Tamoxifen,10540-29-1,IC-0236624

Tamoxifen(TAM) serves as a selective estrogen receptor regulator (SERM), inhibiting estrogen's effects in breast cells while potentially stimulating estrogen activity in cells found in different tissues. Moreover, Tamoxifen can function as an enhancer of Hsp90 chaperone ATPase activity. Furthermore, it has been shown to induce gene knockout in CreER(T2) mice[1-4].
Tamoxifen(1-10µM;24 h) treatment significantly reduced the levels of growth hormone (GH) and adrenocorticotropic hormone (ACTH) secreted by the GH3 and AtT-20 cells respectively[5]. Tamoxifen(0.1-100 µM;48h) decreased the mRNA expression of vascular endothelial growth factor-A (VEGF-A) and increased the mRNA expression of VEGF receptor-1 and placental growth factor (PLGF) in HEECs[6]. Tamoxifen Treatment(1µM; 24/48/96 h) can significantly inhibit the proliferation of MCF7 cells[7]. 5 µM Tamoxifen induces persistent ERK1/2 activation in ER+ breast cancer cells(MCF-7)[8].
Tamoxifen (20, 50 and 100 mg/kg;21 days) treatment not only led to a significant reduction in tumor volume and weight, but also decreased the plasma levels of GH in the tumor-bearing mice[5]. Mice were injected with Tamoxifen (75 mg/kg dissolved in corn oil for 5 days at 6 weeks of age；i.p.) causes floxed exon excision, resulting in gene knockout[9]. Tamoxifen(9 mg/kg；i.g.) exerts an inhibitory effect on the heterotopic bone progression at inflammation and chondrogenesis stages, with the TGF-ß signaling pathway suppressed following the increase in estrogen receptor alpha activity[10].