1586025-45-7

Basic information

• Product Name: N-hydroxy-6-(4-(4-(6-hydroxy-2-(4-hydroxyphenyl)benzo[b]thiophene-3-carbonyl)phenyl)-1H-1,2,3-triazol-1-yl)hexanamide
• Synonyms: N-hydroxy-6-(4-(4-(6-hydroxy-2-(4-hydroxyphenyl)benzo[b]thiophene-3-carbonyl)phenyl)-1H-1,2,3-triazol-1-yl)hexanamide
• CAS NO: 1586025-45-7
• Molecular Weight: 542.615
• Mol File: 1586025-45-7.mol
• Article Data: 1

Chemical Properties

• CAS DataBase Reference: N-hydroxy-6-(4-(4-(6-hydroxy-2-(4-hydroxyphenyl)benzo[b]thiophene-3-carbonyl)phenyl)-1H-1,2,3-triazol-1-yl)hexanamide(CAS DataBase Reference)
• NIST Chemistry Reference: N-hydroxy-6-(4-(4-(6-hydroxy-2-(4-hydroxyphenyl)benzo[b]thiophene-3-carbonyl)phenyl)-1H-1,2,3-triazol-1-yl)hexanamide(1586025-45-7)
• EPA Substance Registry System: N-hydroxy-6-(4-(4-(6-hydroxy-2-(4-hydroxyphenyl)benzo[b]thiophene-3-carbonyl)phenyl)-1H-1,2,3-triazol-1-yl)hexanamide(1586025-45-7)

Safety Data

• Hazardous Substances Data: 1586025-45-7(Hazardous Substances Data)

Upstream product

• 166975-67-3 (4-iodophenyl)(6-methoxy-2-(4-methoxyphenyl)benzo[b]thiophen-3-yl)methanone 
• 1586025-54-8 [6-methoxy-2-(4-methoxyphenyl)benzo[b]thiophen-3-yl][4-[(trimethylsilyl)ethynyl]phenyl]methanone 
• 63675-74-1 2-(4'-methoxyphenyl)-6-methoxybenzothiophene 
• 1711-02-0 4-iodobenzoic acid chloride 

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.