Methyl ganoderate A
Methyl ganoderate A (Ganoderic acid A methyl ester) is a triterpenoid derivative. Methyl ganoderate A can be isolated from the fruiting bodies of G. lucidum. Methyl ganoderate A selectively inhibits CLK2 with an IC50 of 0.69 μM. Methyl ganoderate A inhibits the expression of ADAMTS5, MMP3, and MMP13, and reduces the levels of the cytokines IL-6, TNF-α, and IL-1β. Methyl ganoderate A can be used in research on knee osteoarthritis, Alzheimer's disease, and neuroinflammation.
For research use only. We do not sell to patients.
- CAS No.: 81907-63-3
- Formula: C31H46O7
- Molecular Weight:530.69
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
MMP-3 |
MMP13 |
IL-6 |
IL-1β |
In Vitro
Methyl ganoderate A is a selective CLK2 inhibitor with an IC50 value of 0.69 μM[1].
Methyl ganoderate A (10 μM) inhibits cartilage degradation in rat chondrocytes and BMSCs by reducing the expression of ADAMTS5, MMP3, and MMP13[1].
Methyl ganoderate A competitively inhibits bovine testicular FPT with an IC50 of 38 μM and a Ki of 20 μM[2].
Methyl ganoderate A (200 μM) exhibits moderate inhibitory activity against AChE with an IC50 of 30.26 μM, and shows no inhibitory effect on BChE up to 200 μM[3].
Methyl ganoderate A (100 μM; 3 min preincubation, 30 min reaction) inhibits FAAH activity in vitro, with an inhibition rate of 61% at 100 μM[5].
Methyl ganoderate A (50 μM; 48 h) exhibits no cytotoxicity toward LOVO cells at 50 μM[5].
Methyl ganoderate A (50 μM; 48 h) exhibits no cytotoxicity toward MCF-7 cells at a concentration of 50 μM[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:LOVO
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Concentration:50 μM
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Incubation Time:48 h
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Result:Displayed no cytotoxicity against LOVO human cancer cells.
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Cell Line:MCF-7
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Concentration:50 μM
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Incubation Time:48 h
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Result:Displayed no cytotoxicity against MCF-7 human cancer cells.
Chemical Information
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CAS No. 81907-63-3
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Molecular Weight 530.69
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Formula C31H46O7
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SMILES
C[C@]12C3=C(C(C[C@@]1([C@@](C[C@@H]2O)([H])[C@H](C)CC(C[C@@H](C)C(OC)=O)=O)C)=O)[C@@]4([C@@](C(C)(C(CC4)=O)C)([H])C[C@@H]3O)C
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Synonyms
Ganoderic acid A methyl ester
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Structure Classification
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Initial Source
Ganoderma hainanense J. D. Zhao, L. W. Hsu et X. Q. Zhang
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Research Protocol for Neurological Diseases
PINK1/Parkin-mediated mitophagy pathway is a mitochondrial quality-control signaling axis in which mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, activates Parkin recruitment and E3 ubiquitin ligase activity, promotes ubiquitination of outer mitochondrial membrane proteins, recruits selective autophagy adaptors, and drives lysosomal degradation of damaged mitochondria. In neurological disease research, this pathway is experimentally important because neurons, especially dopaminergic neurons, are highly dependent on mitochondrial integrity, and defective mitochondrial turnover can lead to mitochondrial dysfunction, oxidative stress, impaired neuronal survival, α-synuclein accumulation, and neuroinflammatory damage-associated signals. The genetic disease link is strongest in Parkinson’s disease because mutations in PRKN/parkin cause autosomal recessive juvenile parkinsonism, mutations in PINK1 cause hereditary early-onset Parkinson’s disease, and Drosophila studie
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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
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Alzheimer’s Disease Modeling
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive functions and loss of specific types of neurons and synapses. Alzheimer's symptoms can be simulated in mice by injecting drugs (such as Aβ) or genetically modified.
Purity & Documentation
References
[2]. Lee S, et al. Natural inhibitors for protein prenyltransferase. Planta medica. 1998 May;64(4):303-8.
[3]. Lee I, et al. Selective cholinesterase inhibition by lanostane triterpenes from fruiting bodies of Ganoderma lucidum. Bioorganic & medicinal chemistry letters. 2011 Nov 01;21(21):6603-7. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Methyl ganoderate A Related Classifications
HY-N22053 Related Classifications
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