Myrigalone A
Myrigalone A (MyA) is a plant ethylene biosynthesis inhibitor and natural herbicide. Myrigalone A possesses antioxidant, antifungal, and antimicrobial activities. Myrigalone A interferes with auxin homeostasis during seed germination. Myrigalone A delays seed germination, inhibits the formation of roots, hypocotyls, and root hairs, and causes developmental delay in specific organisms. Myrigalone A triggers the induction of detoxification programs, alters the metabolism of gibberellins, cis-(+)-12-oxophytodienoic acid, and jasmonic acid, disrupts the antioxidant system and oxidative signaling, and impairs the function of aquaporins and water uptake in imbibed seeds. Myrigalone A can be used in studies related to herbicides and plant growth regulators.
For research use only. We do not sell to patients.
- CAS No.: 34328-57-9
- Formula: C18H20O4
- Molecular Weight:300.35
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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
In Vitro
Myrigalone A (0-100 µM; 7 days) potently inhibits the proliferation of Dictyostelium discoideum (Ax3) cells, with an IC50 of 7.1 µM, and induces complete growth inhibition at a concentration of 100 µM. It inhibits the proliferation of Dictyostelium discoideum Aco− mutant cells with lower potency (IC50 = 31.5 µM)[1].
Myrigalone A (100 µM; 0-48 h) causes a reversible 6-hour delay in multicellular development of wild-type Dictyostelium discoideum (Ax3), blocks its developmental progression to mature fruiting bodies at 20 h, and does not induce lethal effects[1].
Myrigalone A (500 µM; 36 h) significantly reduces ethylene production in wild-type Dictyostelium discoideum cells, and the reduction level is consistent with that in Aco− mutant cells[1].
Myrigalone A (0.5 mM; 0-70 h) delays endosperm rupture and inhibits seed germination in Arabidopsis thaliana Col-0, and this effect is reversed by exogenous ethylene or its precursor ACC[1].
Myrigalone A (0.025-0.35 mM; 6 days) significantly inhibits root and hypocotyl growth of Arabidopsis thaliana Col-0 seedlings in a dose-dependent manner, and completely blocks germination at a concentration of 0.35 mM[1].
Myrigalone A (25-100 µM; 3 days) inhibits the formation of basal and ethylene-induced root hairs in Arabidopsis thaliana Col-0 seedlings, and blocks the increase in root hair length and number triggered by ACC or CEPA[1].
Myrigalone A (100 µM; 2 days, with or without 1 µM ACC) significantly reduces ethylene production in Arabidopsis thaliana Col-0 seedlings[1].
Myrigalone A (0.1-1 mM) dose-dependently inhibits endosperm rupture in Lepidium sativum seeds[2].
Myrigalone A (0.5 mM; 6-18 h) alters gibberellin and oxylipin metabolism in germinating Lepidium sativum (garden cress) seeds, leading to the accumulation of specific gibberellin precursors and a reduction in OPDA levels, which triggers the phase-specific induction of genes involved in detoxification, auxin transport, oxidative signaling, and aquaporin transporters, while downregulating specific auxin efflux carriers[2].
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:Dictyostelium discoideum wild-type (Ax3) cells
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Concentration:1 µM, 10 µM, 100 µM
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Incubation Time:7 days
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Result:Produced a concentration-dependent reduction in cell proliferation, with no significant effect at 1 µM, a significant reduction at 10 µM (P < 0.05), and complete inhibition at 100 µM.
Revealed an IC50 of 7.1 µM.
Chemical Information
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CAS No. 34328-57-9
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Molecular Weight 300.35
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Formula C18H20O4
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SMILES
O=C(CCC=1C=CC=CC1)C2C(=O)C(C(=O)C(C2=O)(C)C)C
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Synonyms
MyA
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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
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
References
[1]. Heslop-Harrison G, et al. Functional mechanism study of the allelochemical myrigalone A identifies a group of ultrapotent inhibitors of ethylene biosynthesis in plants. Plant Commun. 2024;5(6):100846. [Content Brief]
[2]. Nakabayashi K, et al. The Phytotoxin Myrigalone A Triggers a Phased Detoxification Programme and Inhibits Lepidium sativum Seed Germination via Multiple Mechanisms including Interference with Auxin Homeostasis. Int J Mol Sci. 2022;23(9):4618. Published 2022 Apr 21. [Content Brief]
[3]. Khaled A, et al. Photodegradation of Myrigalone A, an Allelochemical from Myrica gale: Photoproducts and Effect of Terpenes. J Agric Food Chem. 2019 Jul 3;67(26):7258-7265. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Myrigalone A Related Classifications
HY-N12990 Related Classifications
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