6247-99-0

Basic information

• Product Name: aloe emodin anthrone
• Synonyms: aloe emodin anthrone
• CAS NO: 6247-99-0
• Molecular Formula: C₁₅H₁₂O₄
• Molecular Weight: 256.25338
• Mol File: 6247-99-0.mol
• Article Data: 1

Chemical Properties

• Appearance: /
• CAS DataBase Reference: aloe emodin anthrone(CAS DataBase Reference)
• NIST Chemistry Reference: aloe emodin anthrone(6247-99-0)
• EPA Substance Registry System: aloe emodin anthrone(6247-99-0)

Safety Data

• Hazardous Substances Data: 6247-99-0(Hazardous Substances Data)

Upstream product

• 1415-73-2 10-glucopyranosyl-1,8-dihydroxy-3-(hydroxymethyl)-9(10H)-anthracenone 
• 7732-18-5 water 
• 50-81-7 ascorbic acid 
• 59-88-1 phenylhydrazine hydrochloride 

Downstream Products

• 481-72-1 1,8-dihydroxy-3-hydroxymethyl-9,10-anthracenedione 
• 491-58-7 1,8-dihydroxy-3-methylanthracen-9(10H)-one 
• 13928-72-8 1,8-diacetoxy-3-acetoxymethyl-10-(tetra-O-acetyl-ξ-D-glucopyranosyl)-anthrone 
• 1415-73-2 10-glucopyranosyl-1,8-dihydroxy-3-(hydroxymethyl)-9(10H)-anthracenone 
• 61446-06-8 1,8,9-triacetoxy-3-methyl-anthracene 
• 481-74-3 Chrysophanol 

Relevant articles and documents

Permeation-enhancing effect of aloe-emodin anthrone on water-soluble and poorly permeable compounds in rat colonic mucosa

The aims of this study were to examine the enhancing effects of aloe-emodin enthrone (AEA) on the colonic membrane permeability of water-soluble and poorly permeable compounds and to clarify the mechanism of the permeation-enhancing activity of AEA. The permeation-enhancing activity of AEA was estimated from changes in the permeability coefficient of 5(6)-carboxyfluorescein (CF) in rat colonic mucosa using a Ussing-type chamber. Various inhibitors were used to investigate the mechanism of action of AEA. The structural change in the membrane and the cytotoxicity of AEA in the intestinal mucosa were evaluated by measuring the electrical resistance of the membrane (Rm) and lactate dehydrogenase (LDH) activity, respectively. AEA significantly increased the permeation of CF in a dose-dependent manner. The enhanced permeability was significantly suppressed by a histamine H1 receptor antagonist, pyrilamine, and a mast cell stabilizer, ketotifen, but not by a histamine H 2 receptor antagonist, cimetidine. The enhancing effect was also inhibited by an inhibitor of protein kinase C (PKC). Potential difference and short-circuit current values decreased, while Rm values remained constant throughout the experiment. The addition of AEA to the mucosal solution decreased Rm to 30%, but then remained constant. LDH activity with AEA was not significantly different from that of the control. In conclusion, AEA is a candidate for effective absorption enhancers without damage of the membrane and cytotoxicity. We propose that AEA stimulates mast cells within the colonie mucosa to release histamine, which probably bind to the H1 receptor. The intracellular PKC route activated by H1 receptor activation enhances the permeability of water-soluble and poorly permeable drugs via opening of tight junctions in rat colonic membrane.