116057-69-3

Basic information

• Product Name: Ethanamine, 2-[4-[1-(4-bromophenyl)-2-phenyl-1-butenyl]phenoxy]-N,N-dimethyl-, (E)-
• CAS NO: 116057-69-3
• Molecular Formula: C26H28BrNO
• Molecular Weight: 450.418
• Mol File: 116057-69-3.mol
• Article Data: 3

Chemical Properties

• CAS DataBase Reference: Ethanamine, 2-[4-[1-(4-bromophenyl)-2-phenyl-1-butenyl]phenoxy]-N,N-dimethyl-, (E)-(CAS DataBase Reference)
• NIST Chemistry Reference: Ethanamine, 2-[4-[1-(4-bromophenyl)-2-phenyl-1-butenyl]phenoxy]-N,N-dimethyl-, (E)-(116057-69-3)
• EPA Substance Registry System: Ethanamine, 2-[4-[1-(4-bromophenyl)-2-phenyl-1-butenyl]phenoxy]-N,N-dimethyl-, (E)-(116057-69-3)

Safety Data

• Hazardous Substances Data: 116057-69-3(Hazardous Substances Data)

Upstream product

• 103628-22-4 1--2-phenyl-butan-1-one 
• 68047-07-4 1-[4-[2-(N,N-dimethylamino)ethoxy]phenyl]-2-phenyl-1-butanone 
• 106-37-6 1.4-dibromobenzene 
• 626-00-6 1,3-Diiodobenzene 
• 960245-06-1 1-(4-bromophenyl)-1-(4-methoxyphenyl)-2-phenylbut-1-ene 
• 693818-58-5 4-(4-bromophenyl)-4-(4-methoxyphenyl)-3-phenylbut-1-ene 
• 185223-88-5 1-(4-bromophenyl)-1-(4-hydroxyphenyl)-2-phenylbut-1-ene 
• 40595-34-4 (E)-trimethyl(3-phenylallyl)silane 
• 4584-46-7 (2-chloroethyl)dimethylamine hydrochloride 
• 116057-71-7 cis-4-Bromotamoxifen 
• 116057-70-6 1-(4-Bromo-phenyl)-1-[4-(2-dimethylamino-ethoxy)-phenyl]-2-phenyl-butan-1-ol 

Downstream Products

• 121887-44-3 4-Formyltamoxifen 
• 121887-55-6 trans-4-(Methylthio)tamoxifen 
• 121887-46-5 2-<4-<1-<4-<2-(dimethylamino)ethoxy>phenyl>-2-phenylbut-1-enyl>phenyl>oxirane 
• 121887-45-4 4-(Hydroxymethyl)tamoxifen 
• 121887-43-2 4-<1-<4-<2-(dimethylamino)ethoxy>phenyl>-2-phenylbut-1-enyl>phenyl mercaptan 
• 121887-42-1 bis<4-<1-<4-<2-(dimethylamino)ethoxy>phenyl>-2-phenylbut-1-enyl>phenyl> disulfide 
• 10540-29-1 tamoxifen 

Relevant articles and documents

An expeditious synthesis of tamoxifen, a representative SERM (selective estrogen receptor modulator), via the three-component coupling reaction among aromatic aldehyde, cinnamyltrimethylsilane, and β-chlorophenetole

Two new synthetic pathways to the anti-cancer agent tamoxifen and its derivatives were developed. The first route involved the aldol reaction of benzyl phenyl ketone with acetaldehyde followed by Friedel-Crafts substitution with anisole in the presence of Cl2Si(OTf)2 to produce 1,1,2-triaryl-3-acetoxybutane, a precursor of the tamoxifen derivatives. The second one utilized the novel three-component coupling reaction among aromatic aldehydes, cinnamyltrimethylsilane, and aromatic nucleophiles using HfCl4 as a Lewis acid catalyst to produce 3,4,4-triarylbutene, that is also a valuable intermediate of the tamoxifen derivatives. The former strategy requires a total of 10 steps from the aldol formation to the final conversion to tamoxifen, whereas the latter needs only three or four steps to produce tamoxifen and droloxifene including the installation of the side-chain moiety and the base-induced double-bond migration to form the tetra-substituted olefin structure. This synthetic strategy seems to serve as a new and practical pathway to prepare not only the tamoxifen derivatives but also the other SERMs (selective estrogen receptor modulators) including estrogen-dependent breast cancer and osteoporosis agents.

Derivatives of Tamoxifen. Dependence of Antiestrogenicity on the 4-Substituent

A range of tamoxifen derivatives substituted in the 4-position of the 1-phenyl ring are described.The key steps in the synthesis of 4-iodo-, 4-bromo-, and 4-(methylthio)tamoxifen were reactions of 1,2-diarylbutanones with the (4-halogenophenyl)lithium or magnesium bromide.Oxidized precursors of 4-(methylthio)tamoxifen were used to prepare the methylsulfinyl and methylsulfonyl derivatives.Further derivatives (formyl, hydroxymethyl, oxirane, mercapto) were prepared from 4-bromotamoxifen via the 4-lithio derivative.Several of the derivatives (Br, I, SMe, SoMe, SO2Me, oxirane, CHO, CH2OH) displayed a higher affinity for estrogen receptors (ER) of calf uterine cytosol than did tamoxifen, but there was no relationship between affinity to ER and the ability to inhibit the growth of the MCF-7 breast cancer cell line in vitro.