Momordicoside G  (Synonyms: Momordicacoside G)

Momordicoside G (Momordicacoside G) is an orally active cucurbitane-type triterpene glycoside. Momordicoside G selectively induces apoptosis of M1-like macrophages, without affecting M2-like macrophages. Momordicoside G reduces intracellular ROS levels and promotes autophagy. Momordicoside G also has anticancer activity, inhibiting the growth of cancer cell lines. Momordicoside G stimulates M2-associated lung injury repair and prevents inflammatory lung cancer injury^[1].

Raw264.7 macrophages is stimulated by 10 ng/mL LPS or 10 ng/mL IL-10 for 24 h to obtain M1-like (iNOS+) and M2-like (arginase+) macrophages^[1].
Momordicoside G (10-40 μM; 24 h) inhibits the cell viability of M1 macrophages, but not M2 macrophage^[1].
Momordicoside G (40 μM) induces M1 macrophage apoptosis in vitro, as well as decreasing the level of NO, and increasing the level of IL-12, IL-10, and TGF-β^[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Lung carcinogenic model in ICR mice is induced by Urethane (HY-B1207) (600 mg/kg; i.p.; once weekly for 4 or 8 weeks), or in in macrophage-competent and macrophage-deleted mice is induced by LPS (HY-D1056) (2 mg/kg; intratracheal method) with 4 mg/mouse IEC (i.p.)^[1].
Momordicoside G (50 mg/kg; p.o.; once daily for 4 or 8 weeks) prevents urethane-induced lung injury and carcinoma lesions in mouse lung carcinogenic model^[1].
Momordicoside G (50 mg/kg; p.o.; once daily for 2 weeks) promotes lung injury repair in LPS-induced lung injury model^[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

632.87

C₃₇H₆₀O₈

81371-54-2

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Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Du Z, et al. Momordicoside G Regulates Macrophage Phenotypes to Stimulate Efficient Repair of Lung Injury and Prevent Urethane-Induced Lung Carcinoma Lesions. Front Pharmacol. 2019 Mar 29;10:321.  [Content Brief]