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    CAS No. 559-70-6 Price
    Catalog No.CFN98935Purity>=98%
    Molecular Weight426.7 Type of CompoundTriterpenoids
    FormulaC30H50OPhysical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Featured Products
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    Chlorogenic acid

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    Biological Activity
    Description: beta-Amyrin has antiviral, hepatoprotective, antinociceptive, anti-inflammatory, it retard acute inflammation in rat model of periodontitis. Beta-Amyrin can enhance the total sleeping behavior in pentobarbital-induced sleeping model via the activation of GABAergic neurotransmitter system through GABA content in the brain.alpha- and beta-Amyrin mixture has gastro-protective activity, the mechanism involves at least in part the activation of capsaicin-sensitive primary afferent neurons; it also has sedative and anxiolytic effects, the mechanism may involve an action on benzodiazepine-type receptors, and also an antidepressant effect where noradrenergic mechanisms will probably play a role.
    Targets: GABA Receptor | P450 (e.g. CYP17) | cAMP | PKC | PKA | PGE | TNF-α | Antifection
    In vitro:
    J Pharm Sci. 1974 Mar;63(3):471-3.
    Antiviral activity of triterpenoid saponins containing acylated beta-amyrin aglycones.[Pubmed: 4820390]
    Antiviral activity of triterpenoid saponins containing acylated beta-Amyrin aglycones.
    In vivo:
    Pharm Biol. 2014 Nov;52(11):1478-86.
    beta-Amyrin and alpha-amyrin acetate isolated from the stem bark of Alstonia boonei display profound anti-inflammatory activity.[Pubmed: 25026352]
    Alstonia boonei De Wild (Apocyanaceae) is used in ethnomedicine for the management of malaria, ulcer, rhematic pain, toothache, and inflammatory disorders.To investigate the anti-inflammatory potential of beta-Amyrin and α-amyrin acetate isolated from the stem bark of Alstonia boonei using animal models.
    Chromatographic purification of the crude methanol extract led to the isolation and structure elucidation of beta-Amyrin and α-amyrin acetate. Their anti-inflammatory activities were evaluated in rodents using egg albumen-induced paw edema and xylene-induced ear edema models. The gastric ulcerogenic, in vivo leucocyte migration, and RBC membrane stabilization tests were also investigated. α-Amyrin acetate at 100 mg/kg showed significant (p < 0.05) inhibition of egg albumen-induced paw edema with % inhibition of 40 at the 5th hour. Oral administration up to 100 mg/kg did not produce significant (p > 0.01) irritation of the gastric mucosa while significant (p < 0.01) ulceration was recorded for indomethacin at 40 mg/kg compared with the negative control. At 100 μg/mL, both beta-Amyrin and α-amyrin acetate inhibited heat-induced hemolysis to as much 47.2 and 61.5%, respectively, while diclofenac sodium (100 μg/mL) evoked only 40.5% inhibition. Both compounds at 100 µg/ear produced significant (p < 0.01) inhibition of ear edema in mice by 39.4 and 55.5%, respectively. Also at 100 mg/kg (p.o.) α-amyrin acetate evoked 60.3% reduction in total leucocyte count and significant (p < 0.05) suppression (47.9%) of neutrophil infiltration.
    This study generally provided evidence of profound anti-inflammatory activity of β-amyrin and α-amyrin acetate isolated from the Alstonia boonei stem bark.
    J Pharmacol Exp Ther. 2005 Apr;313(1):310-8.
    Antinociceptive properties of mixture of alpha-amyrin and beta-amyrin triterpenes: evidence for participation of protein kinase C and protein kinase A pathways.[Pubmed: 15626726 ]

    The mixture of the two pentacyclic triterpenes alpha-amyrin and beta-Amyrin, isolated from the resin of Protium kleinii and given by intraperitoneal (i.p.) or oral (p.o.) routes, caused dose-related and significant antinociception against the visceral pain in mice produced by i.p. injection of acetic acid. Moreover, i.p., p.o., intracerebroventricular (i.c.v.), or intrathecal (i.t.) administration of alpha,beta-Amyrin inhibited both neurogenic and inflammatory phases of the overt nociception caused by intraplantar (i.pl.) injection of formalin. Likewise, alpha,beta-Amyrin given by i.p., p.o., i.t., or i.c.v. routes inhibits the neurogenic nociception induced by capsaicin. Moreover, i.p. treatment with alpha,beta-Amyrin was able to reduce the nociception produced by 8-bromo-cAMP (8-Br-cAMP) and by 12-O-tetradecanoylphorbol-13-acetate (TPA) or the hyperalgesia caused by glutamate. On the other hand, in contrast to morphine, alpha,beta-Amyrin failed to cause analgesia in thermal models of pain. The antinociception caused by the mixture of compounds seems to involve mechanisms independent of opioid, alpha-adrenergic, serotoninergic, and nitrergic system mediation, since it was not affected by naloxone, prazosin, yohimbine, DL-p-chlorophenylalanine methyl ester, or L-arginine. Interestingly, the i.p. administration of alpha,beta-Amyrin reduced the mechanical hyperalgesia produced by i.pl. injection of carrageenan, capsaicin, bradykinin, substance P, prostaglandin E2, 8-Br-cAMP, and TPA in rats. However, the mixture of compounds failed to alter the binding sites of [3H]bradykinin, [3H]resiniferatoxin, or [3H]glutamate in vitro.
    It is concluded that the mixture of triterpene alpha-amyrin and beta-Amyrin produced consistent peripheral, spinal, and supraspinal antinociception in rodents, especially when assessed in inflammatory models of pain. The mechanisms involved in their action are not completely understood but seem to involve the inhibition of protein kinase A- and protein kinase C-sensitive pathways.
    Inflammopharmacology. 2008 Feb;16(1):48-52.
    Anti-inflammatory effect of alpha, beta-Amyrin, a pentacyclic triterpene from Protium heptaphyllum in rat model of acute periodontitis.[Pubmed: 18046512 ]
    This study was aimed to evaluate the anti-inflammatory potential of triterpene alpha, beta-Amyrin in rats on acute phase periodontitis.
    Periodontitis was induced by ligature placement around the maxillary right second molar tooth. Rats (n = 8/group) were pretreated with alpha, beta-Amyrin (5 and 10 mg/kg, p. o.), two hours before the induction of periodontal inflammation. Sham-operated and positive controls (lumiracoxib and dexamethasone) were included. Six hours later, plasma levels of TNF-alpha were analysed. Rats were sacrificed at 24 h, and the gingival tissue analysed for myeloperoxidase (MPO) and thiobarbituric acid-reactive substances (TBARS), as measures of neutrophil influx and lipid-peroxidation, respectively alpha, beta-Amyrin as well as dexamethasone significantly inhibited the periodontitis-associated increases of TNF-alpha, and the gingival MPO and TBARS. alpha, beta-Amyrin effect was more prominent at 5 mg/kg. Lumiracoxib manifested varied influence on the studied parameters.
    These results provide evidence to show that alpha, beta-Amyrin retards acute inflammation in rat model of periodontitis and warrant further study on its efficacy to prevent chronic periodontitis-associated bone loss.
    Pharmacol Biochem Behav. 2006 Dec;85(4):827-34.
    A possible mechanism for anxiolytic and antidepressant effects of alpha- and beta-amyrin from Protium heptaphyllum (Aubl.) March.[Pubmed: 17207523 ]
    In the present study, we examined the anxiolytic and antidepressant effects of the mixture of alpha- and beta-Amyrin (AMY), pentacyclic triterpenes isolated from the stem bark resin of Protium heptaphyllum.
    These effects of AMY were demonstrated by the open-field, elevated-plus-maze, rota rod, forced swimming, and pentobarbital-induced sleeping time tests, in mice. In the open-field test, AMY at the doses of 10, 25 and 50 mg/kg, after intraperitoneal or oral administrations, significantly decreased the number of crossings, grooming, and rearing. All these effects were reversed by the pre-treatment with flumazenil (2.5 mg/kg, i.p.), similarly to those observed with diazepam used as a positive standard. In the elevated-plus-maze test, AMY increased the time of permanence and the number of entrances in the open arms. On the contrary, the time of permanence and the number of entrances in the closed arms were decreased. All these effects were also completely reversed by flumazenil, an antagonist of benzodiazepine receptors. In the pentobarbital-induced sleeping time test, AMY at the same doses significantly increased the animals sleeping time duration. In the rota rod test, AMY did not alter motor coordination and, thus, was devoid of effects, as related to controls. Since AMY, at the doses of 10 and 25 mg/kg, showed a sedative effect in the open field test, lower doses (2.5 and 5.0 mg/kg) were used in the forced swimming test, producing a decrease in the immobility time, similarly to that of imipramine, the positive control. The effect of AMI was greater when it was administered 15 min after imipramine (10 mg/kg). However, the antidepressant AMY effects were not altered by the previous administration of paroxetine, a selective blocker of serotonin uptake. In addition, AMY effects in the forced swimming test were totally blocked by reserpine pretreatment, a drug known to induce depletion of biogenic amines.
    In conclusion, the present work evidenced sedative and anxiolytic effects of AMY that might involve an action on benzodiazepine-type receptors, and also an antidepressant effect where noradrenergic mechanisms will probably play a role.
    beta-Amyrin Description
    Source: The stem barks of Alstonia boonei
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.3436 mL 11.7178 mL 23.4357 mL 46.8713 mL 58.5892 mL
    5 mM 0.4687 mL 2.3436 mL 4.6871 mL 9.3743 mL 11.7178 mL
    10 mM 0.2344 mL 1.1718 mL 2.3436 mL 4.6871 mL 5.8589 mL
    50 mM 0.0469 mL 0.2344 mL 0.4687 mL 0.9374 mL 1.1718 mL
    100 mM 0.0234 mL 0.1172 mL 0.2344 mL 0.4687 mL 0.5859 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Animal Research:
    Behav Brain Res. 2015 May 27;291:232-236.
    Positive effects of β-amyrin on pentobarbital-induced sleep in mice via GABAergic neurotransmitter system.[Pubmed: 26026786]
    Sleep loss, insomnia, is considered a sign of imbalance of physiological rhythm, which can be used as pre-clinic diagnosis of various neuropsychiatric disorders. The aim of the present study is to understand the pharmacological actions of α- or beta-Amyrin, natural triterpene compound, on the sleep in mice.
    To analyze the sleeping behavior, we used the well-known pentobarbital-induced sleeping model after single administration of either α- or beta-Amyrin. The sleeping onset time was remarkably decreased and duration was prolonged by beta-Amyrin (1, 3, or 10mg/kg) but not by α-amyrin (1, 3, or 10mg/kg). These effects were significantly blocked by GABAA receptor antagonist, bicuculline. Moreover, beta-Amyrin increased brain GABA level compared to the vehicle administration.
    Overall, the present study suggests that beta-Amyrin would enhance the total sleeping behavior in pentobarbital-induced sleeping model via the activation of GABAergic neurotransmitter system through GABA content in the brain.
    J Ethnopharmacol. 2005 Apr 8;98(1-2):103-8.
    Protective effect of alpha- and beta-amyrin, a triterpene mixture from Protium heptaphyllum (Aubl.) March. trunk wood resin, against acetaminophen-induced liver injury in mice.[Pubmed: 15763370 ]
    In the search of hepatoprotective agents from natural sources, alpha- and beta-Amyrin, a triterpene mixture isolated from the trunk wood resin of folk medicinal plant, Protium heptaphyllum was tested against acetaminophen-induced liver injury in mice. Liver injury was analysed by quantifying the serum enzyme activities and by histopathological observations.
    In mice, acetaminophen (500 mg/kg, p.o.) caused fulminant liver damage characterized by centrilobular necrosis with inflammatory cell infiltration, an increase in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, a decrease in hepatic glutathione (GSH) and 50% mortality. Pretreatment with alpha- and beta-Amyrin (50 and 100 mg/kg, i.p. at 48, 24, and 2 h before acetaminophen) attenuated the acetaminophen-induced acute increase in serum ALT and AST activities, replenished the depleted hepatic GSH, and considerably reduced the histopathological alterations in a manner similar to N-acetylcysteine, a sulfhydryls donor. Also, the acetaminophen-associated mortality was completely suppressed by terpenoid pretreatment. Further, alpha- and beta-Amyrin could potentiate the pentobarbital (50 mg/kg, i.p.) sleeping time, suggesting the possible suppression of liver cytochrome-P450. These findings indicate the hepatoprotective potential of alpha- and beta-Amyrin against toxic liver injury and suggest that the diminution in oxidative stress and toxic metabolite formation as likely mechanisms involved in its hepatoprotection.
    In conclusion, this study supports the traditional use of Protium heptaphyllum resin as a medicinal agent and suggests the feasibility of developing herbal drugs for treatment of liver disorders.
    Planta Med. 2004 Aug;70(8):780-2.
    Gastroprotective effect of the mixture of alpha- and beta-amyrin from Protium heptaphyllum: role of capsaicin-sensitive primary afferent neurons.[Pubmed: 15368675 ]
    This investigation evaluated the role of capsaicin-sensitive afferent neurons in the gastroprotective effect of alpha- and beta-Amyrin, a triterpenoid mixture isolated from Protium heptaphyllum resin.
    Gastric mucosai damage was induced in mice by intragastric ethanol and assessed by planimetry. Mice pretreated orally with the amyrin mixture (50 and 100 mg/kg) or capsaicin (2.5 and 5 mg/kg), the pungent principle from red hot peppers, showed a significantly lower intensity of ethanol-associated gastric mucosal damage, in relation to vehicle-treated controls. At higher doses both these agents produced either a diminished protection or no significant effect.
    The maximal gastroprotection that was observed at the dose of 100 mg/kg amyrin mixture was almost abolished in mice with their sensory afferents chemically ablated by a neurotoxic dose of capsaicin, suggesting that the gastro-protective mechanism of alpha- and beta-Amyrin mixture involves at least in part the activation of capsaicin-sensitive primary afferent neurons.