er in mcf-7 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.

ER covalent antagonist-1 (Compound 39D) acts as an antagonist of the estrogen receptor α (ERα). This compound inhibits the proliferation of ERα-positive MCF-7 cells with an IC50 of 0.98 μM, induces cell cycle arrest at the G0 G1 phase, and triggers apoptosis. Additionally, ER covalent antagonist-1 demonstrates antitumor activity in mouse models.

Nur77 modulator 4 (Compound 15h) is a Nur77 inducer with a KD of 0.477 μM. It significantly promotes Nur77 expression and apoptosis, exhibiting excellent growth inhibitory effects on HepG2 and MCF-7 cells, with an IC50 of less than 5 μM. Nur77 modulator 4 activates Nur77-mediated ER stress through the PERK-ATF4 and IRE1 signaling pathways, leading to apoptosis. This compound is applicable in cancer research.

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.

LSD1 ER-IN-1 (compound 11g) is a potent inhibitor of ER and LSD1, targeting LSD1 with an IC50 of 1.55 μM and exhibiting significant anti-proliferative effects on MCF-7 breast cancer cells with an IC50 of 8.79 μM.

D 15414 is a nonsteroidal weak estrogen of the 2-phenylindole group which was never marketed. It is the major metabolite of the selective estrogen receptor modulator zindoxifene. D-15414 has high affinity for the estrogen receptor and inhibits the growth of ER-positive MCF-7 breast cancer cells in vitro.

Pipendoxifene, also known as ERA-923, is a new antiestrogen with potential anticancer activity. ERA-923 potently inhibits estrogen binding to ER-alpha (IC50 = 14 nM). In ER-alpha-positive human MCF-7 breast carcinoma cells, ERA-923 inhibits estrogen-stimulated growth (IC50 = 0.2 nM) associated with cytostasis. In vitro, a MCF-7 variant with inherent resistance to tamoxifen (10-fold) or 4-OH tamoxifen (>1000-fold) retains complete sensitivity to ERA-923 . In preclinical models, ERA-923 has an improved efficacy and safety compared with tamoxifen. In the combination with temsirolimus, ERA-923 showed excellent anticancer activity in preclinical models.

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].

ER degrader 9 (compound 1) serves as a bifunctional molecule and an effective estrogen receptor (ER) degrader with a DC50 of ≤10 nM in MCF-7 cells. It is utilized in the research of breast cancer.

Uralenol significantly shows the inhibitory activities against the PTP1B enzyme; it also shows inhibitory activities on mushroom tyrosinase using l-tyrosine as substrate( IC50 =49.5 μM). Uralenol shows potent anti-proliferation effects on ER-positive breast cancer MCF-7 cells in vitro.

5,7,3',4'-Tetrahydroxy-3-methoxy-8,5'-diprenylflavone demonstrated a strong anti-proliferative effect on ER-positive breast cancer MCF-7 cells in vitro, with an IC50 value of 4.41 μM. It significantly down-regulated the expression of estrogen receptor-α (ER-α) and inhibited tumor growth in the BCAP-37 human breast cancer cell line xenograft model.

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.