7310-74-9

Usage

Chemical Properties

white crystalline powder

InChI:InChI=1/C27H24P.BrH/c1-5-14-24(15-6-1)16-13-23-28(25-17-7-2-8-18-25,26-19-9-3-10-20-26)27-21-11-4-12-22-27;/h1-22H,23H2;1H/q+1;/p-1/b16-13+;

Upstream product

• 603-35-0 triphenylphosphine 
• 4392-24-9 3-bromo-1-phenyl-1-propenyl bromide 
• 6399-81-1 triphenylphosphine hydrobromide 
• 165754-26-7 [3-(benzyloxy)prop-1-en-1-yl]benzene 

Downstream Products

• 72486-22-7 4-Methyl-1-phenylpenta-1,3-diene 
• 1552-40-5 1--4-phenyl-butadien-(1.3) 
• 53678-07-2 3-methyl-1,6-diphenyl-hexa-1,3,5-triene 
• 27331-25-5 1-(4-chlorophenyl)-4-phenyl-1,3-butadiene 
• 97478-25-6 2-((3E)-4-phenyl-1,3-butadienyl)-1-tosylazetidine 
• 1552-95-0 ethyl 5-phenyl-2,4-pentadienoate 

Relevant academic research and scientific papers

Substituted dienes prepared from betulinic acid – Synthesis, cytotoxicity, mechanism of action, and pharmacological parameters

A set of new substituted dienes were synthesized from betulinic acid by its oxidation to 30-oxobetulinic acid followed by the Wittig reaction. Cytotoxicity of all compounds was tested in vitro in eight cancer cell lines and two noncancer fibroblasts. Almost all dienes were more cytotoxic than betulinic acid. Compounds 4.22, 4.30, 4.33, 4.39 had IC50 below 5 μmol/L; 4.22 and 4.39 were selected for studies of the mechanism of action. Cell cycle analysis revealed an increase in the number of apoptotic cells at 5 × IC50 concentration, where activation of irreversible changes leading to cell death can be expected. Both 4.22 and 4.39 led to the accumulation of cells in the G0/G1 phase with partial inhibition of DNA/RNA synthesis at 1 × IC50 and almost complete inhibition at 5 × IC50. Interestingly, compound 4.39 at 5 × IC50 caused the accumulation of cells in the S phase. Higher concentrations of tested drugs probably inhibit more off-targets than lower concentrations. Mechanisms disrupting cellular metabolism can induce the accumulation of cells in the S phase. Both compounds 4.22 and 4.39 trigger selective apoptosis in cancer cells via intrinsic pathway, which we have demonstrated by changes in the expression of the crucial apoptosis-related protein. Pharmacological parameters of derivative 4.22 were superior to 4.39, therefore 4.22 was the finally selected candidate for the development of anticancer drug.

Cleavage of benzyl ethers by triphenylphosphine hydrobromide

Triphenylphosphine hydrobromide was found to cleave the benzyl ethers derived from 1°, 2° alkyl, and aryl alcohols to the corresponding alcohols and benzyltriphenylphosphonium bromide in good yields. Alkene and allyl phosphonium salts were produced from the benzyl ethers with 3° alkyl and allyl groups, respectively. These results indicate that the formation of the product is determined by the relative stability of the carbocationic intermediate. The anhydrous, stoichiometric amount of PPh3·HBr offers a new and effective method for the deprotection of benzyl ethers.

Palladium-catalyzed silylene-1,3-diene [4 + 1] cycloaddition with use of (aminosilyl)boronic esters as synthetic equivalents of silylene

(Chemical Equation Presented) Silylboronic esters bearing a dialkylamino group on the silicon atoms reacted with 1,3-dienes in the presence of a palladium catalyst to give silacyclopent-3-enes (i.e., 2,5-dihydrosiloles) in high yields via efficient silyle

Microwave irradiation in organophosphorus chemistry. Part 2: Synthesis of phosphonium salts

Several phosphonium salts have been prepared using a domestic microwave oven. The microwave enhanced reaction of triphenylphosphine and an organic halide shows a remarkable rate acceleration under microwave irradiation and allows the general and facile synthesis of both stabilized and non-stabilized phosphonium salts. (C) 2000 Elsevier Science Ltd.