4481-60-1

Upstream product

• 82-57-5 visnagin 
• 78633-78-0 4-allyloxy-2-hydroxy-3-iodo-6-methoxybenzoylacetone 
• 78633-79-1 7-allyloxy-8-iodo-5-methoxy-2-methylchromone 
• 74047-33-9 4-allyloxy-2-hydroxy-3-iodo-6-methoxyacetophenone 
• 54102-21-5 6-allyl-5,7-dihydroxy-2-methyl-4H-chromen-4-one 

Downstream Products

• 1017961-71-5 7-methyl-4-(4-phenoxybutoxy)-5H-furo[3,2-g][1]benzopyran-5-one 
• 1350717-69-9 C₂₄H₂₁NO₆ 
• 1350717-68-8 C₂₅H₂₃NO₅ 
• 1350717-70-2 C₂₄H₂₃NO₅ 
• 1350717-67-7 C₂₅H₁₈N₂O₅ 
• 1350717-66-6 C₂₁H₁₇NO₅ 
• 1350717-63-3 N-[4-oxo-5-(3,4,5-trimethoxyphenyl)thiazolidin-3-yl]-(7-methyl-5-oxo-5H-furo[3,2-g][1]benzopyran-4-yloxy)acetamide 
• 1350717-62-2 C₂₄H₂₂N₂O₈ 
• 82-02-0 Khellin 
• 478-42-2 khellinol 
• 481-71-0 NSC₃₃₀₇₉₆ 

Relevant academic research and scientific papers

Design and molecular modeling of novel P38α MAPK inhibitors targeting breast cancer, synthesized from oxygen heterocyclic natural compounds

Two new series of furochromone and benzofuran derivatives were designed, synthesized and evaluated for their in vitro anticancer activity against MCF-7 and MDA231 breast cancer cell lines. Compounds 5, 6, 7, 9, 15a, 16, 17a and 18 exhibited the best antip

DNA binding, antiviral activities and cytotoxicity of new furochromone and benzofuran derivatives

Bromination of visnagin (1) afforded 9-bromovisnagin (2) which on its alkaline hydrolysis afforded the 3-acetyl benzofuran derivative (3). The condensation of (3) with hydrazine hydrate, phenylhydrazine and/or hydroxylamine hydrochloride afforded the corr

4-Phenoxybutoxy-substituted heterocycles - A structure-activity relationship study of blockers of the lymphocyte potassium channel Kv1.3

The voltage-gated potassium channel Kv1.3 constitutes an attractive pharmacological target for the treatment of effector memory T cell-mediated autoimmune diseases such as multiple sclerosis and psoriasis. Using 5-methoxypsoralen (5-MOP, 1), a compound isolated from Ruta graveolens, as a template we previously synthesized 5-(4-phenoxybutoxy)psoralen (PAP-1, 2) which inhibits Kv1.3 with an IC50 of 2 nM. Since PAP-1 is more than 1000-fold more potent than 5-MOP, we here investigated whether attaching a 4-phenoxybutoxy side chain to other heterocyclic systems would also produce potent Kv1.3 blockers. While 4-phenoxybutoxy-substituted quinolines, quinazolines and phenanthrenes were inactive, 4-phenoxybutoxy-substituted quinolinones, furoquinolines, coumarins or furochromones inhibited Kv1.3 with IC50s of 150 nM to 10 μM in whole-cell patch-clamp experiments. Our most potent new compound is 4-(4-phenoxybutoxy)-7H-furo[3,2-g]chromene-7-thione (73, IC50 17 nM), in which the carbonyl oxygen of PAP-1 is replaced by sulfur. Taken together, our results demonstrate that the psoralen system is a crucial part of the pharmacophore of phenoxyalkoxypsoralen-type Kv1.3 blockers.

NOVEL BENZOFURAN POTASSIUM CHANNEL BLOCKERS AND USES THEREOF

The present invention relates to compounds useful in the modulation of potassium channel activity in cells, in particular the activity of Kv1.3 channels found in T cells. The invention also relates to the use of these compounds in the treatment or prevent

NOVEL CHROMENONE POTASSIUM CHANNEL BLOCKERS AND USES THEREOF

The present invention relates to compounds useful in the modulation of potassium channel activity in cells, in particular the activity of Kv1.3 channels found in T cells. The invention also relates to the use of these compounds in the treatment or prevent

Synthesis and biological activities of flavonoid derivatives as A3 adenosine receptor antagonists

A broad screening of phytochemicals has demonstrated that certain flavone and flavonol derivatives have a relatively high affinity at A3 adenosine receptors, with K(i) values of ≥1 μM (Ji et al. J. Med. Chem. 1996, 39, 781-788). We have further modified the flavone structure to achieve a degree of selectivity for cloned human brain A3 receptors, determined in competitive binding assays versus [125I]AB-MECA [N6-(4-amino-3- iodebenzyl)adenosine-5'-(N-methyluronamide)]. Affinity was determined in radioligand binding assays at rat brain A1 and A(2A) receptors using [3H]- N6-PIA ([3H]-(R)-N6-phenylisopropyladenosine) and [3H]CGS21680 [[3H]-2- [[4-(2-carboxyethyl)phenyl]ethylamino]-5'-(N-ethylcarbamoyl)adenosine], respectively. The triethyl and tripropyl ether derivatives of the flavonol galangin, 4, had K(i) values of 0.3-0.4 μM at human A3 receptors. The presence of a 5-hydroxyl group increased selectivity of flavonols for human A3 receptors. The 2',3,4',7-tetraethyl ether derivative of the flavonol morin, 7, displayed a K(i) value of 4.8 μM at human A3 receptors and was inactive at rat A1/A(2A) receptors. 3,6-Dichloro-2'-(isopropyloxy)-4'- methylflavone, 11e, was both potent and highly selective (~200-fold) for human A3 receptors (K(i) = 0.56 μM). Among dihydroflavonol analogues, the 2-styryl instead of the 2-aryl substituent, in 15, afforded selectivity for human A3 vs rat A1 or A(2A) receptors. The 2-styryl-6-propoxy derivative, 20, of the furanochromone visnagin was 30-fold selective for human A3 receptors vs either rat A1 or A(2A) receptors. Several of the more potent derivatives effectively antagonized the effects of an agonist in a functional A3 receptor assay, i.e. inhibition of adenylyl cyclase in CHO cells expressing cloned rat A3 receptors. In conclusion, these series of flavonoids provide leads for the development of novel potent and subtype selective A3 antagonists.

Kinetic and Thermodynamic Control in the Lithiation of 2,6-Dimethylchromone, and Selective Lithiations in 2-(x-Furyl)chromones and in Furanochromones Related to Khellin

The addition of 2,6-dimethylchromone to lithium di-isopropylamide (LDA) allows formation, under thermodynamic control, of the 2-methylene carbanion (3), but this seems to react at the carbonyl oxygen atom with carbon dioxide so no caboxylic acid can be isolated.With ethyl chloroformate (but not diethyl carbonate) this carbanion does afford the expected ethyl chromon-2-ylacetate (1d).The chromonylacetic acid is also obtainable if the starting chromone bears a free hydroxy group at position 5 as in (4a).From the addition of 2,6-dimethylchromone to a mixture of LDA and diethyl carbonate there results ethyl 2,6-dimethylchromone-3-carboxylate (9b) because the chromone 3-carbanion formed under kinetic control is trapped before it isomerises.The reaction resembles that found in flavones.Flavone (at the 3-position) and furan or benzofuran (at the 2-position) are about equally effective in competing for deprotonation by LDA.Khellin (14a) is probably deprotonated by LDA at both furan and pyrone sites but carboxylation affords only the furan carboxylic acid (14b) and unchanged khellin.This accords with the above results, as does the deprotonation and carboxylation of the phenol (15b), norvisnagin, which affords the chromonylacetic acid (16).With LDA followed by carbon dioxide the 2-(2-furyl)chromone (18a) surprisingly gives only the dicarboxylic acid (18b); apparently the dicarbanion is more stable than either monocarbanion.The isomeric 2-(3-furyl)chromone (20a) under similar conditions affords only the chromone-3-carboxylic acid (20b); the furan ring is untouched.

SELECTIVE CLAISEN MIGRATION IN CHROMONES. A CONVENIENT SYNTHESIS OF THE LINEAR FURANOCHROMONES DESMETHOXYVISNAGIN, NORVISNAGIN, and VISNAGIN

A convenient synthesis of furanochromones, viz. 7-methyl-5H-furobenzopyran-5-one (desmethoxyvisnagin), 4-hydroxy-7-methyl-5H-furobenzopyran-5-one (norvisnagin), and 4-methoxy-7-methyl-5H-furobenzopyran-5-one (visnagin) is described.The synthesis utilises blocking the 8-position of the corresponding 7-allyloxychromone derivative with iodine, Claisen migration, followed by oxidation and subsequent cyclo-dehydration.