inhibitors had higher endocan and/or VCAM-1, but in VV-ECMO patients the raised endocan values seemed unrelated with these factors. Among all COVID-19 hypertensive patients, those with previous RAAS inhibitors treatment had higher endocan.ConclusionsIn our study, endocan stands out as the best marker of endotheliitis in hospitalized COVID-19 patients, being upregulated by VV-ECMO support, hypertension and previous RAAS inhibitor treatment.

01 Jun 2025·Environmental Pollution

In vitro effects of aged low-density polyethylene micro(nano)plastic particles on human airway epithelial cells

Article

Author: Jelinskas, Tadas ; Pajarskienė, Justina ; Vailionytė, Agnė ; Aldonytė, Rūta ; Uogintė, Ieva ; Ignatjev, Ilja ; Bagdonas, Edvardas ; Byčenkienė, Steigvilė

Airborne micro(nano)plastic (MNP) pollution has emerged as a major global concern due to its increasingly worrying adverse health effects. Environmental weathering and UV irradiation of plastic waste, together with tire wear, generate airborne MNPs with irregular shapes and varied sizes, with low-density polyethylene (LDPE) being the predominant plastic type. However, knowledge of MNPs' toxicological effects remains scarce, as current in vitro research mainly focuses on commercial polystyrene beads. In this study, we investigated for the first time the toxicological effects of environmentally relevant aged LDPE MNPs on human bronchial epithelial cells (BEAS-2B). UV-aged LDPE fragments of irregular sizes and shapes were used to mimic real atmospheric particles, and BEAS-2B cells were exposed to 10-1000 μg/cm² of LDPE MNPs. Our results showed that MNPs were internalized by BEAS-2B cells and promoted epithelial-to-mesenchymal transition (EMT), characterized by reduced β-catenin and increased vimentin expression, enhanced motility, and disturbed cell cycle. Moreover, exposure to aged LDPE MNPs significantly increased intracellular ROS levels and reduced cell proliferation rate at the highest dose. LDPE MNPs triggered oxidative stress in BEAS-2B cells through activation of the NRF2 signaling pathway, with impaired autophagic flux indicated by increased expression of p62 and LC3A/B. Importantly, LDPE MNP exposure significantly increased the secretion of pro-inflammatory mediators (CD62E, CD62P, ICAM-1, IL-6, IL-8), accompanied by suppressive effects on mitochondrial respiration and glycolytic function at 1000 μg/cm². Taken together, our findings suggest that inhalation of LDPE MNPs could impact the morphology and function of the human airway epithelium and respiratory health in general.

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