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    Momordin Ic
    Information
    CAS No. 96990-18-0 Price $118 / 20mg
    Catalog No.CFN99726Purity>=98%
    Molecular Weight764.93Type of CompoundTriterpenoids
    FormulaC41H64O13Physical DescriptionBrown powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Momordin Ic has hypoglycemic, anticancer, anti-allergic, anti-pruritogenic, hepatoprotective, antinociceptive and anti-inflammatory effects. It accelerates gastrointestinal transit partially by stimulating synthesis of 5-HT to act through 5-HT(2), possibly 5-HT(2C) and/or 5-HT(2B) receptors, which, in turn, increases synthesis of prostaglandins. Momordin Ic induces apoptosis through oxidative stress-regulated mitochondrial dysfunction involving the MAPK and PI3K-mediated iNOS and HO-1 pathways.
    Targets: Caspase | PARP | ROS | Bcl-2/Bax | p38MAPK | JNK | ERK | Akt | NO | NOS | HO-1 | PI3K | 5-HT Receptor
    In vivo:
    Eur J Pharmacol. 2000 Mar 24;392(1-2):71-7.
    Acceleration of gastrointestinal transit by momordin Ic in mice: possible involvement of 5-hydroxytryptamine, 5-HT(2) receptors and prostaglandins.[Pubmed: 10748274]

    METHODS AND RESULTS:
    Possible involvement of 5-hydroxytryptamine (5-HT), 5-HT receptors and prostaglandins in the acceleration of gastrointestinal transit by Momordin Ic was investigated in mice. Accelerative effect of Momordin Ic (25 mg/kg, p.o.) on gastrointestinal transit was attenuated by pretreatment with a bolus of DL-p-chlorophenylalanine methyl ester (an inhibitor of 5-HT synthesizing enzyme), but not repeated pretreatment with DL-p-chlorophenylalanine methyl ester. Furthermore, cyproheptadine (a nonselective 5-HT(2) receptor antagonist), ritanserin (a 5-HT(2A/2B/2C) receptor antagonist) and clozapine (a 5-HT(2A/2C) receptor antagonist) also attenuated the effect of Momordin Ic, but methiothepin (a 5-HT(1) receptor antagonist), MDL 72222 (3-tropanyl-3,5-dichlorobenzoate) and metoclopramide (5-HT(3) receptor antagonists), tropisetron (a 5-HT(3/4) receptor antagonist), ketanserin and haloperidol (5-HT(2A) receptor antagonists) did not. These results suggested a possible involvement of endogenous 5-HT and 5-HT(2B/2C) over 5-HT(2A) receptors. Attenuation by pretreatment with indomethacin (an inhibitor of prostaglandins synthesis) suggested involvement of prostaglandins.
    CONCLUSIONS:
    It is postulated that Momordin Ic accelerates gastrointestinal transit partially by stimulating synthesis of 5-HT to act through 5-HT(2), possibly 5-HT(2C) and/or 5-HT(2B) receptors, which, in turn, increases synthesis of prostaglandins.
    J Pharmacol Exp Ther. 1999 May;289(2):729-34.
    Inhibition of gastric emptying by triterpene saponin, momordin Ic, in mice: roles of blood glucose, capsaicin-sensitive sensory nerves, and central nervous system.[Pubmed: 10215646]
    The roles of capsaicin-sensitive sensory nerves and the central nervous system in the inhibitory effect of Momordin Ic, a principal saponin constituent in various Chinese and Japanese herbal medicines, such as the fruit of Kochia scoparia (L.) SCHRAD., on gastric emptying were investigated in nonnutrient meal- or nutrient meal-loaded mice.
    METHODS AND RESULTS:
    Momordin Ic (12.5-50 mg/kg) significantly inhibited gastric emptying in 1.5% carboxymethyl cellulose sodium salt test meal-loaded mice by 8.4%-60.6%, 40% glucose test meal-loaded mice by 42.8% (50 mg/kg), milk test meal-loaded mice by 36.4% (50 mg/kg), and 60% ethanol test meal-loaded mice by 37.2% (50 mg/kg). The inhibitory effect on the gastric emptying in 1.5% carboxymethyl cellulose sodium salt test meal-loaded mice was potentiated by glucose (2 g/kg, i.v. or 5 g/kg, i.p.), but markedly attenuated by pretreatment with alloxan (50 mg/kg, i.v.) and streptozotocin (100 mg/kg, i.v.), in which the activity of sympathetic nervous system was decreased, or by insulin (1 or 3 U/kg, s.c.). The effect of insulin (1 U/kg) was markedly reduced by glucose (2 g/kg, i.v.), which can directly nourish the brain, but not by fructose (2 g/kg, i.v.), which cannot be used by the brain. The effect of Momordin Ic was also attenuated by pretreatment with capsaicin (75 mg/kg in total, s.c.).
    CONCLUSIONS:
    These results suggest that the inhibition of gastric emptying by Momordin Ic is relative to serum glucose and, at least in part, mediated by capsaicin-sensitive sensory nerves and the central nervous system.
    Chem Pharm Bull (Tokyo). 1998 Sep;46(9):1399-403.
    Antidiabetic principles of natural medicines. III. Structure-related inhibitory activity and action mode of oleanolic acid glycosides on hypoglycemic activity.[Pubmed: 9775435]

    METHODS AND RESULTS:
    We examined the structure-related activity of oleanolic acid glycosides with respect to their inhibitory effect on the increase in serum glucose in oral glucose-loaded rats and their mechanism of action using oleanolic acid 3-O-glucuronide and Momordin Ic. Both the 3-O-monodesmoside structure and 28-carboxyl group were confirmed to be essential for such activity, and the 3-O-glucuronide was more potent than 3-O-glucoside. On the other hand, the 28-ester glucoside moiety and 6'-methyl ester of the glucuronide moiety reduced such activity. Oleanolic acid 3-O-glucuronide and Momordin Ic, both of which inhibited the increase in serum glucose in oral glucose-loaded rats, did not lower serum glucose in normal or intraperitoneal glucose-loaded rats, or alloxan-induced diabetic mice. These glycosides were found to suppress gastric emptying in rats, and also inhibit glucose uptake in the rat small intestine in vitro.
    CONCLUSIONS:
    These results indicate that oleanolic acid 3-O-glucuronide and Momordin Ic, given orally, have neither insulin-like activity nor insulin releasing-activity. They exhibit their hypoglycemic activity by suppressing the transfer of glucose from the stomach to the small intestine and by inhibiting glucose transport at the brush border of the small intestine.
    Arch Pharm Res. 2002 Jun;25(3):336-42.
    Anti-rheumatoid arthritis effect of the Kochia scoparia fruits and activity comparison of momordin lc, its prosapogenin and sapogenin.[Pubmed: 12135107]

    METHODS AND RESULTS:
    MeOH extract of Kochia scoparia was fractionated into CHCl3-, EtOAc- and BuOH extracts and the last fraction were hydrolyzed by 3%-NaOH (MeOH-H2O) to compare the bioactivities on antinociceptive and anti-inflammatory effects. Silica gel column chromatography of BuOH fraction afforded a large amount of 3-O-beta-D-xylopyranosyl (1-->3)-beta-D-glucuronopyranosyl oleanolic acid (Momordin Ic, 4) and that of acid hydrolysate of BuOH fraction gave 3-O-beta-D-glucuronopyranosyl oleanolic acid (momordin lb, 3), its 6'-O-methyl ester (2) and oleanolic acid (1). Silica gel column chromatography of alkaline hydrolysate afforded a large amount of 4. MeOH extract and both EtOAc- and BuOH fractions were active in the rheumatoidal rat induced Freund's complete adjuvant reagent (FCA) whereas CHCl3 fraction was inactive. Compound 1 and 4 showed significant activities in the same assay but oleanolic acid 3-O-glucuronopyranoside (3) showed no activity. These fashions were also observed in carrageenan-induced edema of the rat and in the antinociceptive activity tests undertaken in hot plate- and writhing methods.
    CONCLUSIONS:
    These results suggest that momordin lc and its aglycone, oleanolic acid, could be active principles for rheumatoid arthritis.
    Momordin Ic Description
    Source: The fruits of Kochia scoparia (L.) Schrad.
    Solvent: DMSO, Pyridine, Methanol, Ethanol, 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 1.3073 mL 6.5365 mL 13.0731 mL 26.1462 mL 32.6827 mL
    5 mM 0.2615 mL 1.3073 mL 2.6146 mL 5.2292 mL 6.5365 mL
    10 mM 0.1307 mL 0.6537 mL 1.3073 mL 2.6146 mL 3.2683 mL
    50 mM 0.0261 mL 0.1307 mL 0.2615 mL 0.5229 mL 0.6537 mL
    100 mM 0.0131 mL 0.0654 mL 0.1307 mL 0.2615 mL 0.3268 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.
    Protocol
    Kinase Assay:
    Apoptosis. 2013 Jun;18(6):751-65.
    Momordin Ic induces HepG2 cell apoptosis through MAPK and PI3K/Akt-mediated mitochondrial pathways.[Pubmed: 23417763]
    Momordin Ic is a natural triterpenoid saponin enriched in various Chinese and Japanese natural medicines such as the fruit of Kochia scoparia (L.) Schrad. So far, there is little scientific evidence for Momordin Ic with regard to the anti-tumor activities. The aim of this work was to elucidate the anti-tumor effect of Momordin Ic and the signal transduction pathways involved.
    METHODS AND RESULTS:
    We found that Momordin Ic induced apoptosis in human hepatocellular carcinoma HepG2 cells, which were supported by DNA fragmentation, caspase-3 activation and PARP cleavage. Meanwhile, Momordin Ic triggered reactive oxygen species (ROS) production together with collapse of mitochondrial membrane potential, cytochrome c release, down-regulation of Bcl-2 and up-regulation of Bax expression. The activation of p38 and JNK, inactivation of Erk1/2 and Akt were also demonstrated. Although ROS production rather than NO was stimulated, the expression of iNOS and HO-1 were altered after Momordin Ic treatment for 4 h. Furthermore, the cytochrome c release, caspase-3 activation, Bax/Bcl-2 expression and PARP cleavage were promoted with LY294002 and U0126 intervention but were blocked by SB203580, SP600125, PI3K activator, NAC and 1,400 W pretreatment, demonstrating the mitochondrial disruption. Furthermore, Momordin Ic combination with NAC influenced MAPK, PI3K/Akt and HO-1, iNOS pathways, MAPK and PI3K/Akt pathways also regulated the expression of HO-1 and iNOS.
    CONCLUSIONS:
    These results indicated that Momordin Ic induced apoptosis through oxidative stress-regulated mitochondrial dysfunction involving the MAPK and PI3K-mediated iNOS and HO-1 pathways. Thus, Momordin Ic might represent a potential source of anticancer candidate.
    Animal Research:
    J Med Food. 2005 Summer;8(2):177-83.
    Momordin Ic and oleanolic acid from Kochiae Fructus reduce carbon tetrachloride-induced hepatotoxicity in rats.[Pubmed: 16117609]
    Hepatoprotective effects of Momordin Ic and oleanolic acid obtained from Kochiae Fructus (KF), the fruit of a traditional Oriental medicinal plant, were evaluated against carbon tetrachloride (CCl4)-induced liver damage in rats.
    METHODS AND RESULTS:
    Male Sprague-Dawley rats were divided into four groups: control, CCl4-treated, CCl4 plus Momordin Ic-treated (MMDIc-CCl4), and CCl4 plus oleanolic acid-treated (OAA-CCl4). Momordin Ic (30 mg/kg of body weight) and oleanolic acid (30 mg/kg of body weight) were orally administered once a day for 14 days. A mixture of 0.2 mL/100 g of body weight of CCl4 in olive oil (1:1, vol/vol) was injected 30 minutes after the final administration of Momordin Ic and oleanolic acid. The Momordin Ic and oleanolic acid pretreatments resulted in significantly lower serum transaminase, lactic dehydrogenase, and gamma-glutamyltransferase levels in the CCl4-treated rats. The CCl4-treated rats had significantly lower activities of glutathione, glutathione reductase, glutathione S-transferase, superoxide dismutase, catalase, and glutathione peroxidase. However, pretreatment with Momordin Ic and oleanolic acid reduced the effect of CCl4 and helped maintain levels of the enzymes. Pretreatment with Momordin Ic and oleanolic acid resulted in significantly lower production of aminopyrine N-demethylase and aniline hydroxylase in the CCl4-treated rats. Pretreatment with Momordin Ic resulted in lower catalase and aminopyrine N-demethylase activity induction by CCl4, towards normalization.
    CONCLUSIONS:
    Momordin Ic and oleanolic acid obtained from KF appear to contribute to alleviating the adverse effects of CCl4 treatment by enhancing the hepatic antioxidant defense system.
    Biol Pharm Bull. 1997 Nov;20(11):1165-70.
    Studies on kochiae fructus. IV. Anti-allergic effects of 70% ethanol extract and its component, momordin Ic from dried fruits of Kochia scoparia L.[Pubmed: 9401725]
    The 70% ethanol extract (KS-ext) from Kochiae Fructus (dried fruits of Kochia scoparia L.) has been screened for activity in experimental models of type I-IV allergy.
    METHODS AND RESULTS:
    In type I allergic models, KS-ext at doses of 200 and 500 mg/kg, p.o. exhibited an inhibitory effect on 48-h homologous passive cutaneous anaphylaxis (PCA) in rats, which is related to IgE, and 1.5-h heterologous PCA in mice, which is related to IgG. In a type III allergic model, KS-ext showed an inhibitory effect on direct passive arthus reaction (DPAR) in rats, while it had no inhibitory effect on reversed cutaneous anaphylaxis (RCA) in a type II allergic model. Furthermore, in a type IV allergic model, KS-ext had an inhibitory effect on the effector phase in picryl chloride-induced contact dermatitis (PC-CD). Also, its anti-pruritogenic component, Momordin Ic (oleanane saponin) exhibited inhibitory effects on 48-h homologous PCA and PC-CD.
    CONCLUSIONS:
    These results indicate that Kochiae Fructus not only inhibits humoral immunity but also influences cellular immunity, and should be recognized as a material for anti-allergic reactions. Also, the mode of its anti-pruritogenic activity may be mediated by anti-allergic action, and its active component may be partially attributed to Momordin Ic.