Cetiedil

Cetiedil (0-500 μM; 1 h) inhibits hypoxic sickling of hemoglobin SS red blood cells in vitro, with the maximum inhibitory effect achieved at 100 μM, and significantly reduces the number of irreversibly sickled cells at concentrations of 100 μM and 200 μM^[1].
Cetiedil (0-1000 μM; 1 h) improves the filterability of deoxyhemoglobin SS red blood cells in vitro, with the peak effect observed at 100 μM^[1].
Cetiedil (125 μM; 1 h) exerts an additive effect with 5 mM sodium cyanate, which reduces the sickling rate and irreversible sickle cell count of deoxyhemoglobin SS red blood cells in vitro and improves their filterability^[1].
Cetiedil (0-90 μM; 4-5 h) competitively inhibits the Ca²⁺-dependent binding of ¹²⁵I-CaM to human erythrocyte ghost membranes, with an IC₅₀ of approximately 40 μM, and this inhibitory effect is reversible via membrane washing^[2].
Cetiedil (0-100 μM; 5 h) competitively inhibits calmodulin (CaM)-stimulated Ca²⁺-ATPase activity in human erythrocyte ghost membranes, with an IC₅₀ of approximately 40 μM. This compound does not affect the basal activity of the enzyme, and its inhibitory effect is reversible by increasing CaM concentration^[2].
Cetiedil (0-200 μM; 15 h) binds directly to human erythrocyte calmodulin and displaces [³H]-trifluoperazine from its CaM binding site^[2].
At concentrations ≥0.25 mM, Cetiedil (0.1-0.5 mM; 6-24 h) increases intracellular Na⁺ levels in both normal red blood cells and sickle cell anemia red blood cells within 24 h; in contrast, 0.1 mM Cetiedil has no effect on ion or water content, while 0.5 mM Cetiedil induces complete hemolysis within 6 h^[3].
Cetiedil (0.1-0.5 mM; 120 min) increases unidirectional sodium influx in both normal red blood cells and sickle cell anemia red blood cells in a dose-dependent manner when ouabain inhibits active Na⁺ efflux (0.1 mM shows no effect, while 0.25 mM and 0.5 mM elevate influx levels)^[3].
Cetiedil (10 μM-0.1 mM; 120 min) inhibits calcium-mediated K⁺ efflux and cell dehydration in both ATP-depleted normal red blood cells and sickle cell anemia red blood cells in a dose-dependent manner in vitro, with the maximum inhibitory effect observed at 0.1 mM and only a weak effect at 10 μM^[3].
Cetiedil (0.1 mM; 0-120 min) immediately blocks the initiated calcium-mediated potassium efflux and cellular dehydration in both ATP-depleted normal red blood cells and sickle cell anemia red blood cells^[3].
Cetiedil (25-200 μM) potently inhibits the activity of calmodulin-stimulated cyclic 3':5'-nucleotide phosphodiesterase purified from bovine brain, with an IC₅₀ of 30 μM. It acts as a competitive inhibitor of calmodulin and cAMP, and does not affect the basal activity of the enzyme or chelate calcium ions^[4].
Cetiedil (25-200 μM; 15 min preincubation on ice) inhibits calmodulin-stimulated Ca²⁺-ATPase activity in the membranes of normal human erythrocytes and erythrocytes from patients with human sickle cell disease, with an IC₅₀ of 60 μM, and exerts no effect on basal enzyme activity; this inhibitory effect is mediated by Cetiedil rather than its citrate counterion^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.