166975-67-3

Basic information

• Product Name: (4-iodophenyl)(6-methoxy-2-(4-methoxyphenyl)benzo[b]thiophen-3-yl)methanone
• Synonyms: (4-iodophenyl)(6-methoxy-2-(4-methoxyphenyl)benzo[b]thiophen-3-yl)methanone
• CAS NO: 166975-67-3
• Molecular Weight: 500.357
• Mol File: 166975-67-3.mol
• Article Data: 2

Chemical Properties

• CAS DataBase Reference: (4-iodophenyl)(6-methoxy-2-(4-methoxyphenyl)benzo[b]thiophen-3-yl)methanone(CAS DataBase Reference)
• NIST Chemistry Reference: (4-iodophenyl)(6-methoxy-2-(4-methoxyphenyl)benzo[b]thiophen-3-yl)methanone(166975-67-3)
• EPA Substance Registry System: (4-iodophenyl)(6-methoxy-2-(4-methoxyphenyl)benzo[b]thiophen-3-yl)methanone(166975-67-3)

Safety Data

• Hazardous Substances Data: 166975-67-3(Hazardous Substances Data)

Upstream product

• 63675-74-1 2-(4'-methoxyphenyl)-6-methoxybenzothiophene 
• 1711-02-0 4-iodobenzoic acid chloride 

Downstream Products

• 1586025-54-8 [6-methoxy-2-(4-methoxyphenyl)benzo[b]thiophen-3-yl][4-[(trimethylsilyl)ethynyl]phenyl]methanone 
• 1586025-45-7 N-hydroxy-6-(4-(4-(6-hydroxy-2-(4-hydroxyphenyl)benzo[b]thiophene-3-carbonyl)phenyl)-1H-1,2,3-triazol-1-yl)hexanamide 
• 1586025-44-6 N-hydroxy-5-(4-(4-(6-hydroxy-2-(4-hydroxyphenyl)benzo[b]thiophene-3-carbonyl)phenyl)-1H-1,2,3-triazol-1-yl)pentanamide 
• 166975-68-4 [4-(3-Hydroxy-prop-1-ynyl)-phenyl]-[6-methoxy-2-(4-methoxy-phenyl)-benzo[b]thiophen-3-yl]-methanone 

Relevant articles and documents

A Chimeric SERM-histone deacetylase inhibitor approach to breast cancer therapy

Breast cancer remains a significant cause of death in women, and few therapeutic options exist for estrogen receptor negative (ER (-)) cancers. Epigenetic reactivation of target genes using histone deacetylase (HDAC) inhibitors has been proposed in ER (-) cancers to resensitize to therapy using selective estrogen receptor modulators (SERMs) that are effective in ER (+) cancer treatment. Based upon preliminary studies in ER (+) and ER (-) breast cancer cells treated with combinations of HDAC inhibitors and SERMs, hybrid drugs, termed SERMostats, were designed with computational guidance. Assay for inhibition of four typea I HDAC isoforms and antagonism of estrogenic activity in two cell lines yielded a SERMostat with 1-3a μM potency across all targets. The superior hybrid caused significant cell death in ER (-) human breast cancer cells and elicited cell death at the same concentration as the parent SERM in combination treatment and at an earlier time point.