diannexin (ASP8597) / Astellas, Surromed, PPD - LARVOL DELTA

Emerging Therapeutic Strategies for Renal Ischemia-Reperfusion Injury in Kidney Transplantation: Progress and Challenges-A Systematic Review. (PubMed, Clin Transplant) - "Most available data remain preclinical and are limited by inconsistent outcome measures and translational bottlenecks. Future efforts should prioritize harmonized animal models, biomarker-defined endpoints, and strategic investment in promising candidates to integrate them into kidney transplant care."

Journal • Review • Cardiovascular • Pediatrics • Reperfusion Injury • Transplantation

CD39-Diannexin alleviates the platelet storage lesion by protecting platelets from activation, a new attempt from a traditional perspective. (PubMed, Platelets) - "Interestingly, we preliminarily discover that CD39-DA may reduce stored platelets' apoptosis and increase aggregatory platelets after activation by thrombin, collagen and calcium, which is marked by GSAO. In conclusion, we confirm that CD39-DA can alleviate PSL by reducing platelet activation."

Journal • ENTPD1 • SELP

Diannexin alleviates myocardial ischemia-reperfusion injury by orchestrating cardiomyocyte oxidative damage, macrophage polarization and fibrotic process by TLR4-NF-kB-mediated inactivation of NLRP3 inflammasome. (PubMed, Int Immunopharmacol) - "The activation of TLR4/NF-κB/NLRP3 inflammasome pathway in MI/R mice was attenuated after Diannexin administration. Together, Diannexin may alleviate the development of MI/R injury by directly regulating cardiomyocyte oxidative injury, fibrotic potential and indirectly affecting macrophage polarization-mediated cardiomyocyte apoptosis, indicating a promising therapeutic strategy for MI/R."

Journal • Cardiovascular • Congestive Heart Failure • Fibrosis • Heart Failure • Immunology • Myocardial Infarction • Myocardial Ischemia • Reperfusion Injury • ANXA5 • IL4 • NLRP3 • TLR4

Recombinant protein diannexin prevents preeclampsia-like symptoms in a pregnant mouse model via reducing the release of microparticles. (PubMed, Front Med) - "Furthermore, diannexin effectively inhibited trophoblast cell activation and NLRP3 inflammasome activation in vitro. These findings suggested that diannexin inhibited MP release and might be an effective therapeutic strategy for preventing PE."

Journal • Preclinical • Gynecology • Inflammation • NLRP3

Diannexin Can Ameliorate Acute Respiratory Distress Syndrome in Rats by Promoting Heme Oxygenase-1 Expression. (PubMed, Mediators Inflamm) - "The partial reversal of diannexin effects by a HO-1 inhibitor suggests that diannexin may promote HO-1 expression to ameliorate ARDS. We showed that diannexin can improve alveolar-capillary permeability, inhibit the oxidative stress response and inflammation, and protect against ARDS-induced lung injury and apoptosis."

Journal • Preclinical • Acute Respiratory Distress Syndrome • Immunology • Inflammation • Pneumonia • Pulmonary Disease • Respiratory Diseases • HMOX1 • MPO

DIANNEXIN DOWN-MODULATES TNF-INDUCED ENDOTHELIAL MICROPARTICLE RELEASE BY BLOCKING MEMBRANE BUDDING PROCESS. (PubMed) - Int J Innov Med Health Sci - "Altogether these data suggest that Diannexin can inhibit endothelial vesiculation by binding PS present either at the cell surface or at the level of the inner leaflet of the plasma membrane."

Journal • Biosimilar • Immunology • Reperfusion Injury • Venous Thromboembolism

Protective effect of phosphatidylserine blockade in sepsis induced organ dysfunction. (PubMed, Surgery) - "In sepsis, phosphatidylserine blockade had a protective effect on gut dysfunction and coagulopathy. Increased phosphatidylserine exposure may be a key mediator of organ dysfunction and coagulopathy during sepsis. These data may provide insights into novel treatment options for septic patients."

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Protective Effect of Phosphatidylserine Blockade in Hemorrhagic Shock. (PubMed, J Surg Res) - "PS blockade with DA decreased renal and gut dysfunction associated with hemorrhagic shock and attenuated the magnitude of LPA generation. Our findings suggest potential for therapeutic targets in the future that could prevent organ dysfunction associated with hemorrhagic shock."

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