Methyl jasmonate targets plant signaling pathways involved in defense responses and secondary metabolite biosynthesis. As a plant hormone, it regulates the expression of genes involved in plant defense, stress responses, and development. In biomedical research, methyl jasmonate has been studied for its anticancer and anti-inflammatory effects. Its mechanism of action in mammalian cells involves modulation of cell signaling pathways such as MAPK and NF-κB, though its precise molecular targets have not been definitively identified. Its plant hormone activity and potential biomedical applications make it a valuable tool for plant biology and pharmacology research.

In vitro, methyl jasmonate exhibits anticancer and anti-inflammatory activities in mammalian cell lines. It induces apoptosis and inhibits the proliferation of cancer cells. The compound's activity is concentration-dependent, with effective concentrations typically in the micromolar range. In plant cell cultures, methyl jasmonate induces the production of secondary metabolites and activates defense-related genes. Its dual activity in plant and mammalian systems makes it a valuable tool for studying plant biology and pharmacology. Detailed IC50 values for specific cancer cell lines are available in published literature.

In vivo, methyl jasmonate has been studied in preclinical models of cancer and inflammation. Its ability to induce apoptosis and inhibit tumor growth makes it a promising candidate for further development as an anticancer agent. However, detailed in vivo efficacy data and pharmacokinetic profiles are limited in publicly available sources. The compound is primarily used as a research tool for plant elicitation and biomedical research. Further studies are needed to fully characterize its therapeutic potential, dosing regimens, and safety profile in vivo.

The in vitro anticancer activity assay for methyl jasmonate typically uses cancer cell lines. Cells are seeded in 96-well plates and treated with varying concentrations of the compound (typically 1 to 100 µM) for 24-72 hours. Cell viability is assessed using MTT or CellTiter-Glo assays. Apoptosis is quantified by Annexin V/PI staining and caspase activity assays. Cell cycle distribution is analyzed by propidium iodide staining and flow cytometry. For plant studies, plant cell cultures or tissues are treated with methyl jasmonate, and the production of secondary metabolites is measured by HPLC or LC-MS. Gene expression is assessed by qRT-PCR. Positive controls and negative controls are included in each assay run.

For in vitro cellular assays, cancer cell lines or plant cell cultures are treated with methyl jasmonate at concentrations ranging from 1 to 100 µM for 24-72 hours. Cell viability is assessed using MTT or CellTiter-Glo assays. Apoptosis is quantified by Annexin V/PI staining and caspase activity assays. Inflammatory markers (TNF-α, IL-6) are measured by ELISA. For plant studies, secondary metabolite production is measured by HPLC or LC-MS. Gene expression is assessed by qRT-PCR. All experiments include appropriate controls (vehicle, untreated cells) and are performed in triplicate.

For in vivo efficacy studies, rodent models of cancer or inflammation are used. Methyl jasmonate is administered orally or intraperitoneally at doses ranging from 1 to 50 mg/kg, typically once or twice daily. Tumor growth is monitored, and inflammatory markers are measured in blood and tissues. For plant studies, methyl jasmonate is applied to plants, and defense responses and secondary metabolite production are assessed. All animal procedures should be conducted in accordance with institutional guidelines.

The pharmacokinetic properties of methyl jasmonate have been partially characterized. The compound has a molecular weight of 224.30 and a LogP of 2.5. Following oral or intraperitoneal administration, it shows moderate absorption with a Tmax of 1-3 hours. Plasma half-life is estimated to be 2-4 hours. The compound distributes into tissues including liver and kidney. Metabolism is primarily hepatic, with oxidation and conjugation as major pathways. The compound is eliminated primarily via biliary and renal excretion. Further PK studies are needed for comprehensive characterization.

Interactions
Researchers investigated the effects of the combined action of methyl jasmonate and sucrose on the expression of defense-related genes, stilbene, and anthocyanin production in grape cell suspensions. Methyl jasmonate/sucrose treatment effectively stimulated the expression of genes for phenylalanine ammonia-lyase, chalcone synthase, stilbene synthase, UDP-glucose:flavonoid-O-glucosyltransferase, protease inhibitors, and chitinase, and induced the accumulation of spruce compounds and anthocyanins intracellularly, as well as the accumulation of trans-resveratrol and spruce compounds in extracellular culture medium…
Capsicum annuum suspension cell cultures were used to evaluate the effects of cyclodextrin and methyl jasmonate as inducers of defense responses. The induced defense responses included the accumulation of sesquiterpenes and phytosterols, as well as the activation of pathogenesis-related proteins, thereby enhancing and altering cell wall structure during induction and protecting cells from biotic stress. The results showed that the addition of both cyclodextrin and methyl jasmonate induced the biosynthesis of two sesquiterpenes—aromatic resins and soravidone. This response exhibits a significant synergistic effect, as the increase in the levels of these compounds is far greater when both inducers are present than when used alone. Phytosterol biosynthesis is also induced in the combined treatment due to an additive effect. Similarly, exogenous application of methyl jasmonate induces the accumulation of disease-related proteins. Extracellular proteomic analysis revealed the presence of amino acid sequences homologous to PR1 and PR4, NtPRp27-like proteins, class I chitinases, peroxidases, hydrolases LEXYL1 and LEXYL2, arabinosidases, pectinases, nectarin IV, and leucine-rich repeat proteins, indicating that methyl jasmonate mediates the expression of defense-related gene products in pepper (C. annuum). In addition to these methyl jasmonate-induced proteins, other PR proteins were found in both control and induced cell cultures of pepper. These enzymes, including class IV chitinases, β-1,3-glucanases, sweet protein-like enzymes, and peroxidases, indicate that their expression is primarily constitutive, as they are involved in plant growth, development, and defense processes. Boron is an essential micronutrient for plants, but excessive boron in the soil is phytotoxic to some plants, such as Artemisia annua, whose aerial parts contain artemisinin (an important antimalarial drug). Artemisinin is a sesquiterpene lactone with an internal peroxide bridge… This study aimed to determine whether exogenous application of methyl jasmonate (MeJA) could counteract the adverse effects of excessive boron stress (B) in the soil. Results showed that boron toxicity induced oxidative stress and significantly reduced stem height, fresh weight, and dry weight. Excess boron in the soil reduced net photosynthetic rate, stomatal conductance, intercellular carbon dioxide concentration, and total chlorophyll content in leaves. Conversely, foliar application of methyl jasmonate (MeJA) improved growth and photosynthetic efficiency in both stressed and unstressed plants. Excessive boron can also increase the activity of antioxidant enzymes (such as catalase, peroxidase, and superoxide dismutase)... Applying MeJA to stressed plants can reduce lipid peroxidation, stimulate the synthesis of antioxidant enzymes, and increase the content and yield of artemisinin. Therefore, it can be concluded that MeJA can be used to alleviate boron toxicity and increase the content and yield of artemisinin in Artemisia annua.

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Preclinical toxicology studies of methyl jasmonate are limited. In acute toxicity studies in rodents, the compound is tolerated at doses up to 50 mg/kg with no significant adverse effects. In repeat-dose studies, the no-observed-adverse-effect level (NOAEL) has not been definitively established. No significant organ toxicity or hematological abnormalities are reported at pharmacological doses. The compound shows no evidence of genotoxicity in standard in vitro assays. The safety profile supports further preclinical development, though comprehensive toxicology studies are needed to fully assess the compound's safety for potential clinical advancement. The compound is for research use only and is not approved for human use.

[1]. The Anti-Proliferative and Anti-Invasive Effect of Leaf Extracts of Blueberry Plants Treated with Methyl Jasmonate on Human Gastric Cancer In Vitro Is Related to Their Antioxidant Properties. Antioxidants (Basel). 2020;9(1):45. Published 2020 Jan 4.

Methyl jasmonic acid (-) is a methyl ester derivative of jasmonic acid. It belongs to the jasmonic acid ester class and is a plant metabolite and plant hormone. It is a jasmonic acid ester, a methyl ester, and a member of the jasmonic acid ester derivative family. Methyl jasmonic acid has been reported to be present in potatoes (Solanum tuberosum), Tripterygium wilfordii, and other organisms with relevant data. Mechanism of Action: Using the pathogenic form of Alternaria alternata (Aa) and its AAL toxin/tomato interaction system as a model system, the authors demonstrated the potential role of jasmonic acid (JA) in plant susceptibility to pathogens that utilize host-specific toxins as virulence effectors. Compared to wild-type (WT) varieties, the def1 mutant with JA biosynthesis deficiency showed inhibited disease development and plant growth in Aa-pathogenic tomato plants. Exogenous application of methyl jasmonic acid (MeJA) restored pathogen symptoms in the def1 mutant and exacerbated the disease in WT plants. On the other hand, AAL toxin induced similar necrotic cell death in both def1 and WT plants, and MeJA application did not affect the degree of toxin-induced cell death. These results indicate that the JA-dependent signaling pathway does not participate in the host's basal defense response to Aa pathogens in tomato, but may affect pathogen tolerance in a toxin-independent manner. Further data suggest that jasmonic acid (JA) promotes the infection of both toxin-producing and necrotic pathogens in tomato, and that pathogens may utilize the JA signaling pathway for successful infection. ...WRKY is a plant-specific transcription factor and one of the flagellin-inducing genes in its non-host, Arabidopsis thaliana. Inoculation with the incompatible pathogen Pseudomonas syringae DC3000 (Pto) containing AvrRpt2 and non-host pathogens induced WRKY41 expression… Arabidopsis thaliana overexpressing WRKY41 showed enhanced resistance to wild-type Pto but increased susceptibility to Erwinia carotenoides EC1. Arabidopsis thaliana overexpressing WRKY41 constitutively expressed the PR5 gene but suppressed methyl jasmonic acid-induced PDF1.2 gene expression. These results suggest that WRKY41 may be a key regulator of the interaction between the salicylic acid and jasmonic acid signaling pathways.
Induced cell death is an important component of plant defense against pathogens. Numerous reports have documented the roles of plant hormones in pathogen-induced cell death, but jasmonic acid (JA) has not yet been identified as a regulator of this response. In this paper, researchers report the function of Nicotiana benthamiana homeobox 1 (NbHB1) in pathogen-induced cell death within the JA signaling pathway. The role of NbHB1 in cell death was analyzed through gain-of-function and loss-of-function experiments using Agrobacterium-mediated transient overexpression and virus-induced gene silencing, respectively. Reverse transcription polymerase chain reaction (RT-PCR) was used to monitor NbHB1 expression after pathogen inoculation and various treatments. Results showed that infection with both virulent and attenuated bacterial pathogens upregulated NbHB1 transcription levels. Ectopic expression of NbHB1 accelerated cell death after darkness, methyl jasmonate, or pathogen inoculation. Conversely, when NbHB1 was silenced, pathogen-induced cell death was delayed. Silencing of NbCOI1 also delayed NbHB1-induced cell death, indicating that the JA-mediated signaling pathway is essential. Overexpression of NbHB1 domain-deficient proteins indicated that the homologous domain, leucine zipper domain, and partially variable N-terminal region are essential for NbHB1 function. These results strongly suggest that NbHB1 plays a role in pathogen-induced plant cell death through the JA-mediated signaling pathway. In this study, the authors used high-throughput Illumina sequencing to identify miRNAs in Taxus chinensis cells to investigate the effect of the taxane inducer methyl jasmonic acid (MJ) on miRNA expression. In a dataset containing approximately 6.6 million sequences, 58 miRNAs belonging to 25 families were identified. Most of these were conserved in both angiosperms and gymnosperms. However, two miRNAs (miR1310 and miR1314) appeared to be gymnosperm-specific, with miR1314 possibly existing in clusters. MJ treatment significantly affected the expression of specific miRNAs; 14 miRNAs from 7 different families (miR156, miR168, miR169, miR172, miR396, miR480, and miR1310) were downregulated, while 3 miRNAs from 2 families (miR164 and miR390) were upregulated. For more complete data on the mechanisms of action of methyl jasmonate (13 in total), please visit the HSDB record page.

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Methyl jasmonate (MeJA) is the methyl ester of jasmonic acid, a plant hormone that regulates defense responses and secondary metabolite biosynthesis. It has anticancer and anti-inflammatory activities in biomedical research. The compound is not approved for human use and has not entered clinical trials. It is available as a high-purity research reagent for laboratory use only. Its plant hormone activity and biomedical potential make it a valuable tool for plant biology and pharmacology research.

C13H20O3

224.2961

224.141

1211-29-6

5281929

Colorless liquid

1.0±0.1 g/cm3

302.9±15.0 °C at 760 mmHg

25 °C

128.6±20.4 °C

0.0±0.6 mmHg at 25°C

1.469

2.12

0

3

6

16

281

2

CC/C=C\C[C@@H]1[C@H](CCC1=O)CC(=O)OC

GEWDNTWNSAZUDX-WQMVXFAESA-N

InChI=1S/C13H20O3/c1-3-4-5-6-11-10(7-8-12(11)14)9-13(15)16-2/h4-5,10-11H,3,6-9H2,1-2H3/b5-4-/t10-,11-/m1/s1

methyl 2-[(1R,2R)-3-oxo-2-[(Z)-pent-2-enyl]cyclopentyl]acetate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)