Compound Monograph

Methyl Jasmonate

Methyl jasmonate is a plant stress-signalling 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.

Where Does It Come From? (2)

Methyl Jasmonate is a naturally occurring oxylipin (jasmonate signalling molecule), found in Jasmine and 1 other source. It is well tolerated orally (low toxicity).

Jasmine Jasminum officinale Widespread trace volatile across flowering plants

Pharmacology & Research

Methyl jasmonate (MeJA) is a plant oxylipin — the methyl ester of jasmonic acid — that functions as a volatile stress-signalling 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-flavour 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.

What the evidence supports
  • A selective anticancer mechanism (preclinical): MeJA detaches hexokinase-2 from the mitochondrial VDAC, causing ATP depletion and p53-independent apoptosis in cancer cells while sparing normal cells 1,2,3Reference 1Rotem R et al. · 2005Jasmonates: novel anticancer agents acting directly and selectively on human cancer-cell mitochondriaView study →Reference 2Goldin N et al. · 2008Methyl jasmonate binds to and detaches mitochondria-bound hexokinaseView study →Reference 3Cesari IM et al. · 2014Methyl jasmonate: putative mechanisms of action on cancer-cell cycle, metabolism and apoptosisView study →.
  • Its actual biological role: a plant-defense signal and agricultural elicitor, used to raise secondary-metabolite (taxane, resveratrol, phytoalexin) yields in plant-cell culture 8,9,10Reference 8Ramirez-Estrada K et al. · 2016Elicitor-mediated production of taxanes in plant cell cultures of Taxus sppView study →Reference 9Almagro L et al. · 2023Factors affecting the bioproduction of resveratrol by grapevine cell cultures under elicitationView study →Reference 10Ho TT et al. · 2021Therapeutic potential of jasmonic acid and its derivativesView study →.
  • The honest headline: no human trials, no oral human PK, µM–mM potency and rapid esterase hydrolysis — and most anticancer work is on synthetic analogues, from a single research group 3,4Reference 3Cesari IM et al. · 2014Methyl jasmonate: putative mechanisms of action on cancer-cell cycle, metabolism and apoptosisView study →Reference 4Flescher E · 2015Methyl jasmonate and its potential in cancer therapyView study →.
1. Selective anticancer (preclinical)

Two decades of cell-line and xenograft work show jasmonates kill cancer cells selectively while sparing normal cells, by acting directly on mitochondria 1,3Reference 1Rotem R et al. · 2005Jasmonates: novel anticancer agents acting directly and selectively on human cancer-cell mitochondriaView study →Reference 3Cesari IM et al. · 2014Methyl jasmonate: putative mechanisms of action on cancer-cell cycle, metabolism and apoptosisView study →. MeJA detaches hexokinase-2 from the mitochondrial voltage-dependent anion channel (VDAC) 2Reference 2Goldin N et al. · 2008Methyl jasmonate binds to and detaches mitochondria-bound hexokinaseView study →, triggering ATP depletion, permeability-transition-pore opening and cytochrome-c release; it kills p53-mutant and wild-type lines alike (p53-independent) 3Reference 3Cesari IM et al. · 2014Methyl jasmonate: putative mechanisms of action on cancer-cell cycle, metabolism and apoptosisView study → and downregulates survival factors such as HPV E6/E7 and survivin in cervical lines 5Reference 5Milrot E et al. · 2012Methyl jasmonate reduces the survival of cervical-cancer cells and downregulates HPV E6/E7 and survivinView study →.

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 1,3Reference 1Rotem R et al. · 2005Jasmonates: novel anticancer agents acting directly and selectively on human cancer-cell mitochondriaView study →Reference 3Cesari IM et al. · 2014Methyl jasmonate: putative mechanisms of action on cancer-cell cycle, metabolism and apoptosisView study →.

2. Plant-defense signalling / elicitor

MeJA’s actual biological function — the honest centre 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 8,9,10Reference 8Ramirez-Estrada K et al. · 2016Elicitor-mediated production of taxanes in plant cell cultures of Taxus sppView study →Reference 9Almagro L et al. · 2023Factors affecting the bioproduction of resveratrol by grapevine cell cultures under elicitationView study →Reference 10Ho TT et al. · 2021Therapeutic potential of jasmonic acid and its derivativesView study →.

Gap: this is agronomy/biotech, not a human-health application — included so the page frames the compound honestly for what it actually does 8,9Reference 8Ramirez-Estrada K et al. · 2016Elicitor-mediated production of taxanes in plant cell cultures of Taxus sppView study →Reference 9Almagro L et al. · 2023Factors affecting the bioproduction of resveratrol by grapevine cell cultures under elicitationView study →.

3. Aroma / flavour volatile

Methyl jasmonate is a characteristic jasmine/gardenia scent constituent and a recognised flavour-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).

4. Antidepressant-like (rodent)

The only “systemic pharmacology” data in mammals: two mouse studies report MeJA reducing depressive-like behaviour, modulating monoaminergic pathways and suppressing TNF-α/oxidative stress 6,7Reference 6Umukoro S et al. · 2018AnimalAntidepressant-like activity of methyl jasmonate involves modulation of monoaminergic pathways in miceView study →Reference 7Eduviere AT et al. · 2017AnimalMethyl jasmonate attenuated lipopolysaccharide-induced depressive-like behaviour in miceView study →.

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 6,7Reference 6Umukoro S et al. · 2018AnimalAntidepressant-like activity of methyl jasmonate involves modulation of monoaminergic pathways in miceView study →Reference 7Eduviere AT et al. · 2017AnimalMethyl jasmonate attenuated lipopolysaccharide-induced depressive-like behaviour in miceView study →.

Mechanisms

Target / pathwayEffectRelevant to
Mitochondria-bound hexokinase-2 / VDACbinds and detaches HK2 from VDAC → loss of glycolytic-mitochondrial couplinganticancer (core mechanism)
Mitochondrial permeability-transition pore (MPTP)direct opening → membrane-potential collapse, cytochrome-c releaseanticancer, selective for cancer mitochondria
Cellular ATPrapid depletion in glycolysis-dependent tumour cellsanticancer selectivity vs normal cells
p53cytotoxicity is p53-independent (kills p53-mutant lines)anticancer
MAPK stress kinases (JNK, p38)activation in lymphoid cellsanticancer apoptosis signalling
HPV E6/E7, survivindownregulation → reduced survival of cervical cancer cellsanticancer (specific line)
Monoaminergic pathways; TNF-α, oxidative stressmodulation/suppressionrodent antidepressant/anti-inflammatory
Plant jasmonate (COI1–JAZ) defense signallingelicits defense-gene expression / secondary-metabolite biosynthesisplant 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 characterised 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.)

CompletedPlannedTerminatedPreclinical
(none)Moderate volume, single-group-dominated, largely analogues

Last checked: July 2026.

Toxicity & Safety

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 flavour/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.

Pregnancy & lactation

No human data → avoid deliberate supplementation. The honest context: MeJA is a normal trace dietary and aromatic-plant volatile, so ordinary incidental exposure (jasmine tea, foods) is not a concern; the caution applies only to intentional concentrated intake, for which no reproductive-safety data exist.

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

  1. 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/
  2. Goldin N, et al. (2008). Methyl jasmonate binds to and detaches mitochondria-bound hexokinase. Oncogene. https://pubmed.ncbi.nlm.nih.gov/18408762/
  3. 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/
  4. Flescher E (2015). Methyl jasmonate and its potential in cancer therapy. Plant Signaling & Behavior. https://pubmed.ncbi.nlm.nih.gov/26208889/
  5. 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/
  6. 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/
  7. 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/
  8. Ramirez-Estrada K, et al. (2016). Elicitor-mediated production of taxanes in plant cell cultures of Taxus spp. Biotechnology Advances. https://pubmed.ncbi.nlm.nih.gov/24681092/
  9. Almagro L, et al. (2023). Factors affecting the bioproduction of resveratrol by grapevine cell cultures under elicitation. Biomolecules. https://pubmed.ncbi.nlm.nih.gov/37892211/
  10. Ho TT, et al. (2021). Therapeutic potential of jasmonic acid and its derivatives. International Journal of Molecular Sciences. https://pubmed.ncbi.nlm.nih.gov/34445138/