Momordicine I 

Momordicine I is a cucurbitane-type triterpenoids. Momordicine I suppresses glioma growth by promoting apoptosis and impairing mitochondrial oxidative phosphorylation. Momordicine I inhibits glycolysis, lipid metabolism, induces autophagy in HNC cells to suppress head and neck cancer growth. Momordicine I alleviates isoproterenol-induced cardiomyocyte hypertrophy through suppression of PLA2G6 and DGK-ζ. Momordicine I exerts its cardiovascular benefits by upregulating nitric oxide, inhibiting the activity of angiotensin-converting enzyme (ACE), activating the PI3K/Akt pathway, reducing oxidative stress and inflammation. Momordicine I inhibits AKT1, IL-6, and SRC, suggesting its potential application in type 2 diabetes^{[1][2][3][4][5]}.

Momordicine I (1.625-25 μg/mL, 24-25 h) has no significant effect on the activity of H9c2 cells in 1.625-12.5 μg/mL and inhibits Isoproterenol (ISO) (HY-B0468)-induced upregulations of mRNA levels and protein expressions of PLA2G6 and DGK-ζ^[1].
Momordicine I exhibits selective cytotoxicity against LN229 cells, GBM 8401 cells and SVGp12 cells with IC₅₀s of 9.2, 9.6 and 14.4 μM^[2].
Momordicine I (0-10 μM, 16-48 h) impedes the migration and invasion of LN229 and GBM8401 cells via alterations in the expression of epithelial-mesenchymal transition (EMT) markers^[2].
Momordicine I (0-10 μM, 48 h) induces apoptotic death and inhibits glioma cell survival through cell cycle modulation in LN229 and GBM8401 cells^[2].
Momordicine I (0-90 μM) increases intracellular ROS generation and senescence and reduces the oxidative phosphorylation (OXPHOS) capacity in LN229 and GBM8401 cells^[2].
Momordicine I (0-8 μM) overcomes the tumorigenicity of Temozolomide (TMZ) (HY-17364)-resistant GBM cells^[2].
Momordicine I (10-15 μg/mL) significantly reduced the expression of key glycolytic molecules (SLC2A1 (GLUT-1), HK1, PFKP, PDK3, PKM, and LDHA) and essential enzymes involved in de novo lipogenesis (including ACLY, ACC1, FASN, SREBP1, and SCD1) in Cal27 and JHU22 cells^[3].
Momordicine I (10-15 μg/mL) induces autophagy, activates AMPK and inhibites mTOR and Akt signaling pathways and leading to apoptosis in Cal27 and JHU22 cells^[3].
Momordicine I stably binds to the AKT1, IL-6 and SRC targets^[4].
Momordicine I might reduce inflammation through the following mechanisms: inhibiting pro-inflammatory cytokines, reducing adhesion molecules expression, suppressing NF-κB activation, modulating the Nrf2 pathway and suppressing c-Met/STAT3 pathway^[5].

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

Momordicine I (30 mg/kg, i.p., once daily for 21 days) induces autophagy in head and neck cancer (HNC) cells and reduces tumor volume in mice^[3].

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

472.70

C₃₀H₄₈O₄

91590-76-0

Solid

White to off-white

O=C[C@@]([C@@](CC[C@@H]1O)([H])C(C(C)1C)=C[C@@H]2O)(CC[C@@]34C)[C@]2([H])[C@@]3(CC[C@]4([H])[C@H](C)C[C@@H](O)/C=C(C)\C)C

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture and light

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

• [1]. Li H, et al. Momordicine I alleviates isoproterenol-induced cardiomyocyte hypertrophy through suppression of PLA2G6 and DGK-ζ. Korean J Physiol Pharmacol. 2023 Jan 1;27(1):75-84.  [Content Brief]

  [2]. Kao Y, et al. Momordicine I suppresses glioma growth by promoting apoptosis and impairing mitochondrial oxidative phosphorylation. EXCLI J. 2023 Jun 6;22:482-498.  [Content Brief]

  [3]. Bandyopadhyay D, et al. Momordicine-I suppresses head and neck cancer growth by modulating key metabolic pathways. Cell Commun Signal. 2024 Dec 18;22(1):597.  [Content Brief]

  [4]. Kao PF, et al. Therapeutic Potential of Momordicine I from Momordica charantia: Cardiovascular Benefits and Mechanisms. Int J Mol Sci. 2024 Sep 29;25(19):10518.  [Content Brief]

  [5]. Niu Y, et al. Comprehensive Studies on the Regulation of Type 2 Diabetes by Cucurbitane-Type Triterpenoids in Momordica charantia L.: Insights from Network Pharmacology and Molecular Docking and Dynamics. Pharmaceuticals (Basel). 2025 Mar 27;18(4):474.  [Content Brief]