TTC-352|CAS 1607819-68-0|DC Chemicals

Cas No.:	1607819-68-0
Chemical Name:	Unii-65ilh3Y0MI
Synonyms:	65ILH3Y0MI;3-(4-fluorophenyl)-2-(4-hydroxyphenoxy)-1-benzothiophen-6-ol;3-(4-fluorophenyl)-2-(4-hydroxyphenoxy)-1-benzothiophene-6-ol;3-(4-Fluorophenyl)-2-(4-hydroxyphenoxy)-benzo[b]thiophene-6-ol;BDBM50145856;J3.603.123I;2-(4-Hydroxyphenoxy)-3-(4-fluorophenyl)benzo[b]thiophene-6-ol;3-(4-Fluorophenyl)-2-(4-hydroxyphenoxy)benzo(b)thiophene-6-ol;3-(4-fluorophenyl)-2-(4-hydroxyphenoxy)benzo[b]thiophen-6-ol;3-(4-fluoro;Unii-65ilh3Y0MI
SMILES:	S1C(=C(C2C=CC(=CC=2)F)C2C=CC(=CC1=2)O)OC1C=CC(=CC=1)O
Formula:	C₂₀H₁₃FO₃S
M.Wt:	352.378827810287
Purity:	>97%
Sotrage:	2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Publication:	1. Balkees Abderrahman, et al. Mol Cancer Ther. 2021 Jan;20(1):11-25.

Description:

TTC-352 is a synthetic selective estrogen mimic acts as estrogen receptor (ER) partial agonist for the treatment of endocrine-resistant breast cancer.TTC-352 yields an H-bond with Glu353, allows Asp351-to-helix 12 (H12) interaction, sealing ERα's ligand-binding domain, recruiting E2-enriched coactivators, and triggering rapid ERα-induced unfolded protein response (UPR) and apoptosis.TTC-352 is a less potent full estrogen agonist compared to E2, allowing H12 to seal the LBD, which recruits many E2-enriched coactivators, and induces rapid ERα-mediated UPR and apoptosis.

References:

1. Balkees Abderrahman, et al. Mol Cancer Ther. 2021 Jan;20(1):11-25.

MSDS

COA

LOT NO.	DOWNLOAD

2018-0101

Cat. No.	Product name	Field of application
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DC70851	TTC-352	TTC352 is a synthetic selective estrogen mimic acts as estrogen receptor (ER) partial agonist for the treatment of endocrine-resistant breast cancer.TTC 352 yields an H-bond with Glu353, allows Asp351-to-helix 12 (H12) interaction, sealing ERα's ligand-binding domain, recruiting E2-enriched coactivators, and triggering rapid ERα-induced unfolded protein response (UPR) and apoptosis.TTC-352 is a less potent full estrogen agonist compared to E2, allowing H12 to seal the LBD, which recruits many E2-enriched coactivators, and induces rapid ERα-mediated UPR and apoptosis.
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