Compound Monograph
Methyl Jasmonate
Methyl jasmonate is a plant stress-signaling oxylipin and jasmine-aroma volatile (the methyl ester of jasmonic acid), best known biomedically for selectively killing cancer cells in preclinical studies by detaching hexokinase from mitochondria. It is primarily a plant hormone, agricultural elicitor and fragrance ingredient — not a supplement, with no human therapeutic use.
Sources · 2
Where Does It Come From?
Methyl Jasmonate is a naturally occurring oxylipin (jasmonate signaling molecule), found in Jasmine and 1 other source. It is well tolerated orally (low toxicity).
Concentration
Content by Source
Concentrations not reported. No percent-dry-weight or mg/g figures have been published for this compound in its source plants.
Methyl Jasmonate at a Glance
Methyl jasmonate is a plant stress-signalling hormone — the volatile the methyl ester of jasmonic acid, released when a plant is wounded and used to warn neighbouring tissue and plants. It is also the jasmine aroma note.
Its biomedical interest is a striking and specific mechanism: it selectively kills cancer cells in preclinical studies by detaching hexokinase from the mitochondrial membrane, collapsing the glycolytic advantage that tumour cells depend on — while leaving normal cells, which rely less on that arrangement, largely unaffected.
What It's Used For
Methyl jasmonate (MeJA) is a plant oxylipin — the methyl ester of jasmonic acid — that functions as a volatile stress-signaling hormone, and it is also a characteristic jasmine/gardenia aroma constituent (structural kin of cis-jasmone). It is best understood as three things: a plant defense signal, an agricultural/biotech elicitor, and a fragrance-and-flavor volatile. Its biomedical hook — real but strictly preclinical — is that jasmonates selectively kill cancer cells by acting directly on mitochondria. The load-bearing caveat is that methyl jasmonate is not a supplement and has no human therapeutic use: every biomedical claim below is cell-line or rodent work.
Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. No human data of any kind, so scores stay low by design.
Two decades of cell-line and xenograft work show jasmonates kill cancer cells selectively while sparing normal cells, by acting directly on mitochondria 1,
Gap: entirely in-vitro/rodent-xenograft, with no human trials, no oral human PK, poor potency (µM–mM), and rapid esterase hydrolysis; most of the more potent work is on synthetic analogues, not parent MeJA, and much of it traces to a single group 1,
MeJA’s actual biological function — the honest center of the page. It is a volatile stress hormone that induces plant defense genes and boosts secondary-metabolite yields, and it is exploited routinely in plant-cell/tissue culture to raise taxane, resveratrol and phytoalexin output 8,
Gap: this is agronomy/biotech, not a human-health application — included so the page frames the compound honestly for what it actually does 8,
Methyl jasmonate is a characteristic jasmine/gardenia scent constituent and a recognized flavor-and-fragrance ingredient; its low-level use in foods and perfumery underlies the low-toxicity designation.
Gap: an organoleptic role only, with no therapeutic claim (and no specific FEMA number asserted here).
The only “systemic pharmacology” data in mammals: two mouse studies report MeJA reducing depressive-like behavior, modulating monoaminergic pathways and suppressing TNF-α/oxidative stress 6,
Gap: rodent-only, single group, small, using injected doses — no mechanism confirmed in humans, no human dosing, and no basis for a mood-supplement use 6,
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| Mitochondria-bound hexokinase-2 / VDAC | binds and detaches HK2 from VDAC → loss of glycolytic-mitochondrial coupling | anticancer (core mechanism) |
| Mitochondrial permeability-transition pore (MPTP) | direct opening → membrane-potential collapse, cytochrome-c release | anticancerselective for cancer mitochondria |
| Cellular ATP | rapid depletion in glycolysis-dependent tumor cells | anticancer selectivity vs normal cells |
| p53 | cytotoxicity is p53-independent (kills p53-mutant lines) | anticancer |
| MAPK stress kinases (JNK, p38) | activation in lymphoid cells | anticancer apoptosis signaling |
| HPV E6/E7, survivin | downregulation → reduced survival of cervical cancer cells | anticancer (specific line) |
| Monoaminergic pathways; TNF-α, oxidative stress | modulation/suppression | rodent antidepressant/anti-inflammatory |
| Plant jasmonate (COI1–JAZ) defense signaling | elicits defense-gene expression / secondary-metabolite biosynthesis | plant biology / agronomy elicitor |
Pharmacokinetics
There is essentially no mammalian PK data. MeJA is a lipophilic methyl ester expected to undergo rapid esterase hydrolysis to jasmonic acid; no verified human absorption, distribution, metabolism or elimination parameters exist. Preclinical anticancer work uses direct in-vitro exposure or local/injected administration in rodents, not characterized systemic oral dosing — so no bioavailability, half-life or Cmax figures can be reported.
Clinical trials
There are none. No human clinical trials of methyl jasmonate exist for any indication; all biomedical evidence is cell-line or rodent-xenograft. (A topical hexokinase-2-modulating MeJA analogue has been explored preclinically for actinic keratoses, but that is the analogue, not parent MeJA, and remains preclinical.)
| Completed | Planned | Terminated | Preclinical |
|---|---|---|---|
| —(none) | — | — | Moderate volume, single-group-dominated, largely analogues |
Last checked: July 2026.
Toxicity & Safety
The low-toxicity flag reflects methyl jasmonate’s status as a trace aroma volatile in ordinary food and plants — it is not an endorsement of supplementation, for which there is no human safety dataset at all.
- A normal trace constituent of edible and aromatic plants. Used at low levels as a flavor and fragrance volatile.
- Avoid deliberate supplementation in pregnancy. No reproductive-safety data.
- No chronic human safety dataset. No established human therapeutic use, and the literature on human toxicity is very limited.
Full Safety & Interactions Detail
Methyl jasmonate carries a low flag: it occurs as a normal trace constituent of edible/aromatic plants and is used at low levels as a flavor/fragrance volatile, consistent with a low-toxicity designation. No signal of significant human toxicity appears in the (very limited) literature, and rodent studies used it without reported acute harm. There is no chronic oral safety dataset in humans, and the compound has no established human therapeutic use — so “low toxicity” reflects its status as a dietary/aroma trace substance, not a safety endorsement for supplementation.
Dosage
There is no established human dose — methyl jasmonate is not a supplement and is not clinically used. No oral human dosing regimen exists; preclinical anticancer concentrations are µM–mM in vitro. No dose should be inferred for human use.
References
- Rotem R, et al. (2005). Jasmonates: novel anticancer agents acting directly and selectively on human cancer-cell mitochondria. Cancer Research. https://pubmed.ncbi.nlm.nih.gov/15753398/
- Goldin N, et al. (2008). Methyl jasmonate binds to and detaches mitochondria-bound hexokinase. Oncogene. https://pubmed.ncbi.nlm.nih.gov/18408762/
- Cesari IM, et al. (2014). Methyl jasmonate: putative mechanisms of action on cancer-cell cycle, metabolism and apoptosis. International Journal of Cell Biology. https://pubmed.ncbi.nlm.nih.gov/24648844/
- Flescher E (2015). Methyl jasmonate and its potential in cancer therapy. Plant Signaling & Behavior. https://pubmed.ncbi.nlm.nih.gov/26208889/
- Milrot E, et al. (2012). Methyl jasmonate reduces the survival of cervical-cancer cells and downregulates HPV E6/E7 and survivin. Cancer Letters. https://pubmed.ncbi.nlm.nih.gov/22198483/
- Umukoro S, et al. (2018). Antidepressant-like activity of methyl jasmonate involves modulation of monoaminergic pathways in mice. Advances in Medical Sciences. https://pubmed.ncbi.nlm.nih.gov/28818747/
- Eduviere AT, et al. (2017). Methyl jasmonate attenuated lipopolysaccharide-induced depressive-like behaviour in mice. Journal of Psychiatric Research. https://pubmed.ncbi.nlm.nih.gov/28647678/
- Cusido, R. M., Onrubia, M., Sabater-Jara, A. B., et al. (2014). A rational approach to improving the biotechnological production of taxanes in plant cell cultures of Taxus spp. — review. Biotechnology Advances. https://pubmed.ncbi.nlm.nih.gov/24681092/
- Vera-Urbina JC, Sellés-Marchart S, Martínez-Márquez A, et al. (2023). Factors affecting the bioproduction of resveratrol by grapevine cell cultures under elicitation. Biomolecules. https://pubmed.ncbi.nlm.nih.gov/37892211/
- Jarocka-Karpowicz I, Markowska A, et al. (2021). Therapeutic potential of jasmonic acid and its derivatives. International Journal of Molecular Sciences. https://pubmed.ncbi.nlm.nih.gov/34445138/
