IHVR-11029 is a potent inhibitor of ER α-glucosidase. IHVR-11029 is active against multiple hemorrhagic fever viruses and efficiently disrupts the morphogenesis of a broad spectrum of enveloped viruses.
Albifylline is a xanthine derivates with anti-asthmatic activity. Albifylline may cause a significant reduction of shock-induced leukocyte adhesions to the sinusoidal endothelium in the liver after hemorrhagic shock. Albifylline also improves microvascula
FGI-106 is a potent, broad-spectrum inhibitor demonstrating activity against various viruses, including Ebola, Rift Valley Fever, and Dengue Fever, exhibiting EC50 values of 100 nM, 800 nM, and 400-900 nM, respectively. Furthermore, it effectively inhibits non-hemorrhagic fever viruses such as HCV and HIV-1, with EC50s of 200 nM and 150 nM, respectively.
IHVR-19029 is an effective endoplasmic reticulum (ER) α-glucosidases I and II inhibitor (IC50: 0.48 μM for ER a-glucosidase I). IHVR-19029 efficiently blocks the replication of several hemorrhagic fever viruses, such as Ebola virus, Dengue virus, and Rift
matrix protein (3-15) [Zaire ebolavirus] is a peptide of the structural proteins linking the viral envelope with the zaire ebolavirus core. Ebola virus (EBOV) is a member of the family Filoviridae in the order Mononegavirales. It is the causative agent of
RO27-3225, also known as RO273225 is a melanocortin type 4 receptor agonist with EC50 = 1 nM. It may alleviate intestinal dysfuntion and brain damage. It has been investigated for an anti-obesity medication. Ro 27-3225 shows some activity at the MC1 receptor. Ro 27-3225 reverses hemorrhagic shock, reduces multiple organ damage, and improves survival.
CM-10-18 is a potent inhibitor of ER α-glucosidase. CM-10-18 demonstrated superior in vitro antiviral activity against representative viruses from four viral families causing hemorrhagic fever. CM-10-18 efficiently protected the lethality of dengue virus
Resolvin E4 (RvE4) is a member of the specialized pro-resolving mediator (SPM) family of bioactive lipids.1It is produced from eicosapentaenoic acid by 15-lipoxygenase (15-LO)via15(S)-HpEPE and 15S-hydroxy, 5S-HpEPE intermediatesin vitroand by isolated human M2 macrophages or polymorphonuclear (PMN) neutrophils under normoxic or hypoxic conditions. RvE4 synthesis is enhanced in M2 macrophage and neutrophil co-cultures, indicating transcellular biosynthesis by a potential 15-LO and 5-LO mechanism. It has been found in mouse inflammatory exudates. RvE4 (10 nM) increases efferocytosis of apoptotic neutrophils or senescent red blood cells (sRBCs) by human M2 macrophages under hypoxic conditionsin vitro. Intraperitoneal administration of RvE4 (100 ng/animal) inhibits increases in inflammatory exudate neutrophil infiltration in a mouse model of hemorrhagic peritonitis induced by zymosan A and thrombin. It also increases inflammatory exudate macrophage infiltration and efferocytosis of apoptotic neutrophils and/or RBCs in the same model. 1.Norris, P.C., Libreros, S., and Serhan, C.N.Resolution metabolomes activated by hypoxic environmentSci. Adv.5(10)eaax4895(2019)