176672-06-3

Basic information

• Product Name: 3-broMo-6-Methoxy-2-(4-Methoxyphenyl)benzo[b]thiophene
• Synonyms: 3-broMo-6-Methoxy-2-(4-Methoxyphenyl)benzo[b]thiophene
• CAS NO: 176672-06-3
• Molecular Formula: C₁₆H₁₃BrO₂S
• Molecular Weight: 349.24222
• Mol File: 176672-06-3.mol
• Article Data: 22

Chemical Properties

• Appearance: /
• Solubility: DCM
• CAS DataBase Reference: 3-broMo-6-Methoxy-2-(4-Methoxyphenyl)benzo[b]thiophene(CAS DataBase Reference)
• NIST Chemistry Reference: 3-broMo-6-Methoxy-2-(4-Methoxyphenyl)benzo[b]thiophene(176672-06-3)
• EPA Substance Registry System: 3-broMo-6-Methoxy-2-(4-Methoxyphenyl)benzo[b]thiophene(176672-06-3)

Safety Data

• Hazardous Substances Data: 176672-06-3(Hazardous Substances Data)

Usage

Description

3-Bromo-6-methoxy-2-(4-methoxyphenyl)benzo[b]thiophene is an organic compound characterized by its unique molecular structure, which features a benzo[b]thiophene core with a bromine atom at the 3-position, a methoxy group at the 6-position, and a 4-methoxyphenyl group at the 2-position. 3-broMo-6-Methoxy-2-(4-Methoxyphenyl)benzo[b]thiophene is known for its potential applications in the pharmaceutical industry due to its structural properties.

Uses

Used in Pharmaceutical Industry:
3-Bromo-6-methoxy-2-(4-methoxyphenyl)benzo[b]thiophene is used as an intermediate in the synthesis of nonsteroidal, selective estrogen receptor modulator (SERM) for the development of Raloxifene (R100000). 3-broMo-6-Methoxy-2-(4-Methoxyphenyl)benzo[b]thiophene plays a crucial role in the production of Raloxifene, a medication used to treat and prevent osteoporosis in postmenopausal women and reduce the risk of breast cancer.
The compound's specific structural features allow it to be a valuable building block in the creation of SERMs, which are important for their ability to modulate estrogen receptor activity in a tissue-specific manner. This makes them useful in treating conditions related to estrogen deficiency while minimizing the risk of hormone-dependent side effects.

Upstream product

• 15570-12-4 3-methoxybenzenethiol 
• 96803-85-9 1-[(2,2-diethoxyethyl)sulfanyl]-3-methoxybenzene 
• 90560-10-4 6-methoxy-benzo[b]thiophene 
• 1163701-10-7 (5-methoxy-2-((4-methoxyphenyl)ethynyl)phenyl)(methyl)-sulfane 
• 1163700-92-2 2-bromo-4-methoxy-1-((4-methoxyphenyl)ethynyl)benzene 
• 696-62-8 para-iodoanisole 
• 63675-74-1 2-(4'-methoxyphenyl)-6-methoxybenzothiophene 

Downstream Products

• 205814-59-1 2-(4-methoxyphenyl)-3-(3-benzyloxyphenyl)-6-methoxybenzo[b]thiophene 
• 189286-85-9 2-(4-methoxyphenyl)-3-[N-(4-benzyloxyphenyl)acetamido]-6-methoxy-benzo[b]thiophene 
• 182133-09-1 C₂₂H₁₇BrO₃S 
• 182133-43-3 [6-methoxy-2-(4-benzyloxyphenyl)-3-bromo]benzo-[b]thiophene 

Relevant articles and documents

Concise synthesis and biological evaluation of 2-Aryl-3-Anilinobenzo[b]thiophene derivatives as potent apoptosis-inducing agents

Many clinically used agents active in cancer chemotherapy exert their activity through the induction of cell death (apoptosis) by targeting microtubules, altering protein function or inhibiting DNA synthesis. The benzo[b]thiophene scaffold holds a pivotal place as a pharmacophore for the development of anticancer agents, and, in addition, this scaffold has many pharmacological activities. We have developed a flexible method for the construction of a new series of 2-aryl-3-(3,4,5-trimethoxyanilino)-6-methoxybenzo[b]thiophenes as potent antiproliferative agents, giving access to a wide range of substitution patterns at the 2-position of the 6-methoxybenzo[b]thiophene common intermediate. In the present study, all the synthesized compounds retained the 3-(3,4,5-trimethoxyanilino)-6-methoxybenzo[b]thiophene moiety, and the structure–activity relationship was examined by modification of the aryl group at its 2-position with electron-withdrawing (F) or electron-releasing (alkyl and alkoxy) groups. We found that small substituents, such as fluorine or methyl, could be placed in the para-position of the 2-phenyl ring, and these modifications only slightly reduced antiproliferative activity relative to the unsubstituted 2-phenyl analogue. Compounds 3a and 3b, bearing the phenyl and para-fluorophenyl at the 2-position of the 6-methoxybenzo[b]thiophene nucleus, respectively, exhibited the greatest antiproliferative activity among the tested compounds. The treatment of both Caco2 (not metastatic) and HCT-116 (metastatic) colon carcinoma cells with 3a or 3b triggered a significant induction of apoptosis as demonstrated by the increased expression of cleaved-poly(ADP-ribose) polymerase (PARP), receptor-interacting protein (RIP) and caspase-3 proteins. The same effect was not observed with non-transformed colon 841 CoN cells. A potential additional effect during mitosis for 3a in metastatic cells and for 3b in non-metastatic cells was also observed.

Synthesis of a 3-(α-Styryl)benzo[ b ]-thiophene Library via Bromocyclization of Alkynes and Palladium-Catalyzed Tosylhydrazones Cross-Couplings: Evaluation as Antitubulin Agents

A library of functionalized 3-(α-styryl)-benzo[b]thiophenes, endowed with a high level of molecular diversity, was efficiently synthesized by applying a synthetic sequence that allowed introduction of various substituents on aromatic A, B, and C-rings. Th

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.