2. Apoptosis Autophagy Metabolic Enzyme/Protease Immunology/Inflammation PI3K/Akt/mTOR Protein Tyrosine Kinase/RTK Epigenetics NF-κB Stem Cell/Wnt JAK/STAT Signaling
  3. Apoptosis Autophagy DGK Mitochondrial Metabolism NO Synthase PI3K Akt Interleukin Related Src AMPK mTOR NF-κB c-Met/HGFR STAT Keap1-Nrf2 Reactive Oxygen Species (ROS) Oxidative Phosphorylation Endogenous Metabolite
  4. 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.

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Momordicine I

Momordicine I 構造式

CAS 番号 : 91590-76-0

容量 価格（税別） 在庫状況 数量
1 mg $500 在庫あり
5 mg $1250 在庫あり
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Based on 2 publication(s) in Google Scholar

Momordicine I 関連抗体

Top Publications Citing Use of Products

NO Synthase アイソフォーム固有の製品をすべて表示:

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PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

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IL-1 IL-2 IL-3 IL-4 IL-5 IL-6 IL-8 IL-10 IL-12 IL-13 IL-15 IL-17 IL-23 IL-7 IL-33 IL-22 IL-18

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Lck Fyn Blk Fgr Hck Lyn Yes SRC-3

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NUAK1 NUAK2 AMPK AMPK α1β1γ1 AMPK α2β1γ1 AMPK α1β2γ1 AMPK α2β2γ1 BRSK1 BRSK2 HUNK AMPKα

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mTOR mTORC1 mTORC2

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NF-κB NF-κB1/p50 RelA/p65 RelB c-Rel

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STAT3 STAT5 STAT6 STAT1

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Human Endogenous Metabolite Microbial Metabolite

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製品説明

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].

IC50 & Target[3][4][5]

PI3K

 

mTOR

 

IL-6

 

Akt1

 

NF-κB

 

STAT3

 

体外実験

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 関連抗体

RT-PCR[1]

Cell Line: H9c2 cells
Concentration: 12.5 μg/mL
Incubation Time: Pretreated for 1 h, and then exposed to Isoproterenol (10 µM) for 24 h
Result: Significantly down-regulated the mRNA expressions of myocardial hypertrophy marker genes (ANP, β-MHC, α-SKA) and PLA2G6, DGK-ζ.

Western Blot Analysis[1]

Cell Line: H9c2 cells
Concentration: 12.5 μg/mL
Incubation Time: Pretreated for 1 h, and then exposed to Isoproterenol (10 µM) for 24 h
Result: Significantly inhibited the upregulation of PLA2G6 and DGK-ζ proteins.

Cell Migration Assay [2]

Cell Line: LN229 cells and GBM 8401 cells
Concentration: 0, 6, 10 μM
Incubation Time: 16 h
Result: Significantly inhibited wound healing.

Cell Invasion Assay[2]

Cell Line: LN229 cells and GBM 8401 cells
Concentration: 0, 6, 10 μM
Incubation Time: 16 h
Result: Significantly inhibited transwell invasion.

Apoptosis Analysis[2]

Cell Line: LN229 cells and GBM 8401 cells
Concentration: 0, 6, 8, 10 μM
Incubation Time: 48 h
Result: Increased the rate of cell apoptosis.

Cell Cycle Analysis[2]

Cell Line: LN229 cells and GBM 8401 cells
Concentration: 0, 6, 8, 10 μM
Incubation Time: 48 h
Result: Significantly increased the proportion of G1 phase cells.

Western Blot Analysis[2]

Cell Line: LN229 cells and GBM 8401 cells
Concentration: 0, 6, 8, 10 μM
Incubation Time: 1, 2, 3, 4, 48 h
Result: Reduced the expression of interstitial markers N-cadherin and Twist.
Downregulated Ki-67 and survivin expression.
体内実験

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.

Animal Model: MOC2 induced xenograft model established in C57BL/6 mice (6-7 weeks)[3]
Dosage: 30 mg/kg
Administration: Intraperitoneal injection (i.p.), once daily for 21 days
Result: Reduced the volume and weight of the tumor.
Reduced Hk1, Pdk3, Fasn, and Acly expression.
分子量

472.70

分子式

C30H48O4
CAS 番号
Appearance

Solid

Color

White to off-white

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
Structure Classification
Initial Source
輸送条件

Room temperature in continental US; may vary elsewhere.
保管条件

-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)
純度とドキュメンテーション

純度: 97.0%

COA (253 KB) RP-HPLC (109 KB)

取扱説明書 (2659 KB)
参考文献
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Momordicine I Related Classifications

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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Momordicine I91590-76-0ApoptosisAutophagyDGKMitochondrial MetabolismNO SynthasePI3KAktInterleukin RelatedSrcAMPKmTORNF-κBc-Met/HGFRSTATKeap1-Nrf2Reactive Oxygen Species (ROS)Oxidative PhosphorylationEndogenous MetaboliteDiacylglycerol kinaseNitric oxide synthasesNOSPhosphoinositide 3-kinasePKBProtein kinase BILAMP-activated protein kinaseMammalian target of RapamycinNuclear factor-κBNuclear factor-kappaBCardiomegalyGlycerophospholipidsRNA sequencingHead and neck cancerGlycolysisLipid metabolismMetabolitesInhibitorinhibitorinhibit

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