MedChemExpress LLC (MCE)

MedChemExpress - Model Momordin Ic - 96990-18-0

Momordin Ic is an orally active triterpenoid saponin that can be isolated from Kochia scoparia. It is also a SUMO specific protease 1 (SENP1) inhibitor, SENP1/c-MYC signaling pathway inhibitor, and apoptosis inducer. Momordin Ic induces autophagy and apoptosis in liver cancer cells through the PI3K/Akt and MAPK signaling pathways mediated by reactive oxygen species. Momordin Ic has the ability to control glucose induced blood glucose elevation, inhibit gastric emptying, resist rheumatoid arthritis, reduce CCl4 (HY-Y0298) induced hepatotoxicity and anti-tumor activity[1][2].

Momordin Ic

MCE China：Momordin Ic

Brand：MedChemExpress (MCE)

Cat. No.HY-N0330

CAS：96990-18-0

Purity：99.71%

Storage：4°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Momordin Ic is an orally active triterpenoid saponin that can be isolated from Kochia scoparia. It is also a SUMO specific protease 1 (SENP1) inhibitor, SENP1/c-MYC signaling pathway inhibitor, and apoptosis inducer. Momordin Ic induces autophagy and apoptosis in liver cancer cells through the PI3K/Akt and MAPK signaling pathways mediated by reactive oxygen species. Momordin Ic has the ability to control glucose induced blood glucose elevation, inhibit gastric emptying, resist rheumatoid arthritis, reduce CCl4 (HY-Y0298) induced hepatotoxicity and anti-tumor activity.

In Vitro：Momordin Ic (0-20 μM, 48 h) relies on cholesterol and ganglioside GM1 to enhance the toxicity of recombinant protein MAP30 in breast cancer cells[2]. Momordin Ic (10 μM, 24 h) induces colon cancer cell cycle arrest and apoptosis by inhibiting the SENP1/c-MYC signaling pathway[3].

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].

References：

[1]. Mi Y, et al. Momordin Ic couples apoptosis with autophagy in human hepatoblastoma cancer cells by reactive oxygen species (ROS)-mediated PI3K/Akt and MAPK signaling pathways. Free Radic Biol Med. 2016 Jan;90:230-42. [Content Brief]

[2]. Wang W, et al. Cytotoxic effects of recombinant proteins enhanced by momordin Ic are dependent on cholesterol and ganglioside GM1. Toxicon. 2023 Jun 15;229:107129. [Content Brief]

[3]. Xianjun F, et al. Momordin Ic induces G0/1 phase arrest and apoptosis in colon cancer cells by suppressing SENP1/c-MYC signaling pathway. J Pharmacol Sci. 2021 Aug;146(4):249-258. [Content Brief]

[4]. Li Y, et al. Acceleration of gastrointestinal transit by momordin Ic in mice: possible involvement of 5-hydroxytryptamine, 5-HT(2) receptors and prostaglandins. Eur J Pharmacol. 2000 Mar 24;392(1-2):71-7. [Content Brief]

[5]. Matsuda H, et al. Roles of capsaicin-sensitive sensory nerves, endogenous nitric oxide, sulfhydryls, and prostaglandins in gastroprotection by momordin Ic, an oleanolic acid oligoglycoside, on ethanol-induced gastric mucosal lesions in rats. Life Sci. 1999;65(2):PL27-32. [Content Brief]

[6]. Kim NY, et al. Momordin Ic and oleanolic acid from Kochiae Fructus reduce carbon tetrachloride-induced hepatotoxicity in rats. J Med Food. 2005 Summer;8(2):177-83. [Content Brief]

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