1125-74-2

Upstream product

• 1126-20-1 2-allyloxyphenol 
• 108059-04-7 2-allyloxy-3-hydroxybenzaldehyde 
• 4827-99-0 α-<2.5-Diaethoxy-tetrahydro>-furfuroyl-α-allyl-essigsaeure-aethylester 
• 579-60-2 6-allylguaicol 
• 2848-25-1 2-acetoxyphenol 
• 106-95-6 allyl bromide 
• 120-80-9 benzene-1,2-diol 
• 90-05-1 2-methoxy-phenol 
• 23343-06-8 2-allyloxy-3-methoxy-benzaldehyde 
• 4125-43-3 O-allyl guaiacol 

Downstream Products

• 2896-63-1 3-propylbenzene-1,2-diol 
• 50916-57-9 3,6-diallylbenzene-1,2-diol 
• 13620-82-1 4-allyl-1,2-phenylene diacetate 
• 860603-26-5 1,4-diallyl-2,3-bis-allyloxy-benzene 

Relevant academic research and scientific papers

Structure–activity relationships and docking studies of hydroxychavicol and its analogs as xanthine oxidase inhibitors

Hydroxychavicol (HC), which is obtained from the leaves of Piper betle LINN. (Piperaceae), inhibits xanthine oxidase (XO) with an IC50 value of 16.7μM, making it more potent than the clinically used allopurinol (IC50=30.7μM). Herein, a structure–activity relationship analysis of the polar part analogs of HC was conducted and an inhibitor was discovered with a potency 13 times that of HC. Kinetic studies have revealed that HC and its active analog inhibit XO in an uncompetitive manner. The binding structure prediction of these inhibitor molecules to the XO complex with xanthine suggested that both compounds (HC and its analog) could simultaneously form hydrogen bonds with xanthine and XO.

Structure–Activity Relationship of Anti-malarial Allylpyrocatechol Isolated from Piper betle

Malaria disease remains a serious worldwide health problem. In South-East Asia, one of the malaria infection “hot-spots,” medicinal plants such as Piper betle have traditionally been used for the treatment of malaria, and allylpyrocatechol (1), a constituent of P. betle, has been shown to exhibit anti-malarial activities. In this study, we verified that 1 showed in vivo anti-malarial activity through not only intraperitoneal (i.p.) but also peroral (p.o.) administration. Additionally, some analogs of 1 were synthesized and the structure–activity relationship was analyzed to disclose the crucial sub-structures for the potent activity.

Hybridization of β-Adrenergic Agonists and Antagonists Confers G Protein Bias

Starting from the β-adrenoceptor agonist isoprenaline and beta-blocker carvedilol, we designed and synthesized three different chemotypes of agonist/antagonist hybrids. Investigations of ligand-mediated receptor activation using bioluminescence resonance energy transfer biosensors revealed a predominant effect of the aromatic head group on the intrinsic activity of our ligands, as ligands with a carvedilol head group were devoid of agonistic activity. Ligands composed of a catechol head group and an antagonist-like oxypropylene spacer possess significant intrinsic activity for the activation of Gαs, while they only show weak or even no β-arrestin-2 recruitment at both β1- and β2-AR. Molecular dynamics simulations suggest that the difference in G protein efficacy and β-arrestin recruitment of the hybrid (S)-22, the full agonist epinephrine, and the β2-selective, G protein-biased partial agonist salmeterol depends on specific hydrogen bonding between Ser5.46 and Asn6.55, and the aromatic head group of the ligands.

SUBSTITUTED CATHECHOLS AS INHIBITORS OF IL-4 AND IL-5 FOR THE TREATMENT BRONCHIAL ASTHMA

The present invention relates to compounds of general formula 1 for the treatment of bronchial asthma by inhibition of IL-4 or IL-5 pathway inhibition. The present invention also relates to the use of compound of general formula 1 for the treatment of bronchial by inhibition of IL-4 or IL-5 pathway. The present invention also relates to the method of treating asthma by inhibition of IL-4 or IL-5 pathway by administration of compound or said composition through oral, intranasal, route or by inhalation to a mammal in need thereof. Compound of general formula 1 may be used for reducing perivascular and peribronchial inflammation.

INHIBITORS OF PHOSPHATIDYLINOSITOL-3-KINASE (PI3) AND INDUCERS OF NITRIC OXIDE (NO)

The present invention relates to compounds of general formula 1 for the treatment of malignancy by inhibition of PI3-Akt pathway and or induction of NO. The present invention also relates to the use of compound of general formula 1 for the treatment of malignancy by inhibition of PI3-Akt pathway and or induction of NO. The present invention further relates to a method of treating malignancy by inhibition of PI3-Akt pathway and or induction of NO by administration of compound or said composition to a mammal in need thereof.