er in t47d er+ cells

ERD-308 induces >95% of ER degradation at concentrations as low as 5 nM in both cell lines (DC50 (concentration causing 50% of protein degradation) of 0.17 nM and 0.43 nM in MCF-7 and T47D ER+ cells, respectively).ERD-308 is a highly potent PROTAC degrade

(E Z)-Droloxifene is a mixture comprising (E)-Droloxifene, known as a selective estrogen receptor modulator, and (Z)-Droloxifene. (E)-Droloxifene binds to estrogen receptors (ER) in rabbit uterine homogenate with an IC50 of 24 nM. It increases uterine weight in immature rats and reduces the uterine weight increase caused by estradiol in juvenile rats. Additionally, (E)-Droloxifene inhibits the growth of human breast cancer cells MCF-7, ZR-75-1, and T47D stimulated by 17β-estradiol. In contrast, (Z)-Droloxifene shows weak binding to ER and exhibits neither estrogenic nor anti-estrogenic activity.

17β-hydroxy Exemestane is the primary active metabolite of exemestane . It is formed by metabolism of exemestane by the cytochrome P450 (CYP) isoforms CYP1A and CYP4A11. 17β-hydroxy Exemestane is an aromatase inhibitor (IC50 = 69 nM using human placental microsomes) and an androgen receptor (AR) agonist (IC50 = 39.6 nM) that is selective for AR over estrogen receptor α (ERα; IC50 = 21.2 μM). It stimulates growth of AR- and ERα-positive MCF-7 (EC50 = 2.7 μM) and T47D breast cancer cells (EC50s = 0.43 and 1,500 nM for AR- and ER-mediated growth, respectively) and inhibits proliferation of testosterone-treated aromatase-overexpressing MCF-7aro cells in a concentration-dependent manner. 17β-hydroxy Exemestane (20 mg/kg) inhibits increases in serum cholesterol and LDL levels and prevents decreases in bone mineral density in the lumbar vertebrae and femur, as well as femoral bending strength and compressive strength of the fifth lumbar vertebrae, in ovariectomized rats.

ER degrader 7 (Compound 35t) is a selective degrader of both ERα and ERβ and functions as a tubulin polymerization inhibitor. It inhibits cell viability with IC50 values of 0.06 μM for MCF-7, 2.56 μM for T47D, 15.84 μM for MCF-10A, 1.59 μM for LCC2, 1.67 μM for T47D D538G, and 1.37 μM for T47D Y537S cells. Additionally, ER degrader 7 demonstrates efficacy in suppressing breast cancer tumor growth [1].

ERα17p (ERα 295-311), the epitope of the CaM binding site located on estrogen receptor α (ER), interacts with calmodulin (CaM) in a calcium-dependent fashion. This peptide is involved in regulating the migration of various cancer cell lines including MCF-7, SK-BR-3, T47D, and MDA-MB-231 via the Rho ROCK and PI3K Akt signaling pathways. Additionally, ERα17p plays a role in suppressing proliferation and inducing apoptosis in breast cancer cells, as well as inhibiting tumor growth in mouse models.