Fosfructose

Fosfructose is an orally active cyclooxygenase-2 inhibitor and Toll-like receptor 4 modulator. Fosfructose reduces the expression of cyclooxygenase-2, thereby decreasing prostaglandin production. By inhibiting the Toll-like receptor 4 signaling pathway, Fosfructose downregulates LPS-induced adhesion molecule expression. Fosfructose is applicable to research related to ischemic stroke, epilepsy, sepsis, myocardial injury, osteoporosis, and ultraviolet B-induced skin damage^[1]. IC50 & Target: Endogenous Metabolite^[1] In Vitro: Fosfructose (0.5-2%) concentration-dependently inhibits protein oxidation in cell-free human serum albumin assays^[1].
Fosfructose (5-10 mM) concentration-dependently increases metabolism in hypoxic rat cardiomyocytes and increases membrane fluidity in lipid vesicles^[1].
Fosfructose (3.5 mM) inhibits cyanide- and iodoacetate-induced intracellular calcium increases in cultured astrocytes and adult rat brain slices^[1].
Fosfructose (1-20 mM; 24 h post-irradiation for 10 mM) dose-dependently reduces UVB-induced intracellular oxidation in HaCaT cells, and 10 mM (24 h post-irradiation) inhibits COX-2 expression, prostaglandin production, and increases GSH levels^[1].
Fosfructose (10-20 mM; 24 h post-treatment) concentration-dependently protects mouse cortical neurons from NMDA-induced excitotoxicity by reducing ROS production and neuronal death^[1].
Fosfructose (10 mM; 20 min reperfusion) improves ATP + ADP preservation and ATP recovery in isolated rat liver mitochondria following ischemia-reperfusion injury^[1].
Fosfructose (5 mM) reduces K⁺ permeability, preserves Na⁺/K⁺ ATPase activity, and inhibits TNF-α-induced apoptosis in GalN-treated isolated rat hepatocytes^[1]. In Vivo: Fosfructose (2 g/kg; i.p.; single post-insult dose) reverses galactosamine-induced hepatitis in Wistar rats by improving hepatic carbohydrate metabolism and reducing apoptotic and necrotic liver damage^[1].
Fosfructose (0.5 g/kg; i.p.; single dose) reduces sepsis-induced inflammatory markers and achieves 50% 7-day survival in Wistar rats^[1].
Fosfructose (2 g/kg; i.p.; single dose; at sepsis induction) inhibits sepsis-induced platelet aggregation and coagulation abnormalities in Wistar rats^[1].
Fosfructose (500 mg/kg; i.p.; single pre-insult dose) drastically improves long-term survival in mice with Candida albicans-induced candidemia^[1].
Fosfructose (i.p.) reverses cisplatin-induced acute renal failure in Wistar rats^[1].
Fosfructose (i.p.) reduces doxorubicin-induced cardiac histological damage in Wistar rats^[1].
Fosfructose (2 g/kg; i.p.; single dose) reverses hypothermia-induced oxidative stress and metabolic acidosis in Wistar rats^[1].
Fosfructose (1.0 g/kg; i.p.; single pre-kindling dose) delays seizure acquisition in a rat rapid hippocampal kindling model by modulating BDNF/TrkB signaling and cation-chloride cotransporter expression^[1].
Fosfructose (0.5-1 g/kg; i.p.; single pre-insult dose) exerts a dose-dependent anticonvulsant effect in rats with chemically induced acute seizures, increasing seizure latency and reducing seizure duration and severity^[1].
Fosfructose (0.5-1 g/kg; i.p.; single pre-convulsion dose) protects hippocampal mitochondrial function and synaptic structure in immature rats with repeated febrile convulsions^[1].
Fosfructose (350 mg/kg; i.v.; twice daily; 7 days), combined with an immunosuppressant, quadruples heterotropic heart transplant survival in Mus musculus (mice) by inhibiting T-lymphocyte proliferation and IL-2 production^[1].
Fosfructose (9 mM; topical; once daily for 3 days pre-irradiation; immediately post-irradiation) preserves skin antioxidant capacity and reduces UVB-induced oxidative stress in hairless mice^[1].