| Identification | Back Directory | [Name]
MOMORDINIC | [CAS]
96990-18-0 | [Synonyms]
MOMORDINIC
Momordin 1c
MorModin Ic
Kochioside Ic
Ic Momordin Ic
Saponin Ic of Fructus Scutellariae
28-norolean-12-en-3-yl 3-O-β-D-xylopyranosyl-
β-D-Glucopyranosiduronic acid, (3β)-17-carboxy-
Momordin IC, 98%, from Kochia scoparia(L.)Schrad.
28-Noroleanane,β-D-glucopyranosiduronic acid deriv
(3β)-17-carboxy-28-norolean-12-en-3-yl 3'-O-(β-D-xylopyranosyl)-β-D-glucuronide
β-D-Glucopyranosiduronic acid, (3β)-17-carboxy-28-norolean-12-en-3-yl 3-O-β-D-xylopyranosyl-
(2S,3S,4S,5R,6R)-6-[[(3S,4aR,6aR,6bS,8aS,12aS,14aR,14bR)-8a-carboxy-4,4,6a,6b,11,11,14b-heptamethyl-1,2,3,4a,5,6,7,8,9,10,12,12a,14,14a-tetradecahydropicen-3-yl]oxy]-3,5-dihydroxy-4-[(2S,3R,4S,5R)-3,4,5-trihydroxyoxan-2-yl]oxyoxane-2-carboxylic acid | [Molecular Formula]
C41H64O13 | [MDL Number]
MFCD11042256 | [MOL File]
96990-18-0.mol | [Molecular Weight]
764.94 |
| Chemical Properties | Back Directory | [Melting point ]
238-240 °C | [Boiling point ]
886.2±65.0 °C(Predicted) | [density ]
1.35±0.1 g/cm3(Predicted) | [storage temp. ]
Sealed in dry,2-8°C | [solubility ]
Methanol (Slightly, Heated, Sonicated), Pyridine (Slightly) | [form ]
Solid | [pka]
2.75±0.70(Predicted) | [color ]
White to Pale Yellow | [optical activity]
[α]/D 12 to 17° in methanol (c=0.5 g/100mL) | [Stability:]
Hygroscopic |
| Hazard Information | Back Directory | [Uses]
Mormodin Ic is used as an anti-cancer agent, and is shown to induce HepG2 apoptosis in a PI3K and MAPK pathway-dependant manner. | [Definition]
ChEBI: Momordin ic is a triterpenoid saponin. | [Biological Activity]
Potent inhibitor of SUMO-specific protease 1 (SENP1) th at increases SUMOylated proteins in PC3 cells | [in vivo]
Momordin Ic (12.5, 25, 50 mg/kg, p.o.) accelerates gastrointestinal transport and inhibits gastric emptying in mice by stimulating the synthesis of serotonin (5-HT)[4].
Momordin Ic (10 mg/kg, p.o.) can inhibit ethanol induced gastric mucosal lesions in rats[5].
Momordin Ic (30 mg/kg, once a day for 14 days, p.o.) can reduce CCl4-induced hepatotoxicity in rats[6]. | Animal Model: | Male ddY mice[4]. | | Dosage: | 12.5, 25, 50 mg/kg | | Administration: | Oral gavage (p.o.) | | Result: | Accelerated gastrointestinal transit in fasted mice. |
| Animal Model: | Male Sprague-Dawley rat[5]. | | Dosage: | 10 mg/kg | | Administration: | Oral gavage (p.o.) | | Result: | Reduced the length of the lesions. |
| Animal Model: | Male Sprague–Dawley rat[6]. | | Dosage: | 30 mg/kg | | Administration: | Oral gavage (p.o.), once a day for 14 days | | Result: | Reduced serum transaminase, lactic dehydrogenase, and γ-glutamyltransferase levels in the CCl4-treated rats. |
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