A Multi-Center, Randomized, Double-Blind, Parallel, Placebo-Controlled, Phase III Clinical Study to Evaluate Efficacy and Safety of SP-8203 (Otaplimastat) in Patients with Acute Ischemic Stroke Requiring Thrombolytic Therapy As Standard of Care

This clinical study is designed to evaluate the efficacy and safety of the combination therapy of SP-8203 (otaplimastat) and thrombolytic standard of care in acute ischemic stroke patient.
As a standard of care, thrombolytic therapy (for instance, recombinant tissue plasminogen activator) will be administered. When reperfusion is not achieved in spite of thrombolytic therapy, endovascular therapy can be performed.

Start Date30 Dec 2024

Sponsor / Collaborator

Shin Poog Pharmaceutical Co., Ltd.

NCT04479449 / CompletedPhase 2

A Prospective, Randomized, Double-blind Phase 2b Clinical Trial to Investigate the Efficacy and Safety of SP-8203 in Patients With Acute Ischemic Stroke Requiring Recombinant Tissue Plasminogen Activator (rtPA) Standard of Care

This clinical trial is designed to evaluate the efficacy and safety of the combination therapy of SP-8203 (Otaplimastat) and recombinant tissue Plasminogen Activator (rtPA) standard of care. In this clinical trial, rtPA will be injected intravenously using an infusion device. If reperfusion is not occur in spite of rtPA therapy, endovascular therapy can be performed.

Start Date18 Mar 2019

Sponsor / Collaborator

Shin Poog Pharmaceutical Co., Ltd.

NCT02787278 / CompletedPhase 2

A Prospective, Randomized, Double-blinded Phase IIa Clinical Trial to Investigate the Safety and Efficacy of Two Doses of SP-8203 in Patients With Ischemic Stroke Requiring rtPA Standard of Care

The current study aims to evaluate the safety of SP-8203, designing in two stages (stage-1, stage-2) to evaluate the safety and efficacy of the combination therapy of SP-8203 and rtPA for the occurrence of cerebral hemorrhage in patients with acute ischemic stroke receiving rtPA standard of care.

Start Date05 Jun 2016

Sponsor / Collaborator

Shin Poog Pharmaceutical Co., Ltd.

100 Clinical Results associated with Reactive oxygen species x SOD1

100 Translational Medicine associated with Reactive oxygen species x SOD1

0 Patents (Medical) associated with Reactive oxygen species x SOD1

Literatures (Medical) associated with Reactive oxygen species x SOD1

01 Nov 2023·Shock

CEBPD REGULATES OXIDATIVE STRESS AND INFLAMMATORY RESPONSES IN HYPERTENSIVE CARDIAC REMODELING

Article

Author: Zhang, Rongyi ; Hu, Jilin ; Deng, Jianping ; Zhao, Jinghong

ABSTRACTHypertension seems to inevitably cause cardiac remodeling, increasing the mortality of patients. This study aimed to explore the molecular mechanism of CCAAT/enhancer-binding protein delta (CEBPD)–mediated oxidative stress and inflammation in hypertensive cardiac remodeling. The hypertensive murine model was established through angiotensin-II injection, and hypertensive mice underwent overexpressed CEBPD vector injection, cardiac function evaluation, and observation of histological changes. The cell model was established by angiotensin-II treatment and transfected with overexpressed CEBPD vector. Cell viability and surface area and oxidative stress (reactive oxygen species/superoxide dismutase/lactate dehydrogenase/malondialdehyde) were assessed, and inflammatory factors (TNF-α/IL-1β/IL-6/IL-10) were determined bothin vivoandin vitro. The levels of CEBPD, miR-96-5p, inositol 1,4,5-trisphosphate receptor 1 (IP3R), natriuretic peptide B, and natriuretic peptide A, collagen I, and collagen III in tissues and cells were determined. The binding relationships of CEBPD/miR-96-5p/IP3R 3′ untranslated region were validated. CEBPD was reduced in cardiac tissue of hypertensive mice, and CEBPD upregulation improved cardiac function and attenuated fibrosis and hypertrophy, along with reductions of reactive oxygen species/lactate dehydrogenase/malondialdehyde/TNF-α/IL-1β/IL-6 and increases in superoxide dismutase/IL-10. CEBPD enriched on the miR-96-5p promoter to promote miR-96-5p expression, whereas CEBPD and miR-96-5p negatively regulated IP3R. miR-96-5p silencing/IP3R overexpression reversed the alleviative role of CEBPD overexpression in hypertensive mice. In summary, CEBPD promoted miR-96-5p to negatively regulate IP3R expression to inhibit oxidative stress and inflammation, thereby alleviating hypertensive cardiac remodeling.

01 Jun 2022·Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan

Efficacy of phospholipid complex of flavonoids from persimmon leaves on atherosclerosis, and possible mechanism.

Article

Author: Yi, Liu ; Chengwang, Tian ; Song, Jin ; Jinpeng, Chen ; Xiaohong, Gai ; Kexia, Zhang ; Tao, Ren

OBJECTIVETo investigate the efficacy of phospholipid complex of flavonoids from persimmon leaves (PLF-PC) on atherosclerosis, and to study its mechanism behind the action.METHODSTo clarify the constituents of the flavonoids from persimmon leaves (PLF), an ultra-performance liquid chromatography/quadrupole-time-of-flight mass spectrometry method was established. To enhance the anti-atherosclerotic effect of PLF, a newly emerging approach based on the combination of phospholipid complexation technique was employed. PLF-PC was prepared by the solvent-evaporation method then characterized using Fourier transform infrared spectroscopy, Powder X-Ray Diffractometry and Scanning electron microscopy. A model of oxidized low-density lipoprotein-induced injury on human umbilical vein endothelial cells was established to investigate the anti-atherosclerotic effect of PLF-PC versus PLF. The levels of nitric oxide, endothelial nitric oxide synthase, intracellular adhesion molecule-1, reactive oxygen species, superoxide dismutase, tumor necrosis factor-αand nuclear factor-κB were observed assay kits.RESULTSA total of 31 compounds were identified in PLF. PLF-PC showed better anti-atherosclerotic power compared with PLF, moreover, enzyme linked immune-osorbent assay analysis showed that the PLF-PC may effect on endothelial dysfunction and atherosclerosis antioxidant-related mechanisms.CONCLUSIONSOur findings elucidated that PLF-PC significantly enhanced the PLF's efficacy on atherosclerosis.

01 Dec 2020·Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan

Jianpi Huazhuo Tiaozhi granules reduce oxidative stress injury in macrophages by inhibiting the nicotinamide adenine dinucleotide phosphate oxidase/reactive oxygen species-nuclear transcription factor kappa B pathway.

Article

Author: Liu, Yanwei ; Liu, Zhongyong

OBJECTIVETo assess the effect of Jianpi Huazhuo Tiaozhi granules (JHTG) on oxidative stress damage to macrophages and explore the relationship between the levels of this damage and the nicotinamide adenine dinucleotide phosphate oxidase (NOX)/reactive oxygen species (ROS)- nuclear transcription factor kappa B (NF-κB) signaling pathway.METHODSMacrophages cultured in vitro were divided into seven groups: control, model control, inhibitor, positive control, 2.5% JHTG, 5% JHTG, and 10% JHTG. An oxidative stress injury model was established by stimulating macrophages with oxidized low-density lipoprotein. Cell survival and apoptosis were detected by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide and flow cytometry assays, respectively. Malondialdehyde and superoxide dismutase levels were detected by enzyme-linked immunosorbent assays, while ROS levels were detected using a fluorescence probe. Proteins and mRNAs associated with the NOX/ROS-NF-κB pathway, including NOX4, p22phox, inhibitor of NF-κB kinase-α (IKK-α), inhibitor of NF-κB kinase-β (IKK-β), and NF-κB were detected by Western blot and PCR, respectively.RESULTSAfter JHTG treatment, there were fewer damaged and apoptotic macrophages, while superoxide dismutase levels were elevated. The JHTG-treated groups also showed reduced ROS levels. The molecular changes following JHTG treatment included decreased expression of NOX4 and p22phox at the protein level and decreased IKK-α, IKK-β, and NF-κB expression at the mRNA level. All of these effects were correlated with the JHTG concentration.CONCLUSIONThese results demonstrated that the molecular mechanism underlying the antioxidant activity of JHTG in macrophages is through inhibiting the NOX/ROS-NF-κB pathway.

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