GNE-274

Modify Date: 2024-01-14 06:30:28

GNE-274 Structure
GNE-274 structure
Common Name GNE-274
CAS Number 2369048-69-9 Molecular Weight 457.56
Density N/A Boiling Point N/A
Molecular Formula C29H31NO4 Melting Point N/A
MSDS N/A Flash Point N/A

 Use of GNE-274


GNE-274 is a non-degrader that is structurally related to GDC-0927 (ER degrader). GNE-274 does not induce ER turnover and functions as a partial ER agonist in breast cancer cell lines. GNE-274 increase chromatin accessibility at ER-DNA binding sites, while GDC-0927 do not. GNE-274 is a potent inhibitor of ER-ligand binding domain (LBD). GNE-274 can be used for cancer research[1][2].

 Names

Name GNE-274

 GNE-274 Biological Activity

Description GNE-274 is a non-degrader that is structurally related to GDC-0927 (ER degrader). GNE-274 does not induce ER turnover and functions as a partial ER agonist in breast cancer cell lines. GNE-274 increase chromatin accessibility at ER-DNA binding sites, while GDC-0927 do not. GNE-274 is a potent inhibitor of ER-ligand binding domain (LBD). GNE-274 can be used for cancer research[1][2].
Related Catalog
In Vitro GNE-274 (0.1 nM-1000 nM; 4 hours) fails to trigger increased ER turnover in MCF7, MD-134, HCC1500 and CAMA cells[1]. GNE-274 (1-1000 nM; 7-10 days) potently inhibits cellular proliferation, exhibiting greater potency than fulvestrant, 4-OHT, AZD9496, and GDC-0810 in E2-stimulated ER+ breast cancer cell lines[1]. In transposaseaccessible chromatin sequencing (ATAC-seq) assay, GNE-274 increase chromatin accessibility at ER-DNA binding sites, it significantly alters chromatin accessibility at 594 sites. But GDC-0927 has considerably less impact on chromatin accessibility[1]. Cell Viability Assay[1] Cell Line: MCF7, MB-134, HCC1500, EFM-19, CAMA-1, T-47D cells Concentration: 1 nM; 10 nM; 100 nM; 1000 nM Incubation Time: 7-10 days Result: Exhibited IC50 values approximately ranging from 5nM to 20 nM in different cells.
References

[1]. Jane Guan, et al. Therapeutic Ligands Antagonize Estrogen Receptor Function by Impairing Its Mobility. Cell. 2019 Aug 8;178(4):949-963.e18.

[2]. Jane Guan, et al. Abstract NG05: Not all “SERDs” are equal: Context-independent ER degradation and full ER antagonism define the next generation of ER therapeutics. Cancer research.

 Chemical & Physical Properties

Molecular Formula C29H31NO4
Molecular Weight 457.56
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