IngredientsCitral is a naturally occurring acyclic monoterpene aldehyde. It is not a single compound but a mixture of two geometric isomers: geranial (citral A) and neral (citral B). The E-isomer is named geranial (trans-citral; α-citral), also called citral A. The Z-isomer is named neral.
Structurally, the two isomers are identical except that one bond near the oxygen atom is attached differently to the linking carbon atom, producing a subtly different shape. Like geranial, neral also has a fresh, lemon smell, but it is more subtle and sweet. In practical terms, geranial is the more potent of the two isomers, with a strong, sharp lemon odor, while neral is softer and slightly sweeter.
Its chemical formula is C₁₀H₁₆O. It is a pale yellow, oily liquid at room temperature with a strong lemon aroma and a boiling point of 226–228°C. It is insoluble in water but highly soluble in organic solvents like ethanol, ether, and mineral oil. Citral is an α,β-unsaturated aldehyde with highly reactive chemical properties. Citral is susceptible to oxidation and deterioration due to its conjugated double bonds and aldehyde groups.
Citral carries CAS number 5392-40-5 and EINECS number 226-394-6. Its alternative common name is lemonal, a term reflecting its characteristic citrus scent. Being a monoterpene, citral is made of two isoprene units.
Citral is present in the oils of several plants, including lemon myrtle (90–98%), Litsea citrata (90%), Litsea cubeba (70–85%), lemongrass (65–85%), lemon tea-tree (70–80%), Ocimum gratissimum (66.5%), Lindera citriodora (about 65%), petitgrain (36%), lemon verbena (30–35%), lemon ironbark (26%), lemon balm (11%), lime (6–9%), lemon (2–5%), and orange.
Of the myriad sources of citral, the Australian myrtaceous tree Lemon Myrtle, Backhousia citriodora F. Muell. (Myrtaceae), is considered superior. Lemon oil itself, cold pressed from the peel of Citrus limon L. (Rutaceae), contains only 2–3% of citral (geranial + neral).
Lemongrass (Cymbopogon flexuosus) is a perennial herb and one of the commercially important aromatic grasses belonging to the Poaceae family, due to its citral-rich (around 70–80%) essential oil, making it the primary source of citral. Besides citral, the lemongrass essential oil also contains minor amounts of other monoterpenes such as geraniol, citronellal, and myrcene.
The formation of citral in plants has been reported to involve the enzymatic oxidation of geraniol and/or nerol to citral by enzymes belonging to the NADP-dependent alcohol dehydrogenases (ADHs) class.
Commercially, citral is obtained via steam distillation of botanical sources — lemongrass oil from India and Sri Lanka contains high concentrations of citral; Litsea cubeba from China is another major commercial source; lemon myrtle plantations in Australia also yield citral-rich oils. Citral is also manufactured synthetically on a large scale from petrochemical feedstocks including isobutylene and formaldehyde. Citral can also be synthesized from myrcene.
Synthetic citral is chemically identical to the natural compound and dominates commercial fragrance supply because of price and consistency. Citral is isolated from lemongrass oil, which is obtained from lemongrass by steam distillation.
Most commercial citral is a blend of both isomers, with the ratio between them varying depending on the natural source or the synthetic production method.
Citral appears in commerce and research in several forms:
Citral is a precursor in the industrial production of vitamins A, E, and K, and is also a precursor to lycopene, ionone, and methylionone.
Lemongrass has been used traditionally in folk medicine in India, Thailand, Brazil, and beyond for centuries. Native to India and Sri Lanka, this botanical thrives in tropical climates and is synonymous with traditional tropical Asian cuisines.
Lemongrass essential oil has been used since ancient times in folk medicine as a remedy to improve circulation, stabilize menstrual cycles, promote digestion, and increase immunity. Traditional use shifted over time from ritual bathing to more clinical applications: poultices for headaches, decoctions for fever and dysentery, and inhalations for congestion.
The lemongrass plant is deeply rooted in India's culinary, medicinal, and agricultural traditions, appearing in Ayurvedic remedies, herbal teas, Indian curries, and sustainable farming systems. Key active constituents recognized within this tradition include citral (neral + geranial), myrcene, and limonene, each conferring unique therapeutic actions linked to lemongrass's reputation in balancing doshas.
In Thailand, lemongrass (takhrai) is an essential ingredient of traditional dishes such as tom yam and tom kha kai. Traditional uses of citral-rich plants in ethnopharmacology, particularly in Asia, Africa, and South America, have long underpinned their application in managing symptoms of inflammation.
Lippia alba, a citral-bearing plant used in South American and African herbal traditions, is empirically used for infusions, teas, macerates, and hydroalcoholic extracts because of its antispasmodic, analgesic, sedative, and anxiolytic effects. Citral is the main constituent of L. alba essential oil and is considered to account for its analgesic, anxiolytic, anticonvulsant, and sedative effects in these traditions.
Ionone and methylionone, made from citral, are used in perfumery; ionone is also converted into synthetic vitamin A. Citral is a crucial starting material in the industrial synthesis of Vitamin A (retinol). The process leverages citral's specific carbon skeleton and functional group, beginning by reacting citral with acetone to form pseudoionone, which is then cyclized to create β-ionone, the characteristic ring structure found in Vitamin A.
Citral itself is the primary bioactive molecule of interest. When derived from essential oils, it coexists with other minor monoterpenes whose synergistic contributions may be relevant in some contexts. The following describes the two principal isomers and their distinct characteristics:
When citral is derived from lemongrass oil, it is accompanied by: myrcene, citronellal, citronellol, linalool, and geraniol as additional co-occurring terpene constituents.
Citral has been shown to modulate key inflammatory pathways, including the inhibition of COX-2 and NF-κB, reduction of pro-inflammatory cytokines, and activation of peroxisome proliferator-activated receptors (PPARs).
COX-2 promoter activity was suppressed by lemongrass oil in cell-based transfection assays, and citral was identified as the major component responsible for the suppression of COX-2 expression and as an activator of PPARα and γ. In human macrophage-like U937 cells, citral suppressed both LPS-induced COX-2 mRNA and protein expression in a dose-dependent manner. Moreover, citral induced the mRNA expression of the PPARα-responsive carnitine palmitoyltransferase 1 gene and the PPARγ-responsive fatty acid binding protein 4 gene, indicating that citral activates PPARα and γ and thereby regulates COX-2 expression.
The anti-inflammatory mechanism of citral is attributed to the inhibition of NF-κB signaling. Citral activates peroxisome proliferator-activated receptor (PPAR-γ) and inhibits IκB phosphorylation, which independently blocks NF-κB activity with the consequent inhibition of gene expression of inflammatory mediators.
Citral also inhibited NLRP3 inflammasome activation and levels of ROS, NAD(P)H oxidase subunit p47(phox), and COX-2, and enhanced the activation of nuclear factor E2-related factor 2 (Nrf2).
As a bioactive component of lemongrass, citral inhibits oxidant activity, NF-κB activation, and COX-2 expression, while it activates PPAR-α and γ. Additionally, citral produces long-lasting inhibition of transient receptor potential (TRP) channels found in sensory neurons, such as TRPV1-3 and TRPM8, while transiently blocking TRPV4 and TRPA1.
One of the pivotal aspects of citral's antimicrobial efficacy lies in its diverse mechanisms of action: citral disrupts cell membrane integrity, inhibits essential enzymes in microbial metabolism, and interferes with quorum sensing, among other mechanisms.
In antifungal studies involving Candida albicans, involvement with the cell wall and ergosterol binding were excluded as possible mechanisms of action. Citral was observed to inhibit pseudohyphae and chlamydoconidia formation. Against filamentous fungi, increased membrane permeability, with increases in extracellular electrical conductivity and a decrease in soluble protein content, was demonstrated. A decrease in the range of ergosterol levels showed that citral altered the physiology of the cell membrane, and a reduction in the levels of enzymes associated with respiration resulted in the disruption of energy metabolism.
Treatment with citral causes an increase in intracellular oxygen radicals, and the resulting oxidative stress is the initiating and essential factor that leads to decreased proliferation and cancer cell death. Citral-induced oxidative stress also activates p53 to induce apoptosis; in cancer cells lacking this tumor suppressor, it inhibits proliferation by inducing endoplasmic reticulum stress.
Citral treatment induces decreased mitochondrial membrane potential, indicating that it induces apoptosis via the mitochondrial pathway. Bax up-regulation and Bcl-2 down-regulation at the mRNA level, and NF-κB down-regulation at the protein level, have been observed in citral-treated cancer cells.
In metabolic contexts, citral's activation of PPARα and PPARγ is relevant. These nuclear receptors regulate genes involved in lipid metabolism, adipogenesis, and insulin sensitivity. Research findings suggest that citral increased energy dissipation and reduced lipid accumulation, consequently preventing and ameliorating diet-induced obesity. In addition, it improved insulin sensitivity and glucose tolerance in animal models.
Research has examined whether the GABAA-benzodiazepine and 5-HT1A receptors are involved in the anxiolytic-like effects of citral. Citral dose-dependently decreased anxiety-related behaviors in mouse tests, with results suggesting that its anxiolytic activity occurs via GABAA and 5-HT1A receptor modulation.
In vitro and in silico analyses have indicated the ability of citral to counteract low levels of the neurotransmitter acetylcholine, pointing to potential acetylcholinesterase (AChE) inhibitory activity.
Investigations have demonstrated that citral exhibits several biological activities including antibacterial, antifungal, antibiofilm, antiparasitic, antiproliferative, anti-inflammatory, and antioxidant properties, documented by in vitro and in vivo assays.
Evidence level: Predominantly in vitro and in vivo (animal); no clinical human trials.
In a study investigating activity against Candida albicans, the MIC and MFC of citral were 64 µg/mL and 256 µg/mL, respectively. Involvement with the cell wall and ergosterol binding were excluded as mechanisms of action. In the morphological interference assay, citral inhibited pseudohyphae and chlamydoconidia formation. An earlier study found different MIC/MFC values: the MIC and MFC of citral against C. albicans were 512 and 1024 µg/mL, respectively — variability that reflects differences in strain and methodology between laboratories.
Among tested pathogens relevant to oral medicine, citral showed activity against Candida spp. and bacteria such as Staphylococcus aureus, Streptococcus mutans, and Lactobacillus spp. The precise mechanism of action has not been determined, and one of the studies reported low cytotoxicity.
In yeast models, the antifungal activity of 20 monoterpenes (including citral) was evaluated against the model yeast Saccharomyces cerevisiae; oxygenated monoterpenes exhibited greater fungistatic and fungicidal activities than hydrocarbons, and among the most effective oxygenated monoterpenes was citral, with an MIC and minimum fungicidal concentration (MFC) of 0.64 mM. Time response experiments showed that the selected monoterpenes rapidly reduced the viability of yeast cells in a time- and dose-dependent manner, with reduced viability associated with loss of cell membrane integrity.
Evidence level: Mechanistic in vitro and preclinical in vivo data; no randomized human clinical trials for citral alone.
In one animal study, citral (40 mg/kg) was administered intraperitoneally in rats, while a cell line was incubated with 3, 6, and 12 µM of citral for 12 hours. Citral treatment reduced the counts of white blood cells and the inflammatory cytokines IL-6 and TNF-α in rats. Furthermore, TNF-α and IL-8 expression and NF-κB activation induced by LPS were significantly reduced by citral in human umbilical vein endothelial cells (HUVECs). Results concluded that the anti-inflammatory activity of citral was attributed to the activation of the PPAR-γ receptor, which attenuates NF-κB activation and inflammatory mediator production.
These molecular actions support citral's ability to alleviate inflammation in various systems, including respiratory, gastrointestinal, neuroinflammatory, and orofacial conditions. Despite these promising findings, the full therapeutic potential of citral remains underexplored, with limited clinical studies and a lack of clarity regarding its long-term safety and bioavailability.
Evidence level: In vitro (cell line) studies and limited in vivo animal studies only; no human clinical trials.
Multiple cancer cell line studies have been published:
In in vivo animal experiments, while there was significant reduction in tumor volume, even high doses of nanoparticles loaded with citral, neral, or geranial did not cause noticeable toxicity in the animals. Overall, these studies have suggested that citral and its constituents neral and geranial may be considered as cytotoxic agents for the treatment of solid tumors. A major hurdle in the use of citral as an anticancer therapeutic is the lack of understanding of the full mechanism by which this monoterpenoid induces cancer cell death. No human clinical trials have been conducted.
Evidence level: Animal (rodent) studies; no human clinical trials.
In a streptozotocin/high-fat-diet diabetic rat model, citral was administered orally at a dose of 45 mg/kg body weight for 28 days. Blood glucose, plasma insulin, and lipid profile were studied. The results confirmed that administration of citral significantly (P<0.05) decreased the blood glucose level and increased plasma insulin in diabetic rats. Citral also improved oxidative markers along with antioxidative enzymes of the liver, adipose tissue, and pancreas, and regulated the activity of glucose-metabolic enzymes in the liver.
In a diet-induced obesity model, after obesity was induced, rats were treated with daily doses of citral at 10, 15, and 20 mg/kg body weight for a period of 28 days and then subjected to metabolic experiments. Citral-treated groups showed a dose-dependent reduction in body weight gain. They significantly had lower fasting glucose levels, improved glucose tolerance, lower fasting plasma glucose, higher metabolic rate, and smaller adipocytes after drug administration.
A more recent (2025) study using male C57BL/6J mice fed a high-fat diet investigated the effects of citral on intestinal and metabolic impairment induced by LPS and high-fat diet in vitro and in vivo models. Mice were fed a standard diet or HFD for 17 weeks, with daily oral administration of citral treatment at 25, 100, or 300 mg/kg or vehicle. The authors noted that some more studies are necessary to understand the precise mechanism of antidiabetic and antidyslipidemic activity of citral.
Evidence level: Animal (rodent) studies; evidence for isolated citral is mixed. No human clinical trials.
Studies have introduced citral as a functional component of some essential oils in anxiolytic and antidepressant therapies; however, the neuropharmacological characteristics of citral have not yet been fully reported. In one study, the anxiolytic activities of citral were evaluated in comparison to two standard anxiolytics, diazepam and buspirone, in Swiss albino mice by intraperitoneal administration of 1, 2, 5, 10, and 20 mg/kg using the elevated plus maze (EPM) and open-field test (OFT). Citral dose-dependently decreased the number of border crossings and time spent in borders, and the number of grooming and rearing events in the OFT without altering motor activity, with results suggesting anxiolytic activity via GABAA and 5-HT1A receptor modulation.
In the open field test, citral significantly reduced locomotor activity at a dose of 400 mg/kg. Citral also increased pentobarbital-induced sleeping time at the same dose, indicating sedative and hypnotic effects. In the forced swimming test, citral reduced immobility time at doses of 100–400 mg/kg, suggesting antidepressant activity. However, citral did not exhibit significant effects in the elevated plus maze test at these doses.
Importantly, a systematic review noted a key limitation: one study did not observe an anxiolytic-like effect in the elevated plus-maze with isolated citral, limonene, or myrcene, which suggests that other constituents may contribute to the anxiolytic-like effect of C. citratus whole oil. Furthermore, the anxiolytic-like effect was not seen after repeated (21-day) treatment, suggesting tolerance development, and the effect appeared to be mediated by GABA-A/benzodiazepine transmission, as it was blocked by flumazenil pretreatment.
Studies evaluated the effects of the essential oil of Lippia alba and citral on compound action potentials (CAPs) in Wistar rat sciatic nerves. Both drugs inhibited CAPs in a concentration-dependent manner. The calculated half-maximal inhibitory concentration (IC₅₀) for citral was 35.00 µg/mL (or 230 µM). These results provide a pharmacological basis for the traditional use of citral-bearing plants in pain relief.
The terpenoid component citral shows antioxidant activity, which is a result of co-oxidation with the target substrate and cross-termination of the oxidative chain. The antioxidant properties of lemongrass essential oil have been studied by many researchers, though there are some discrepancies between the results, probably due to the different geographical origin of the plant, different extraction methods, and methodology used to evaluate its antioxidant activity. Citral is considered a proven antioxidant, as further confirmed by increased DPPH inhibition with increased citral concentration (IC₅₀: 6.9 ± 1.68 µg/mL, p < 0.05).
Animal data from a lupus nephritis model showed that citral (3,7-dimethyl-2,6-octadienal), a major active compound in the Chinese herbal medicine Litsea cubeba, was used to test renoprotective effects in a lipopolysaccharide (LPS)-induced mouse model of accelerated and severe lupus nephritis, examining NLRP3 inflammasome activation, ROS and COX-2 production, and Nrf2 activation. The analysis of mechanisms of action also involved its effects on IL-1β secretion and signaling pathways of the NLRP3 inflammasome in LPS-primed peritoneal macrophages. These findings remain at the preclinical level.
No established clinical dosages exist for citral as a standalone dietary supplement. The following dosages are those reported in experimental studies and should be understood strictly in that research context:
Citral has acceptable drug-likeness properties and does not present any violations of Lipinski's rules, which could theoretically be used in drug development pipelines.
Citral is recognized as safe (GRAS) by the Food and Drug Administration (FDA). Citral is generally recognized as a safe food additive and has been approved by the Food and Drug Administration for use in foods (FDA GRAS, 21 CFR 182.60).
The most significant documented safety concern for citral is its potential as a skin sensitizer. The core concern with citral is contact sensitization, meaning that repeated exposure can trigger allergic reactions in a subset of people even at low concentrations. Citral is associated with allergies and contact dermatitis.
Based on a weight of evidence approach, the data demonstrate that the human NOEL (No Observed Effect Level) for induction of dermal sensitization to citral is 1400 µg/cm². The identification of this induction threshold allows risk assessments to focus on primary prevention of contact allergy to citral based on a Quantitative Risk Assessment (QRA) paradigm. This assessment forms the basis of a risk management approach specifically via a new IFRA (International Fragrance Association) standard on the use of citral in consumer products.
The International Fragrance Association (IFRA) has issued a standard on the use of citral in fragrance formulations based on its allergenic potential. Citral is one of 26 fragrance materials identified as a suspected cause of allergic contact dermatitis by the European Commission's advisory committee.
Data on citral provide a calculated margin of exposure greater than 100 for repeated dose toxicity and developmental and reproductive toxicity endpoints. The SCCS concluded that, based on the QRA2 methodology, citral is considered safe at the proposed concentrations in cosmetic products, though they noted the methodology still requires further clarification and refinement.
Cross-reactivity is a relevant concern: sensitivity to citral often overlaps with issues around geraniol, hydroxycitronellal, and citrus peel extracts.
Citral is not genotoxic, according to available safety evaluations by the Research Institute for Fragrance Materials Expert Panel (REXPAN).
The regulatory picture for citral is notably different on each side of the Atlantic. The FDA includes citral in its list of substances considered Generally Recognized as Safe as a synthetic flavoring substance. In the European Union, several fragrance allergens require labeling in a cosmetic product's ingredient list if they are present above a certain threshold concentration.
Citral is susceptible to oxidation and deterioration due to its conjugated double bonds and aldehyde groups. Oxidative degradation products may themselves be more potent sensitizers than the parent compound, which is a relevant consideration in both cosmetic and food applications where citral may be exposed to light, air, or heat over extended storage periods.
Despite its promising benefits, the full therapeutic potential of citral remains underexplored, with limited clinical studies and a lack of clarity regarding its long-term safety and bioavailability in humans. The overwhelming majority of pharmacological studies are conducted in cell cultures or rodent models. No peer-reviewed, randomized, controlled clinical trials in humans examining citral as an isolated therapeutic agent had been identified in the published literature as of the time of this writing. Extrapolation of rodent dosing data to humans requires significant caution, and the identified mechanisms and effects — while scientifically plausible — cannot be considered clinically established.
Health conditions that Citral may help support.
Body systems that Citral may help support.
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