Skip to main content
Free shipping on all orders
888-559-3802
VitabaseIngredients

Myrcene

Table of contents

Other Names

1,6-Octadiene, 7-methyl-3-methylene-1,7-Octadiene, 2-methyl-6-methylene-2-Methyl-6-methylene-1,7-octadiene2-Methyl-6-methylene-2,7-octadiene2-methyl-6-methylideneocta-1,7-diene3-Methylene-7-methyl-1,6-octadiene7-Methyl-3-methylen-1,6-octadien7-Methyl-3-methylene-1,6-octadiene7-Méthyl-3-méthylène-1,6-octadiène7-Methyl-3-methylene-octa-1,6-diene7-Methyl-3-methyleneocta-1,6-diene7-Methyl-3-methyleneoctadiene-(1,6)7-Methyl-3-methylideneocta-1,6-dienea-Myrcenealpha-Myrceneb-Geranioleneb-Myrcenebeta-MyrceneMyrcene, β-NSC 406264α-Myrceneβ-Geranioleneβ-mirceneβ-Myrcene

Synopsis

Myrcene (β-Myrcene)

1. Identity: Chemical and Botanical Profile

Chemical Names and Classification

Chemically classified under IUPAC nomenclature as 7-methyl-3-methylene-1,6-octadiene, myrcene serves as a key intermediate in terpene-based aroma chemistry, contributing characteristic peppery and balsamic notes to beer and certain flavor applications. Its synonyms include β-myrcene, beta-myrcene, 2-methyl-6-methylene-2,7-octadiene, and 3-methylene-7-methyl-1,6-octadiene.

Myrcene is a monoterpene, a type of terpene consisting of two isoprene units with the chemical formula C₁₀H₁₆, and is classified as a monoterpenoid and a major component in the essential oils of various plants. It has a molecular weight of 136.23 grams per mole. As a volatile compound, myrcene easily evaporates, shaping the overall scent profile of plants that contain it.

In biosynthesis, terpenes form from precursor molecules like geranyl pyrophosphate (GPP) for monoterpenes; myrcene is one common outcome of monoterpene biosynthesis pathways.

Discovery and Naming

Myrcene derives its name from the Brazilian shrub Myrcia sphaerocarpa, where it was first isolated in 1897. The systematic study of myrcene began in the early 20th century as part of broader investigations into terpene chemistry, and while naturally occurring myrcene was identified in various essential oils including bay leaf (Pimenta racemosa) and verbena, early researchers recognized the practical limitations of isolation from botanical sources.

Natural Sources and Occurrence

β-Myrcene is present in various plant species, such as lemongrass oil (Cymbopogon citratus), rosemary (Rosmarinus officinalis), and is also the major component of hop and bay oils, which are used in the manufacture of alcoholic beverages. Myrcene is found in small amounts in a number of essential oils, including rosemary, frankincense, juniper, rose, ginger, and verbena, all of which have traditional analgesic qualities.

Its most abundant and well-studied botanical sources include:

  • Hops (Humulus lupulus), where myrcene is responsible for the peppery, spicy, balsam fragrance in beer.
  • Cannabis (Cannabis sativa), where myrcene is one of the most abundant terpenes, accounting for up to 50% of a strain's total terpene profile.
  • In modern commercial cannabis strains tested at scale, myrcene represents on average over 20% of the terpene profile, though individual samples vary widely.
  • Hops and cannabis are both members of the family Cannabaceae.

Aroma Profile

Myrcene is described as having an earthy, musky, herbal, clove-like aroma, but can be very pungent in higher concentrations, as in heavily hopped beers. In purified form, its odor profile is sweet-balsamic and fruity-resinous with green mango nuances, light citrus notes, and slightly ethereal, mushroomy undertones.

Common Forms and Preparations

β-Myrcene is an abundant monoterpene which occurs as a major constituent in many plant species, including hops and cannabis, and is a popular flavouring and aroma agent used in the manufacture of food and beverages. Its uses include fragrance intermediate, extender for bay leaf oil and citrus accords, masking agent in industrial products, and precursor for terpene alcohols (geraniol, nerol, linalool, citronellol), aldehydes (citral, citronellal), and menthol.

β-Myrcene has been used as a synthetic flavor chemical in the U.S. for well over 50 years, having been approved by the FDA in 1964 along with many other flavoring substances. In supplement and research contexts, pure β-myrcene has been administered in capsule form in at least one clinical study.


2. Traditional and Historical Use

Brazilian Folk Medicine

Myrcene gets its name from Myrcia sphaerocarpa, a shrub from Brazil that contains large amounts of it and has long been used as a folk remedy for hypertension, diabetes, and diarrhea. Traditional Brazilian healers also use the myrcia leaf to treat a similar range of maladies.

One of the most culturally rich uses of myrcene can be found in the consumption of lemongrass tea, particularly in Brazil and Mexico, where this myrcene-rich brew has been a traditional remedy to soothe the mind, mitigate pain, and combat insomnia.

Hops in European Tradition

Long before hops became a flavoring agent in beer, it was a prized herbal remedy in ancient Egypt, and became a staple of European folk medicine for its treatment of digestive disorders and liver diseases. It is common for Germans, who are the second largest hops growers in the world (the US is first), to use myrcene-rich hop preparations as a sleep aid.

Thyme in Roman and Mediterranean Traditions

The therapeutic use of myrcene-rich plants dates back thousands of years; two thousand-year-old Roman texts describe the medicinal virtues of thyme, a herb that can contain up to 40% myrcene by weight.

Asian and Ayurvedic Traditions

Asian and Ayurvedic healing traditions use calming lemongrass teas and administer essential lemongrass extracts as remedies for numerous conditions, from stomachaches and coughs to high blood pressure and joint pain.

Traditional Pain Use

β-Myrcene has been extensively used throughout history by folk medicine as a pain-killer; most commonly, traditional medicine has used essential oils which contain high percentages of myrcene along with an array of other terpenes. Myrcene has a long history of traditional use in herbal medicine through plants like lemongrass and hops, both of which have been brewed for centuries to encourage calm and rest.

Important note: In all traditional contexts, myrcene was consumed as a constituent of whole-plant preparations (teas, essential oils, decoctions) rather than as an isolated compound. The attribution of specific effects to myrcene itself, as distinct from other co-occurring compounds in these preparations, is an interpretation of modern phytochemical analysis.


3. Key Active Constituents and Mechanisms of Action

β-Myrcene's reported biological activities include analgesic, sedative, antidiabetic, antioxidant, anti-inflammatory, antibacterial, and anticancer effects. The following sections address the primary mechanisms proposed in peer-reviewed research.

Analgesic (Pain-Relieving) Mechanisms

β-Myrcene has shown central and peripheral analgesic effects; intraperitoneal administration of β-myrcene (10 mg/kg; 73 μmol/kg) provided antinociception in mice undergoing tests of acute pain.

This effect was antagonised centrally by prior administration of naloxone (an opioid antagonist) and yohimbine (an α2-adrenergic antagonist), implying the role of the opioid and noradrenergic systems; the results imply that the antinociceptive effect is mediated by the release of endogenous opioids through the α2-adrenoreceptors.

The peripheral analgesic effect of myrcene was further confirmed by testing a standard commercial preparation on the hyperalgesia induced by prostaglandin in the rat paw test and upon the contortions induced by intraperitoneal injections of iloprost in mice. Myrcene's analgesic and anti-inflammatory actions can also be attributed to reduction of peripheral nociception by inhibition of prostaglandin release.

While myrcene seems to act chiefly through non-cannabinoid routes, it has been shown to interact with local cannabinoid receptors (likely CB2) in murine models of joint inflammation, reducing pain and swelling, though without synergy with CBD. Overall, myrcene's analgesic action probably involves a combination of peripheral opioid receptor engagement, a reduction in inflammatory sensitization, and possibly TRPV1 modulation, although its precise molecular targets remain undefined.

Anti-Inflammatory Mechanisms

Several experimental investigations, both in vitro and in vivo, have demonstrated that β-myrcene effectively modulates inflammatory responses by targeting key molecular mediators and signaling pathways. It significantly suppresses the production of major pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), while concurrently inhibiting the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), enzymes crucial in the synthesis of inflammatory mediators.

β-Myrcene administration suppressed mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB) pathways to limit inflammation. Mechanistic studies further revealed that these protective effects were mediated through the inhibition of NF-κB p65 subunit translocation into the nucleus and suppression of MAPK signaling cascades, including ERK, JNK, and p38.

Sedative / Hypnotic Mechanisms

Beta-myrcene reduced the damage to hypothalamic neuron cells and increased neurotransmitter levels of GABA, 5-HT, and glutamate (Glu) in the serum and hypothalamus of insomnia model mice. Beta-myrcene exerted an improvement in insomnia by upregulating relevant genes and protein expression in the serotonergic synaptic pathway.

Myrcene appears to work in part by enhancing activity of the inhibitory GABA-A receptor, a mechanism shared with benzodiazepines, which are sedative drugs used for anxiety and sleep.

Antioxidant Mechanisms

In systemic inflammatory conditions such as diabetic nephropathy and adrenalectomy-induced oxidative stress, myrcene demonstrated significant antioxidant and anti-inflammatory benefits by restoring the activities of key antioxidant enzymes—superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH)—and by reducing the lipid peroxidation marker malondialdehyde (MDA), thereby protecting tissues from oxidative injury.

Blood–Brain Barrier Permeability

It appears that myrcene lowers resistance across the blood-brain barrier, improving permeability, so that β-myrcene itself and many other chemicals (including the analgesic THC) may cross the barrier more effectively. This proposed mechanism has implications for the so-called "entourage effect" in cannabis pharmacology, but remains to be directly confirmed in human studies.


4. Scientific Evidence by Area of Use

General note on evidence quality: No data is currently available that correlates the therapeutic use of pure β-myrcene with health benefits in human participants; most of the studies on health benefits of β-myrcene have been conducted in animal models or cell culture. Few studies conducted in humans (n=2 at the time of the review) were found, and these included humans inhaling plant essential oil extracts containing less than 25% β-myrcene; thus, more robust, randomised, controlled clinical trials using pure β-myrcene preparations are needed.

4.1 Pain and Analgesia

Preclinical evidence (animal/in vitro): In preclinical studies, administration of essential oils rich in myrcene have been found to have analgesic and anti-inflammatory properties; for example, Eremanthus erythropappus (10% myrcene) and Bougainvillea glabra (4% myrcene) increased hindpaw withdrawal time in mice and rats in response to noxious stimuli.

The monoterpene myrcene can reduce nociception produced by noxious thermal and mechanical stimuli as well as reducing acute inflammation; a 2022 study from Dalhousie University examined the role of myrcene and cannabidiol (CBD) in controlling chronic joint inflammation and pain. In summary, myrcene was found to have anti-inflammatory and analgesic effects in inflammatory joint disease by activating articular cannabinoid receptors. While chronic myrcene treatment had no effect on joint pathology, long-term administration of the compound had a more profound effect on inflammatory parameters, and peripheral myrcene had no effect on circulating cytokine levels, so the anti-inflammatory mechanism of action still needs to be resolved.

Lorenzetti et al. (1991) concluded their work with the suggestion that terpenes should be investigated with the "possibility of developing a new class of analgesic with myrcene as the prototype."

Human evidence: It is not clear that any controlled studies have pinpointed myrcene as having a causal role in driving pain relief in humans; there are no well-controlled human clinical trials that clearly demonstrate a pure analgesic effect of myrcene.

Evidence strength: Preliminary. Preclinical data are consistent and mechanistically plausible, but human clinical validation is absent.

4.2 Inflammation — Bowel and Systemic

Preclinical evidence: Using DSS-induced colitis and TNF-α challenged HT-29 adenocarcinoma cells as in vivo and in vitro models, administration of β-myrcene in dextran sodium sulfate-treated mice restored colon length, decreased disease activity index (DAI), myeloperoxidase (MPO) enzyme activity and suppressed proinflammatory mediators. β-Myrcene also suppressed mRNA expression of proinflammatory chemokines in TNF-α challenged HT-29 adenocarcinoma cells.

Human evidence: None identified in the literature reviewed.

Evidence strength: Preliminary. Animal and cell models only.

4.3 Osteoarthritis and Joint Health

In vitro (human cell) evidence: In an in vitro cartilage degradation model of osteoarthritis, myrcene (25–50 μg/mL; 183.5–367 μmol/kg) showed anti-inflammatory and anticatabolic effects on human chondrocytes, slowing down cartilage degradation and osteoarthritis progression. Myrcene decreased interleukin IL-1β-induced NF-κB and JNK, further decreased ERK1/2, p38 activation and the expression of inflammatory iNOS, decreased catabolic responses (matrix metalloprotease MMP1 and MMP13), whilst increasing the expression of anticatabolic genes (tissue inhibitor of metalloproteases TIMP1 and TIMP3), and decreased the expression of non-cartilage specific collagen I induced by IL-1β, thus promoting the maintenance of the differentiated chondrocyte phenotype.

In cell-based studies using human chondrocytes, myrcene mitigated interleukin-1β-induced inflammation by reducing nitric oxide release and downregulating the expression of matrix metalloproteinases MMP-1 and MMP-13, enzymes implicated in cartilage degradation and joint inflammation.

Human evidence: None identified. The chondrocyte findings are in vitro using isolated cells, not in human clinical trials.

Evidence strength: Preliminary. Human cell-line data are mechanistically suggestive but cannot be extrapolated directly to clinical outcomes.

4.4 Sleep and Sedation

Preclinical evidence: In a 2024 study, among 15 potential active ingredients in lavender essential oil, beta-myrcene had strong sedative–hypnotic effects through the serotonergic synaptic pathway according to network pharmacological prediction; PCPA-induced insomnia mice were then treated with beta-myrcene for one or seven days. The quiet state of insomnia mice was increased effectively, and the hypnotic effect was enhanced by sodium pentobarbital, prolonging sleep duration, decreasing sleep latency, and increasing the rate of falling asleep; beta-myrcene also increased neurotransmitter levels of GABA, 5-HT, and Glu in the serum and hypothalamus.

Studies in rodents have shown that myrcene has several properties associated with sedatives, evidenced by induction of cytochrome P-450 (P-450 2B subfamily) enzyme, slowed motor activity, increased muscle relaxation, and increased sleeping time.

Human evidence: No well-controlled human clinical trials have clearly demonstrated a sedative effect of myrcene.

Evidence strength: Weak for humans. Rodent and cell data support a biological plausibility for sedative and sleep-promoting effects, but no direct human clinical evidence exists for isolated myrcene.

4.5 Psychomotor Effects and Driving Impairment

Human clinical evidence (the only direct human trial identified): A double-blind, placebo-controlled crossover pilot study was conducted on a small sample of 10 participants, each randomized to receive 15 mg of pure β-myrcene in a capsule versus a canola oil control; each session, participants completed a baseline block and three follow-up blocks on a STISIM driving simulator. β-Myrcene was associated with statistically significant reductions in speed control and increased errors on a divided attention task; other measures did not approach statistical significance but fit the pattern of results consistent with the hypothesis that β-myrcene impairs simulated driving.

To the authors' knowledge, this was the first research examining the effects of a cannabis terpene on behavior related to driving; importantly, β-myrcene was dosed outside of any cannabis product, based on earlier research that β-myrcene alone might have sedating properties.

The authors acknowledged that the pilot study was underpowered and the design suffered several limitations. One small pilot study examined beta-myrcene's effects on driving performance and divided attention in humans but did not collect data on subjective side effects like drowsiness, so the clinical evidence on how people actually feel after taking isolated myrcene remains thin.

Evidence strength: Very preliminary (n=10, single study). Proof-of-principle only; larger, better-powered trials are needed.

4.6 Anticancer Activity

In vitro evidence: In a 2023 PMC-published study, the biological efficacy of myrcene was studied in human cell lines (HeLa, SH-SY5Y, and HDFa) using cytotoxicity, cell proliferation, cell migration, and morphology assays; results showed that myrcene has potential biological activity especially in HeLa cells, where it leads to an arrest of proliferation, a decrease in motility and morphological changes with loss of sphericity and thickness, and DNA damage.

A separate study demonstrated that compared with control cells, myrcene induces cell death in A549 lung adenocarcinoma cells in a dose-dependent manner while inducing ROS levels, and that the metabolic activity of the cancer cells was diminished. The maximum number of nonviable A549 cells was observed at a myrcene concentration of 1 µg/mL, with a half-maximal inhibitory concentration of 0.5 µg/mL.

Human evidence: None. All anticancer evidence is from cell lines only.

Evidence strength: Very preliminary (in vitro cell lines). Results cannot be extrapolated to clinical anticancer efficacy in humans.

4.7 Antioxidant Effects

These findings collectively suggest that β-myrcene exerts its anti-inflammatory activity through a multifaceted mechanism involving suppression of pro-inflammatory mediators, inhibition of NF-κB and MAPK pathways, and enhancement of the cellular antioxidant defense system.

Evidence strength: Preclinical only. Consistent findings across multiple animal and cell models, but no human interventional data.


5. Body Systems and Health Areas Associated with Myrcene

  • Central Nervous System: Sedation, sleep promotion, modulation of GABA-A receptors and serotonergic pathways (preclinical).
  • Musculoskeletal / Joints: Anti-inflammatory and anticatabolic effects in chondrocytes; analgesic activity in arthritis models (preclinical and in vitro).
  • Gastrointestinal: Reduction of colonic inflammation, inhibition of gastric ulcer formation, and antibacterial effects against Helicobacter pylori (preclinical). An antibacterial effect of β-myrcene against Helicobacter pylori has been reported.
  • Immune / Inflammatory: Modulation of cytokine production (TNF-α, IL-1β, IL-6), suppression of NF-κB and MAPK pathways (preclinical).
  • Cardiovascular / Oxidative Stress: In rodent models, administration of β-myrcene was reported to protect against oxidative and histological damage in heart tissue after global ischemia-reperfusion.
  • Oncology (in vitro): Antiproliferative and proapoptotic activity in cervical and lung cancer cell lines; not validated in humans.
  • Skin: β-Myrcene has a potential protective effect on UVB-induced human skin photoaging (based on in vitro/preclinical data).

6. Dosage Forms and Dosages Reported in Studies

The following dosages are reported solely as they appeared in the cited scientific literature. No standardized clinical dosing regimen for myrcene exists, and no therapeutic dose has been established for humans.

  • Animal analgesic study (intraperitoneal, mice): Intraperitoneal administration of β-myrcene at 10 mg/kg (73 μmol/kg) provided antinociception in mice in tests of acute pain.
  • In vitro osteoarthritis model (human chondrocytes): Myrcene at concentrations of 25–50 μg/mL (183.5–367 μmol/kg) showed anti-inflammatory and anticatabolic effects on human chondrocytes.
  • In vitro lung cancer model (A549 cells): The maximum cytotoxic effect was observed at 1 µg/mL, with a half-maximal inhibitory concentration (IC50) of 0.5 µg/mL.
  • Human pilot study (oral capsule): Participants received 15 mg of pure β-myrcene in a capsule in the only identified direct human dosing trial.
  • Rat oral NOEL (no-observed-effect level): The oral NOEL for both sexes of rats was the highest dose tested: 115 and 136 mg/kg body weight/day for males and females respectively, a level that is several orders of magnitude greater than typical human exposures from β-myrcene.

7. Safety Considerations and Regulatory Status

General GRAS Status

Myrcene is listed as "Generally Recognized as Safe" (GRAS) by the U.S. Food and Drug Administration (FDA) for use in food and cosmetic products. However, the regulatory history of synthetic myrcene as a direct food additive is complex (see below).

NTP Carcinogenicity Studies and FDA Regulatory Action

Myrcene was nominated by the National Institute of Environmental Health Sciences in 1997 for study by the National Toxicology Program (NTP) based on its high production volume, high level of human exposure, and a structural relationship to d-limonene.

Following 2-year carcinogenicity studies of β-myrcene in mice and rats, NTP published Technical Report TR-557 in 2010; the FDA concluded that synthetic myrcene was shown to cause cancer in laboratory animals under the conditions of the NTP carcinogenicity studies. The FDA also confirmed that myrcene is not genotoxic, yet definitive modes of action were not established for rodent carcinogenicity.

Based on increased incidence of renal tubule neoplasms, NTP concluded that there was clear evidence of carcinogenic activity of myrcene in male F344/N rats and equivocal evidence of carcinogenic activity of myrcene in female rats.

In 2018, the FDA took regulatory action to no longer permit the use of β-myrcene as a food additive, based on legal action taken under the Delaney Clause (a federal health statute which prohibits FDA approval of any food additive that caused cancer in humans or animals). Importantly, the FDA confirmed that there was no safety concern for β-myrcene to public health under the conditions of its intended use.

The FDA's revocation of the listings providing for the use of these synthetic flavoring substances does not affect the legal status of foods containing natural counterparts or non-synthetic flavoring substances extracted from food, and there is nothing in the data FDA reviewed that causes FDA concern about the safety of foods that contain natural counterparts or extracts from such foods.

Scientific Critique of NTP Findings — Dose Relevance and Species Specificity

The dosages applied in the NTP study were five–six orders of magnitude greater than human exposure, and there are also doubts about the purity of the β-myrcene used, thus casting serious doubts on the relevance to humans.

The NTP concluded that the renal tumours in the low-dose group of male F344 rats were possibly due to α2u-globulin nephropathy, a mechanism not applicable to humans, as the protein α2u-globulin responsible for this effect in rodents is not present in humans.

The B6C3F1 male mice included in the NTP study are recognised for having a high and variable background incidence of hepatocellular tumors; on this basis the European Food Safety Authority (EFSA) has rejected their relevance for human health.

The FEMA Expert Panel (2020) reaffirmed β-myrcene as Generally Recognized as Safe (GRAS), stating "no change is necessary in the FEMA GRAS status of beta-myrcene" following the FDA's regulatory action.

Psychomotor and CNS Safety

Evaluation of exploratory, emotional and anxiolytic activity in rodents using tests such as the elevated plus maze, conditioned avoidance, and open space showed that β-myrcene does not provoke any mind-altering behavior.

In the only human pilot study, a 15 mg oral dose was associated with statistically significant reductions in simulated driving speed control and increased errors on a divided attention task, though other measures did not reach significance. This finding, while preliminary given the study's very small sample (n=10) and acknowledged limitations, suggests that isolated myrcene may impair psychomotor performance at supplemental doses.

Myrcene is widely described as having sedative properties in cannabis culture, but controlled human data supporting that claim is limited.

Natural Occurrence vs. Concentrated Supplementation

If using terpene-enriched products, the dose matters more than the substance itself; the safety profile that regulators have endorsed applies to flavoring-level exposures, not to concentrated supplementation.


References

Health Conditions

Health conditions that Myrcene may help support.

  • No conditions available.

Body Systems

Body systems that Myrcene may help support.

  • No body systems available.
Join our newsletter

Stay informed. Stay healthy.

Get expert supplement tips, exclusive discounts, and product recommendations delivered to your inbox

Myrcene | Vitabase