Cat. No.: HY-N21887

Gypenoside LVI

Gypenoside LVI is an orally active dammarane-type triterpenoid compound found in Gynostemma pentaphyllum. Gypenoside LVI inhibits ERK and JNK phosphorylation, the NLRP3 inflammasome, and modulates M1 to M2 microglial polarization. Gypenoside LVI downregulates PCSK9 expression through a SREBP-independent pathway. Gypenoside LVI promotes cholesterol efflux via ABCG1 and SRB1, upregulates LXRα-mediated reverse cholesterol transport, and attenuates foam cell formation by reducing lipid accumulation and cholesterol uptake. Gypenoside LVI inhibits IL-6 and IL-1β secretion, reduces oxidative stress, neuroinflammation, microglial and astrocyte activation, and inhibits LPS-induced microglial proliferation. Gypenoside LVI can be used for research on atherosclerosis, hypercholesterolemia, depression, and non-small cell lung cancer.

For research use only. We do not sell to patients.

CAS No.: 105214-48-0
Formula: C₅₃H₉₀O₂₃
Molecular Weight:1095.28

Storage:

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

Gypenoside LVI Chemical Structure

CAS No.: 105214-48-0

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target

^[1]^[2]^[3]^[5]^[4]

ERK

JNK

NLRP3

PCSK9

ABCG1

SRB1

LXRα

IL-6

IL-1β

All ERK Isoforms :

All JNK Isoforms :

All NOD-like Receptor (NLR) Isoforms :

All Interleukin Related Isoforms :

In Vitro

Lipid MetabolismInnate ImmunityAnti-cancerOxidative StressApoptosisCytokines & ChemokinesOthers

Lipid Metabolism

Innate Immunity

Gypenoside LVI (GPLVI) (24 h) inhibits ox-LDL-induced foam cell formation in RAW264.7 cells^[1].

Innate Immunity

Lipid Metabolism

Gypenoside LVI (100 μg/mL; 24 h) dose-dependently reduces TG content in ox-LDL-induced RAW264.7 macrophages^[1].
Gypenoside LVI (100 μg/mL; 24 h) attenuated the elevated CE/TC ratio in ox-LDL-induced RAW264.7 macrophages^[1].
Gypenoside LVI (25-100 μg/mL; 4 h) dose-dependently reduces the uptake of Dil-ox-LDL by RAW264.7 macrophages^[1].
Gypenoside LVI (25-100 μg/mL; 24 h) enhances HDL-mediated cholesterol efflux at 50 μg/mL, whereas 25 and 100 μg/mL reduce cholesterol efflux in RAW264.7 macrophages^[1].
Gypenoside LVI (25-100 μg/mL; 24 h) upregulated the mRNA expression of ABCG1, SRB1, and LXRα in ox-LDL-induced RAW264.7 macrophages^[1].
Gypenoside LVI (25-100 μg/mL; 24 h) upregulates the protein expression of ABCG1, SRB1, and LXRα in RAW264.7 macrophages^[1].
Gypenoside LVI (25-100 μg/mL; 24 h) inhibits ERK and JNK phosphorylation in ox-LDL-induced RAW264.7 macrophages^[1].
Gypenoside LVI (25-100 μg/mL; 24 h) inhibits IL-6 and IL-1β production in ox-LDL-induced RAW264.7 macrophages, but does not reduce TNF-α production^[1].

Anti-cancer

Gypenoside LVI (compound 2) (20-100 μM; 24 h) inhibited the viability of HepG2 cells^[2].
Gypenoside LVI (5-20 μM; 24 h) inhibits PCSK9 secretion in LPDS-induced HepG2 cells^[2].
Gypenoside LVI (5-20 μM; 24 h) reduces PCSK9 protein expression in HepG2 cells^[2].
Gypenoside LVI (5-20 μM; 24 h) increases LDLR protein expression in HepG2 cells^[2].
Gypenoside LVI (5-20 μM; 24 h) reduces Simvastatin (HY-17502)-induced PCSK9 expression in HepG2 cells^[2].
Gypenoside LVI (5-20 μM; 24 h) reduces PCSK9 mRNA expression in HepG2 cells^[2].

Lipid Metabolism

Gypenoside LVI (5-20 μM; 24 h) protects LDLR from lysosomal degradation in HepG2 cells via a post-translational pathway^[2].
Gypenoside LVI (5-20 μM; 24 h) increases the abundance of LDLR in HepG2 cells^[2].
Gypenoside LVI (5-20 μM; 20 h) promotes LDL uptake in HepG2 cells^[2].

Innate Immunity

Oxidative Stress

Gypenoside LVI (10-50 μM; 3 h) inhibits LPS-induced NO release in BV-2 microglial cells at concentrations of 20 μM and above^[3].

Anti-cancer

Lipid Metabolism

Gypenoside LVI (5-20 μM; 24 h) increases cell surface LDLR levels in HepG2 cells^[2].

Apoptosis

Cytokines & Chemokines

Innate Immunity

Gypenoside LVI (Gyp-LVI) (10-50 μM; 3 h) exerts anti-inflammatory and neuroprotective effects in LPS-induced BV-2 cells by regulating apoptosis-related proteins and downregulating key inflammatory factors^[3].
Gypenoside LVI (10-50 μM; 3 h) inhibits LPS-induced activation of the NLRP3 inflammasome signaling pathway in BV-2 microglia^[3].

Innate Immunity

Gypenoside LVI (10-50 μM; 3 h) regulates LPS-induced M1/M2 phenotypic polarization in BV-2 microglia by inhibiting M1 markers (iNOS, CD86) and promoting M2 markers (Arg-1)^[3].

Others

Gypenoside LVI (5-20 μM; 24 h) does not affect SREBP-2 protein expression in HepG2 cells^[2].
Gypenoside LVI (5-20 μM; 24 h) does not affect the expression of SREBP-2 or LDLR mRNA in HepG2 cells^[2].

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

Real Time qPCR^[1]

Cell Line:

RAW264.7 murine macrophages
Concentration:

25, 50, 100 μg/mL
Incubation Time:

24 h
Result:

Significantly and dose-dependently promoted ABCG1 gene expression.
Increased SRB1 gene expression.
Up-regulated LXRα gene expression to 0.984 at 25 μg/mL and increased by about 2-fold (1.172) at 100 μg/mL compared to ox-LDL-treated cells (0.633).

Western Blot Analysis^[1]

Cell Line:

RAW264.7 murine macrophages
Concentration:

25, 50, 100 μg/mL
Incubation Time:

24 h
Result:

Displayed stimulatory effect on ABCG1 protein expression at 25 μg/mL.
Significantly up-regulated SRB1 protein expression in a dose-dependent manner.
Significantly elevated LXRα protein expression to 0.213, 0.201 and 0.334 at 25, 50 and 100 μg/mL, respectively.\nDramatically suppressed phosphorylation of ERK and JNK.

ELISA Assay^[1]

Cell Line:

RAW264.7 murine macrophages
Concentration:

25, 50, 100 μg/mL
Incubation Time:

24 h
Result:

Markedly decreased ox-LDL-induced production of IL-6 and IL-1β.
Accumulation of TNF-α was not reduced but instead slightly increased at 25 μg/mL and 50 μg/mL.
Inhibition ratio on IL-1β reached 74.4% at 100 μg/mL.
Attenuated about 11.21%, 22.2% and 55.81% of ox-LDL-induced accumulation of IL-6 at 25, 50 and 100 μg/mL, respectively.

Cell Viability Assay^[2]

Cell Line:

HepG2
Concentration:

20, 40, 60, 80, 100 μM
Incubation Time:

24 h
Result:

Inhibited the viability of HepG2 cells.

ELISA Assay^[2]

Cell Line:

HepG2
Concentration:

5, 10, 20 μM
Incubation Time:

24 h
Result:

Significantly decreased the levels of secreted PCSK9 in a dose-dependent manner.

Western Blot Analysis^[2]

Cell Line:

HepG2
Concentration:

5, 20 μM
Incubation Time:

24 h
Result:

Evidently reduced the expression of PCSK9 in total cell lysate compared to the control group.\nSignificantly enhanced LDLR protein levels compared with vehicle-treated cells.\nFailed to alter SREBP-2 protein expression.\nFurther inhibited degradation of LDLR compared with BA1 alone.\nMarkedly decreased the PCSK9 upregulation induced by 1 μM simvastatin.

Real Time qPCR^[2]

Cell Line:

HepG2
Concentration:

5, 20 μM
Incubation Time:

24 h
Result:

Remarkably declined the mRNA level of PCSK9.\nFailed to alter SREBP-2 mRNA expression and exhibited no influence on the mRNA expression of LDLR.

Immunofluorescence^[2]

Cell Line:

HepG2
Concentration:

5, 20 μM
Incubation Time:

24 h
Result:

Increased fluorescence intensity of LDLR on the membrane.

ELISA Assay^[3]

Cell Line:

LPS-induced BV-2 microglial cells
Concentration:

10, 20, 50 μM
Incubation Time:

3 h
Result:

Exhibited a significant inhibitory effect on NO release at concentrations of 20 μM and above.

Real Time qPCR^[3]

Cell Line:

LPS-induced BV-2 microglial cells
Concentration:

10, 20, 50 μM
Incubation Time:

3 h
Result:

LVI-H (50 μM) significantly reversed the upregulation of Bax and antagonized the downregulation of Bcl-2.
LVI-H (50 μM) significantly suppressed the LPS-induced upregulation of TNF-α, IL-6, and iNOS mRNA.
All tested concentrations significantly downregulated the transcription levels of iNOS and IL-1β.
Western blot confirmed that LPS-induced high expression of IL-1β was significantly inhibited by Gyp-LVI at all concentrations.

Immunofluorescence^[3]

Cell Line:

LPS-induced BV-2 microglial cells
Concentration:

10, 20, 50 μM
Incubation Time:

3 h
Result:

LVI-L (10 μM) and LVI-M (20 μM) markedly inhibited the increased fluorescence intensity of iNOS.
All treatment groups significantly downregulated CD86 expression.
Western blot confirmed that LVI-H (50 μM) significantly reduced CD86 protein levels.
All concentrations of Gyp-LVI significantly upregulated Arg-1 expression.\nLVI-M (20 μM) and LVI-H (50 μM) markedly suppressed the intracellular fluorescence signal of NLRP3.
All concentrations of Gyp-LVI significantly antagonized the upregulation of NLRP3 mRNA expression.
All concentrations of Gyp-LVI significantly downregulated the protein expression of both NLRP3 and Caspase-1.
Only LVI-M (20 μM) showed a statistically significant inhibitory effect on ASC.

In Vivo

Innate ImmunityAdaptive ImmunityOxidative Stress

Innate Immunity

Adaptive Immunity

Oxidative Stress

Gyp-LVI (10-40 mg/kg; i.g.; daily; 10 days) exerts significant antidepressant effects in CUMS mice by mitigating peripheral and central inflammation, modulating oxidative stress, regulating microglial phenotypic polarization, and inhibiting the NLRP3/Caspase-1/ASC signaling pathway, with the 20 mg/kg dose demonstrating particularly stable regulatory efficacy^[3].

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

Animal Model:

C57/BL6J (female, 7 months old, chronic unpredictable mild stress (CUMS) model)^[3]
Dosage:

10, 20, 40 mg/kg
Administration:

i.g.; daily; 10 days
Result:

Reversed CUMS-induced decrease in total movement distance at 10 and 20 mg/kg in the open field test.
Increased central zone exploration distance at 10 and 20 mg/kg.
Increased licking time at all doses in the sucrose splash test, with a dose-dependent trend.
Shortened immobility time at all doses in the tail suspension test.
Alleviated CUMS-induced body weight abnormality at 10 mg/kg at the end of the fourth week.
Reversed slow weight gain at 10 mg/kg by the fifth week.
Increased rate of body weight change at 10 mg/kg.
Downregulated iNOS and CD86 and upregulated Arg-1 expression in the hippocampus at 20 mg/kg.
Regulated iNOS, CD86, and Arg-1 in the PFC at 20 mg/kg.
Improved various morphological parameters of microglia in the PFC region at 40 mg/kg.
Downregulated NLRP3, Caspase-1, and ASC protein expression in the PFC at 20 mg/kg.
Reversed all measured oxidative stress indices in serum at 20 mg/kg.
Improved most oxidative stress indices in PFC tissue at 20 mg/kg.

Related Protocols :

Chemical Information

CAS No. 105214-48-0
Molecular Weight 1095.28
Formula C₅₃H₉₀O₂₃
SMILES

C[C@]12[C@@]([C@]3(C)[C@@](CC1)(C(C)(C)[C@@H](O[C@H]4[C@H](O[C@@H]5O[C@H](CO)[C@@H](O)[C@H](O)[C@H]5O)[C@@H](O)[C@H](O)[C@@H](CO)O4)[C@H](O)C3)[H])(C[C@@H](O)[C@]6([C@@]2(C)CC[C@@]6([C@@](O[C@@H]7O[C@H](CO[C@H]8[C@H](O)[C@@H](O)[C@H](O)CO8)[C@@H](O)[C@H](O)[C@H]7O)(CCC=C(C)C)C)[H])[H])[H]
Structure Classification
- Terpenoids
- Tetracyclic Triterpenoids
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

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

Purity & Documentation

Handling Instructions (2659 KB)

References

[1]. Shen C‑Y, et al. Gypenoside LVI attenuates foam cell formation by promoting cholesterol export and inhibiting inflammation response. Journal of Functional Foods. 2018 Nov;50:71‑77.

[2]. Wang J, et al. Gypenoside LVI improves hepatic LDL uptake by decreasing PCSK9 and upregulating LDLR expression. Phytomedicine : international journal of phytotherapy and phytopharmacology. 2021 Oct;91:153688.

[3]. Guo M, et al. Gypenosides ameliorate depression by modulating microglial state transition via the NLRP3/Caspase-1/ASC signaling pathway. Phytomedicine : international journal of phytotherapy and phytopharmacology. 2026 Jul;156:158189.

[4]. Zhou P, et al. Chromosome-Level Genome Assembly of the Allotetraploid Gynostemma pentaphyllum Provides Novel Insights Into the Biosynthesis of Ginsenoside and Gypenoside LVI. Plant biotechnology journal. 2026 Jun;24(6):4204-4220.

[5]. Chen DJ, et al. Metabolite profiling of gypenoside LVI in rat after oral and intravenous administration. Archives of pharmacal research. 2015 Jun;38(6):1157-67.

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How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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Gypenoside LVI

All ERK Isoforms

All JNK Isoforms

All NOD-like Receptor (NLR) Isoforms

All Interleukin Related Isoforms