CT-1

Overexpression of CT-1 (48 h post-transfection) significantly promotes the proliferation and migration of HUVECs, enhances the capillary-like tube formation ability of cells, significantly upregulates the expression of eNOS mRNA, and increases the protein expression levels of DDAH I, DDAH II and VEGF^[1].
Overexpression of CT-1 (48 h post-transfection) significantly reduces the level of ADMA in HUVECs, enhances DDAH activity, and increases NOS activity and NO production^[1].
CT-1 (0.78-12.5 μM; 0-300 s) binds to purified human FTH1 and wild-type FTH1, with K_d values of 17.15 μM and 5.46 μM, respectively^[2].
CT-1 (100 μM at room temperature; 1 h) interacts with FTH1 in 4T1 cell lysates and reduces the stability of FTH1 against pronase-mediated proteolysis^[2].
CT-1 (0.5-16 μM; 24 h) inhibits the viability of 4T1, MDA-MB-231, and N2-type tumor-associated neutrophils (polarized HL-60 cells) in a dose-dependent manner^[2].
CT-1 (24 h) inhibits the viability of primary mouse N2-like neutrophils with an IC₅₀ of 7.16 μM^[2].
CT-1 (0-8 μM; 24 h) increases intracellular Fe²⁺ levels and the GSSG/GSH ratio (a marker of oxidative stress), reduces mitochondrial membrane potential, promotes intracellular ROS production, induces cellular lipid peroxidation, and facilitates lysosomal autophagic degradation of FTH1 in 4T1 cells^[2].
CT-1 (1-4 μM; 24 h) induces lipid peroxidation in N2-type tumor-associated neutrophils (polarized HL-60 cells)^[2].
CT-1 (0.25-32 μM; 6 days) inhibits the growth and viability of triple-negative breast cancer organoids in a dose-dependent manner, with IC₅₀ values ranging from 2.35 to 6.74 μM across 3 PDO cell lines after 6 days of treatment^[2].
CT-1 (0.1 nM or lower) potently induces volume overload-like hypertrophy in neonatal cardiomyocytes, enhances the survival rate of neonatal rat cardiomyocytes in serum-free medium by reducing apoptosis, and upregulates the expression of ANP, BNP, hsp70 and hsp90 genes in cultured cardiomyocytes^[3].
CT-1 (30 min) protects neonatal cardiomyocytes cultured in vitro from cell death and apoptosis induced by simulated hypoxia/ischemia stress, and this effect depends on the activation of the p42/p44 MAPK pathway (which can be inhibited by 50 μM PD98059 (HY-12028))^[3].

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