Momordicine I
Based on 2 publication(s) in Google Scholar
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.
For research use only. We do not sell to patients.
- Purity: 97.0%
- CAS No.: 91590-76-0
- Formula: C30H48O4
- Molecular Weight:472.70
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Storage:
-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)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Publications Citing Use of MedChemExpress (MCE) Momordicine I
MoreAll Endogenous Metabolite Isoforms
MoreAll AMPK Isoforms
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Biological Activity
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PI3K |
mTOR |
IL-6 |
Akt1 |
NF-κB |
STAT3 |
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.
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Cell Line:H9c2 cells
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Concentration:12.5 μg/mL
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Incubation Time:Pretreated for 1 h, and then exposed to Isoproterenol (10 µM) for 24 h
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Result:Significantly down-regulated the mRNA expressions of myocardial hypertrophy marker genes (ANP, β-MHC, α-SKA) and PLA2G6, DGK-ζ.
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Cell Line:H9c2 cells
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Concentration:12.5 μg/mL
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Incubation Time:Pretreated for 1 h, and then exposed to Isoproterenol (10 µM) for 24 h
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Result:Significantly inhibited the upregulation of PLA2G6 and DGK-ζ proteins.
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Cell Line:LN229 cells and GBM 8401 cells
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Concentration:0, 6, 10 μM
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Incubation Time:16 h
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Result:Significantly inhibited wound healing.
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Cell Line:LN229 cells and GBM 8401 cells
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Concentration:0, 6, 10 μM
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Incubation Time:16 h
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Result:Significantly inhibited transwell invasion.
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Cell Line:LN229 cells and GBM 8401 cells
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Concentration:0, 6, 8, 10 μM
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Incubation Time:48 h
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Result:Increased the rate of cell apoptosis.
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Cell Line:LN229 cells and GBM 8401 cells
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Concentration:0, 6, 8, 10 μM
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Incubation Time:48 h
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Result:Significantly increased the proportion of G1 phase cells.
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Cell Line:LN229 cells and GBM 8401 cells
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Concentration:0, 6, 8, 10 μM
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Incubation Time:1, 2, 3, 4, 48 h
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Result:Reduced the expression of interstitial markers N-cadherin and Twist.
Downregulated Ki-67 and survivin expression.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:MOC2 induced xenograft model established in C57BL/6 mice (6-7 weeks)[3]
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Dosage:30 mg/kg
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Administration:Intraperitoneal injection (i.p.), once daily for 21 days
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Result:Reduced the volume and weight of the tumor.
Reduced Hk1, Pdk3, Fasn, and Acly expression.
Chemical Information
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CAS No. 91590-76-0
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Appearance Solid
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Molecular Weight 472.70
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Formula C30H48O4
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Color White to off-white
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SMILES
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
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-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)
Publications (2)
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Journal Impact Factor
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Most Recent
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Food Funct
Momordicine I, a triterpene from bitter melon (Momordica charantia L.), ameliorates alcohol-associated liver disease: research on the possible liver benefits. [Abstract]2026 Feb 23;17(4):2018-2036. PMID: 41637150 -
Poult Sci
PhospholipaseA2VI mediates the lipid peroxidation-ferroptosis axis to regulate rooster sperm motility. [Abstract]2025 Aug 28;104(11):105751. PMID: 40961763
Purity & Documentation
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Data Sheet (286 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[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]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Momordicine I Related Classifications
HY-122949 Related Classifications
Powered by Bioz
- Momordicine I
- 91590-76-0
- Reactive Oxygen Species (ROS)
- NF-κB
- Oxidative Phosphorylation
- Interleukin Related
- Src
- NO Synthase
- Autophagy
- Mitochondrial Metabolism
- DGK
- Keap1-Nrf2
- Apoptosis
- PI3K
- Endogenous Metabolite
- c-Met/HGFR
- AMPK
- STAT
- Akt
- mTOR
- Cardiomegaly
- Glycerophospholipids
- RNA sequencing
- Head and neck cancer
- Glycolysis
- Lipid metabolism
- Metabolites
- Inhibitor
- inhibitor
- inhibit