73490-49-0

Upstream product

• 120-08-1 Scoparone 
• 74-88-4 methyl iodide 
• 141-82-2 malonic acid 
• 4460-86-0 asaraldehyde 

Downstream Products

• 80749-75-3 (E)-3-(2,4,5-trimethoxy-phenyl)-acrylic acid methyl ester 
• 1026278-45-4 (E)-N-(6-Amino-2,4-dioxo-1,3-dipropyl-1,2,3,4-tetrahydro-pyrimidin-5-yl)-3-(2,4,5-trimethoxy-phenyl)-acrylamide 
• 1213775-86-0 (E)-3-(2,4,5-trimethoxyphenyl)acryloyl fluoride 
• 1418317-25-5 (E)-1,2,4-trimethoxy-5-(3,3,3-trifluoroprop-1-en-1-yl)benzene 
• 941278-58-6 2,4,5-trimethoxycynnamoyl chloride 
• 20491-91-2 2,4,5-trimethoxyphenol 
• 147700-53-6 (E)-1,3-Dipropyl-8-(2,4,5-trimethoxystyryl)xanthine 
• 147700-54-7 (E)-7-Methyl-1,3-dipropyl-8-(2,4,5-trimethoxystyryl)xanthine 
• 14469-89-7 trans-2,4,5-trimethoxycinnamic acid ethyl ester 

Relevant academic research and scientific papers

Discovery of caffeic acid phenethyl ester derivatives as novel myeloid differentiation protein 2 inhibitors for treatment of acute lung injury

Myeloid differentiation protein 2 (MD2) is an essential molecule which recognizes lipopolysaccharide (LPS), leading to initiation of inflammation through the activation of Toll-like receptor 4 (TLR4) signaling. Caffeic acid phenethyl ester (CAPE) from propolis of honeybee hives could interfere interactions between LPS and the TLR4/MD2 complex, and thereby has promising anti-inflammatory properties. In this study, we designed and synthesized 48 CAPE derivatives and evaluated their anti-inflammatory activities in mouse primary peritoneal macrophages (MPMs) activated by LPS. The most active compound, 10s, was found to bind with MD2 with high affinity, which prevented formation of the LPS/MD2/TLR4 complex. The binding mode of 10s revealed that the major interactions with MD2 were established via two key hydrogen bonds and hydrophobic interactions. Furthermore, 10s showed remarkable protective effects against LPS-caused ALI (acute lung injury) in vivo. Taken together, this work provides new lead structures and candidates as MD2 inhibitors for the development of anti-inflammatory drugs.

Synthesis, antiepileptic effects, and structure-activity relationships of α-asarone derivatives: In vitro and in vivo neuroprotective effect of selected derivatives

In the present study, we compared the antiepileptic effects of α-asarone derivatives to explore their structure-activity relationships using the PTZ-induced seizure model. Our research revealed that electron-donating methoxy groups in the 3,4,5-position on phenyl ring increased antiepileptic potency but the placement of other groups at different positions decreased activity. Besides, in allyl moiety, the optimal activity was reached with either an allyl or a 1-butenyl group in conjugation with the benzene ring. The compounds 5 and 19 exerted better neuroprotective effects against epilepsy in vitro (cell) and in vivo (mouse) models. This study provides valuable data for further exploration and application of these compounds as potential anti-seizure medicines.

Synthesis, mitochondrial localization of fluorescent derivatives of cinnamamide as anticancer agents

Mitochondria are considered as a therapeutic target for new drug design toward all kinds of cancer. Hence in order to enhance the dosage in mitochondrial fraction of cinnamamides, the mitochondria-targeted derivatives were designed by the incorporation of cinnamamides into a fluorophore carrier of coumarin-3-carboxamide with a 1:1 stoichiometry. Using the amide linkers, twenty-one compounds were synthesized and the cytotoxicity against a panel of cancer cells (MCF-7, Hela, HepG2, HL-60) was tested. In particular, compound 18c displayed the potent cytotoxicity toward HL-60 leukaemia cells, which could quickly and efficiently entry into HL-60 cells and specifically localize within mitochondria. And 18c preferred enrichment in HL-60 cells than in PBMC normal cells, accounting for the higher toxicity to cancer cells than to normal cells. Moreover, the dissipations of mitochondrial membrane potential and enhancement of cellular ROS level were also preceded upon 18c treatment, leading to cell cycle arrest and apoptosis/necrosis in HL-60 cells. Besides, acted as a Michael acceptor, 18c initiated a thia-Michael addition reaction toward cysteamine (1:2 stoichiometry), detecting by the UV-Vis spectrum and HRMS analysis. This could result in the blue emission of 18c in mitochondria after the procedure of cell fixation, owing to the formation of covalent bond with mitochondrial thiols. Our study reported 18c might be useful for the further development into a mitochondria-targeted anti-leukemia agent and the Michael acceptor might be a versatile functional group.

Cinnamoylated chloroquine analogues: A new structural class of antimalarial agents

A novel series of cinnamoylated chloroquine hybrid analogues were synthesized and evaluated as antimalarial agents. The trans cinnamic acid derivatives (3–8) were synthesized by utilizing substituted aldehydes and malanoic acid in DMF catalysed by DABCO. The final cinnamoylated chloroquine analogues (9–14) were synthesized by utilizing DCC coupling reagent. The amido chloroquine (17) was prepared from acid (16) and compound 2 in benzene using SOCl2 as chlorinating agent. The corresponding ester (15) was prepared from 2-hydroxy acetophenone and 2-bromoacetates in actonitrile in presence of K2CO3?as?base followed by basic hydrolysis. The preparation of amide based chloroquine-chalcone analogues (18–22), were obtained by the combination of amido chloroquine (17) and aldehydes in 10% aq. KOH in methanol at room temperature. Further we prepared epichlorohydrin based chloroquine-chalcone analogues (25–28), by reacting the epoxide (24a, 24b and 24c) with 2 and methelenedioxy aniline. In?vitro antimalarial activity against chloroquine sensitive strain 3D7, chloroquine resistant strain K1 of P.?falciparum and in?vitro cytotoxicity of compounds using VERO cell line was carried out. The synthesized molecules showed significant in?vitro antimalarial activity especially against CQ resistant strain (K1). Among tested compounds, 13, 9 and 10 were found to be the most potent compounds of the series with IC50 value of 44.06, 48.04 and 59.37?nM against chloroquine resistant K1 strain.

ANTI-HIV COMPOUNDS

This invention provides, among other things, tetrahydroisoquinolines useful for treating viral infections, pharmaceutical formulations containing such compounds, as well as methods of inhibiting the replication of a virus, such as HIV, or treating a disease, such as AIDS.

Metabolites of orally administered Perilla frutescens extract in rats and humans

As a part of our search for bioactive substances from the leaves of Perilla frutescens BRITTON var. acuta KUDO, (Perillae Herba, Labiatae), the aqueous extract was orally administered to rats and humans, and metabolites in the urine, plasma, and/or bile were analyzed by a high-performance liquid chromatograph (HPLC) equipped with a photodiode array detector. When the extract was administered to rats, 10 metabolites, trans-caffeic acid-4-O- sulfate (1), trans-p-coumaric acid-4-O-sulfate (2), trans-ferulic acid-4-O- sulfate (3), trans-m-coumaric acid-3-O-sulfate (4), trans-caffeic acid (5), m-hydroxyphenylpropionic acid (6), trans-p-coumaric acid (7), trans-m- coumaric acid (8), luteolin (9), and apigenin (10) were detected in the urine, whereas four metabolites, scutellarein-6, 7-di-O-β-glucuronide (11), apigenin-4'-O-sulfate-7-O-β-glucuronide (12), apigenin-7-O-β-glucuronide (13), and diosmetin-7-Oβ-glucuronide (14) were found in the bile. Compounds 1-8 and 11-14 were also found in the plasma. When the extract was given to humans, however, two metabolites, 1-O-(2,4,5-trimethoxycinnamoyl)-β- glucuronic acid (15) and apigenin-4'-O-β-glucuronide (16), were found in the urine and plasma. Thus, a species difference in the metabolism of the extract constituents was observed between rats and humans. Structures 1-16 were identified based on their chemical and spectral data.