TOLERABILITY OF ENECADIN (INN) IN ACUTE ISCHEMIC STROKE TRIAL - TEST- PHASE IIA : A multicentre, double-blind, randomised, placebo-controlled, dose-escalating parallel- group study to investigate the tolerability of enecadin (INN) in acute ischemic stroke - TEST

Start Date20 Apr 2007

Sponsor / Collaborator

Paion Deutschland GmbH

NCT00331721

/ TerminatedPhase 2

A Multicentre, Double-Blind, Randomised, Placebo-Controlled, Dose-Escalating Parallel-Group Study to Investigate the Tolerability of Enecadin (INN) in Acute Ischemic Stroke

The main objective of this study is to investigate the tolerability of enecadin in patients with acute ischemic stroke. Furthermore, the pharmacokinetics of enecadin in both male and female patients with acute ischemic stroke will be assessed. Efficacy trends will be evaluated up to day 30 post stroke.

Start Date01 May 2006

Sponsor / Collaborator

Paion Deutschland GmbH

100 Clinical Results associated with CAPN1 x CAPN2

100 Translational Medicine associated with CAPN1 x CAPN2

0 Patents (Medical) associated with CAPN1 x CAPN2

1,000

Literatures (Medical) associated with CAPN1 x CAPN2

31 Dec 2025·OncoImmunology

Calpain 2 regulates IL-1α secretion and inhibits tumor development via modulating calpain 1 expression in the tumor microenvironment

Article

Author: Teo, Huey Yee ; Chiu, Jing Wen ; Liu, Haiyan ; Lu, Jinhua ; Binte Hanafi, Zuhairah ; Mei, Yu ; Zhu, Ying ; Yong Lionel, Chew Chin

Tumor-promoting inflammation significantly impacts cancer progression, and targeting inflammatory cytokines has emerged as a promising therapeutic approach in clinical trials. Interleukin (IL)-1α, a member of the IL-1 cytokine family, plays a crucial role in both inflammation and carcinogenesis. How IL-1α is secreted in the tumor microenvironment has been poorly understood, and we previously showed that calpain 1 cleaves pro-IL-1α for mature IL-1α secretion, which exacerbates hepatocellular carcinoma by recruiting myeloid-derived suppressor cells. In this study, we report that calpain 2 also modulates IL-1α secretion. Notably, a deficiency in calpain 2 resulted in enhanced hepatocellular carcinoma development within an IL-1α-enriched tumor microenvironment. Further investigations revealed that calpain 2 deficiency increased calpain 1 expression, implying a compensatory mechanism between the two calpains. Mechanistically, calpain 2 deficiency led to increased expression of FoxO3, which is a forkhead transcription factor that promotes calpain 1 expression. Collectively, these results suggest that calpain 2 modulates calpain 1 expression, and therefore IL-1α secretion through the induction of FoxO3, offering novel potential therapeutic targets for cancer treatment.

03 Jan 2025·Science Advances

Determinants of increased muscle insulin sensitivity of exercise-trained versus sedentary normal weight and overweight individuals

Article

Author: Schrauwen-Hinderling, Vera ; Szendroedi, Julia ; Anadol-Schmitz, Evrim ; Weiss, Jürgen ; Pesta, Dominik ; Sarabhai, Theresia ; Phielix, Esther ; Lyu, Kun ; Habets, Ivo ; Roden, Michael ; Zaharia, Oana-Patricia ; Gaspar, Rafael Calais ; Op den Kamp, Yvo ; Trinks, Nina ; Schrauwen, Patrick ; Dewidar, Bedair ; Op den Kamp-Bruls, Yvonne M. H. ; Al-Hasani, Hadi ; Mastrototaro, Lucia ; Gancheva, Sofiya ; Strassburger, Klaus ; Shulman, Gerald I. ; Zhang, Dongyan ; Kupriyanova, Yuliya

The athlete’s paradox states that intramyocellular triglyceride accumulation associates with insulin resistance in sedentary but not in endurance-trained humans. Underlying mechanisms and the role of muscle lipid distribution and composition on glucose metabolism remain unclear. We compared highly trained athletes (ATHL) with sedentary normal weight (LEAN) and overweight-to-obese (OVWE) male and female individuals. This observational study found that ATHL show higher insulin sensitivity, muscle mitochondrial content, and capacity, but lower activation of novel protein kinase C (nPKC) isoforms, despite higher diacylglycerol concentrations. Notably, sedentary but insulin sensitive OVWE feature lower plasma membrane-to-mitochondria sn -1,2-diacylglycerol ratios. In ATHL, calpain-2, which cleaves nPKC, negatively associates with PKCε activation and positively with insulin sensitivity along with higher GLUT4 and hexokinase II content. These findings contribute to explaining the athletes’ paradox by demonstrating lower nPKC activation, increased calpain, and mitochondrial partitioning of bioactive diacylglycerols, the latter further identifying an obesity subtype with increased insulin sensitivity (NCT03314714).

01 Jan 2025·American Journal of Physiology-Lung Cellular and Molecular Physiology

Neutrophil elastase activates macrophage calpain as a mechanism for phagocytic failure

Article

Author: Ghio, Andrew J. ; Deshpande, Laxmikant S. ; Kummarapurugu, Apparao B. ; Zheng, Shuo ; Ma, Jonathan ; Voynow, Judith A.

Neutrophil elastase, a cystic fibrosis airway inflammation biomarker, increases macrophage Calpain activity, and Calpain inhibition partially restores the decreased phagocytosis in neutrophil elastase-challenged macrophages. Neutrophil elastase increases Calpain-2 protein, degrades the Calpain inhibitor, Calpastatin, and increases intracellular calcium as potential mechanisms of Calpain activation. This presents a novel mechanism for macrophage dysfunction relevant to cystic fibrosis.

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