Iron sucrose

Research use only, not for human use.

Iron sucrose is treatment of iron deficiency anemia.

Iron sucrose is treatment of iron deficiency anemia.(In Vitro):Intravenous Iron sucrose results in a statistically significant increase in hemoglobin, mean corpuscular volume, serum iron, ferritin, and % iron saturation, with a corresponding decrease in total iron binding capacity.In vitro survival assays show that 10 mM ascorbate exposure (2h) clonogenically inactivated 40-80% of exponentially growing colon cancer cell lines (HCT116 and HT29). When colon cancer cells are treated in the presence or absence of 250 μM Iron sucrose, then rinsed, and treated with 10 mM ascorbate, the cells demonstrate increased levels of labile iron that results in significantly increased clonogenic cell killing, compared to pharmacological ascorbate alone.The expression levels of intracellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and adhesion of U937 cells increased in Iron sucrose-treated human aortic endothelial cells through upregulated NADPH oxidase (NOx) and NF-κB signaling. Iron sucrose significantly induces a time-dependent increase in intracellular ROS production in HAECs between 1 and 3 hours at a concentration of 160 μg/mL, but the effect diminished at 4 hours.(In Vivo):Iron sucrose significantly increases tissue superoxide production, expression of tissue cell adhesion molecules, and endothelial adhesiveness in mice with subtotal nephrectomy. Iron sucrose exacerbates atherosclerosis in the aorta of ApoE-/- mice with uninephrectomy.

Intravenous Iron sucrose results in a statistically significant increase in hemoglobin, mean corpuscular volume, serum iron, ferritin, and % iron saturation, with a corresponding decrease in total iron binding capacity. In vitro survival assays show that 10 mM ascorbate exposure (2h) clonogenically inactivated 40-80% of exponentially growing colon cancer cell lines (HCT116 and HT29). When colon cancer cells are treated in the presence or absence of 250 μM Iron sucrose, then rinsed, and treated with 10 mM ascorbate, the cells demonstrate increased levels of labile iron that results in significantly increased clonogenic cell killing, compared to pharmacological ascorbate alone. The expression levels of intracellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and adhesion of U937 cells increased in Iron sucrose-treated human aortic endothelial cells through upregulated NADPH oxidase (NOx) and NF-κB signaling. Iron sucrose significantly induces a time-dependent increase in intracellular ROS production in HAECs between 1 and 3 hours at a concentration of 160 μg/mL, but the effect diminished at 4 hours.

Iron sucrose significantly increases tissue superoxide production, expression of tissue cell adhesion molecules, and endothelial adhesiveness in mice with subtotal nephrectomy. Iron sucrose exacerbates atherosclerosis in the aorta of ApoE-/- mice with uninephrectomy.

Iron saccharate | Sucroferric oxyhydroxide

Others

Other Targets

others

Cardiovascular Disease

Iron?Deficiency Anemia

8047-67-4

736.1

C18H24Fe2O24

>98% (HPLC)

DMSO:100 mg/mL (135.85 mM)H2O:100 mg/mL (135.85 mM)

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——

(-20℃)

With Ice Pack

≥ 2 years