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Theacrine
Theacrine
Theacrine
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Theacrine
Chemical structure of theacrine.
Names
Preferred IUPAC name
1,3,7,9-Tetramethyl-7,9-dihydro-1H-purine-2,6,8(3H)-trione
Other names
1,3,7,9-Tetramethyluric acid; Temurin; Temorine; Tetramethyluric acid; Tetramethyl uric acid; TeaCrine (trade name)
Identifiers
3D model (JSmol)
ChEBI
ChemSpider
ECHA InfoCard 100.017.268 Edit this at Wikidata
UNII
  • InChI=1S/C9H12N4O3/c1-10-5-6(11(2)8(10)15)12(3)9(16)13(4)7(5)14/h1-4H3
    Key: QGDOQULISIQFHQ-UHFFFAOYSA-N
  • InChI=1/C9H12N4O3/c1-10-5-6(11(2)8(10)15)12(3)9(16)13(4)7(5)14/h1-4H3
    Key: QGDOQULISIQFHQ-UHFFFAOYAN
  • CN1C2=C(N(C1=O)C)N(C(=O)N(C2=O)C)C
Properties
C9H12N4O3
Molar mass 224.220 g·mol−1
Melting point 226 °C (439 °F; 499 K)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).

Theacrine, also known as 1,3,7,9-tetramethyluric acid, is a purine alkaloid found in cupuaçu (Theobroma grandiflorum) and in a Chinese kucha tea (Chinese: 苦茶; pinyin: kǔ chá; lit. 'bitter tea') (Camellia assamica var. kucha).[1][2] It shows anti-inflammatory and analgesic effects and appears to affect adenosine signalling in a manner similar to caffeine.[2][3] In kucha leaves, theacrine is synthesized from caffeine in what is thought to be a three-step pathway.[2] Theacrine and caffeine are structurally similar.

Caffeine vs theacrine

Pharmacology

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Pharmacodynamics

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The exact mechanism of action of theacrine is uncertain, as no binding affinities have been published. However, animal research involving selective A1 and A2A adenosine agonists found theacrine pretreatment attenuated the expected motor depression induced by adenosine agonism, indicating that theacrine is likely an adenosine antagonist.[2]

Administration of selective dopamine D1 and D2 antagonists demonstrate that, similarly to caffeine,[4] the behavioural effects of theacrine are in part mediated by dopamine receptors.[2]

Pharmacokinetics

[edit]

Theacrine has half-life of 30 to 33 hours.[5]

Safety

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Theacrine has demonstrated clinical safety and non-habituating effects in healthy humans over eight weeks of daily use at up to 300 mg/day.[6] Moreover, there was no evidence of the tachyphylaxis typical of neuroactive agents like caffeine and other stimulants.[6]

In animal studies, theacrine has an LD50 of 810 mg/kg,[3][6] compared to 265 mg/kg for caffeine.[7]

See also

[edit]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Theacrine

View on Grokipedia
from Grokipedia
Theacrine is a purine alkaloid, chemically known as 1,3,7,9-tetramethyluric acid with the molecular formula C₉H₁₂N₄O₃ and a molecular weight of 224.22, structurally analogous to caffeine but featuring a methyl group at the N-9 position. It occurs naturally, first identified in the seeds of cupuaçu (Theobroma grandiflorum), at concentrations of 1.3–3.4% dry weight primarily in the leaves of the wild tea plant Camellia kucha Hung T. Chang, a species endemic to Yunnan Province in China, and in trace amounts in other plants such as Camellia sinensis var. puanensis, Ilex vomitoria, Camellia gymnogyna, and Theobroma grandiflorum. Unlike caffeine, theacrine exhibits a longer half-life, reduced potential for habituation, and fewer adverse side effects, positioning it as a component in dietary supplements for cognitive and physical enhancement. Theacrine is biosynthesized from through enzymatic processes involving N-methylation at the N-9 position, catalyzed by enzymes like CkTcS (a methyltransferase) using S-adenosyl-L-methionine as the methyl donor. This pathway underscores its role as a downstream in within , where it contributes to the plant's defense mechanisms against herbivores and environmental stressors. Commercially, theacrine is extracted from C. kucha leaves or synthesized for use in nutraceuticals, often under brand names like TeaCrine®, and is included in and products due to its antagonism similar to but with sustained effects. Human consumption typically ranges from 65–300 mg per dose, derived from supplements rather than traditional tea brews where levels are low. Pharmacologically, theacrine demonstrates promising effects on cognitive performance, mood, and resistance through mechanisms including system modulation, antagonism, and actions. Clinical studies in healthy adults have shown that acute doses of 200–300 mg improve focus, , and positive mood while reducing subjective , with benefits observed in tasks requiring sustained . In exercise contexts, it may enhance by increasing time-to-exhaustion by 27–38% in some trials, though results on physical performance metrics like sprint speed or agility are inconsistent across studies. Animal models further support its , , and neuroprotective properties, potentially mitigating stress-induced central via regulation of neurotransmitters. Regarding safety, theacrine has a favorable profile with an oral LD₅₀ of 810.6 mg/kg in mice and a of 180 mg/kg/day in rats. In trials, daily doses of 200–300 mg for up to 8 weeks in healthy adults (n=60) produced no significant changes in , liver or function, or hematology markers, with no reports of jitteriness, increased , or . Minor reductions in LDL and total were noted in some participants at higher doses, but no adverse events on or mood were observed long-term. Overall, theacrine is considered safe for short- and medium-term use in healthy populations at recommended doses.

Natural occurrence and sources

Primary plant sources

Theacrine, a structurally similar to , was first identified in 1937 as a minor component in the leaves of tea plants. Its primary natural source, however, is the wild tea plant Camellia kucha Hung T. Chang (formerly known as Camellia assamica var. kucha; commonly known as Kucha tea), native to the mountainous regions of Yunnan Province in , where it accumulates in significantly higher concentrations in the leaves and young shoots. In C. kucha, theacrine levels in tender shoots with two leaves and a bud range from 1.3% to 3.4% of dry weight, making it the dominant alongside . This plant's unique profile contributes to the bitter taste of Kucha tea, traditionally consumed for its stimulating effects. Trace amounts of theacrine have also been detected in other plant species, including the seeds of cupuaçu (), a native to the , var. puanensis, , Camellia gymnogyna, and (as of 2025, the first coffee species confirmed to contain it). These secondary sources contain only minor quantities compared to Kucha , often less than 0.1% dry weight, and are not commercially significant for extraction. No substantial presence has been confirmed in (maca) roots based on available analyses. Commercially, theacrine is primarily harvested from the leaves of cultivated Camellia kucha through solvent extraction processes that isolate the while preserving its purity. The resulting extract is standardized and branded as TeaCrine®, a patented form containing at least 98% theacrine, used in dietary supplements for its purported energy-enhancing properties without the associated with . This commercial production relies on sustainable cultivation of Kucha tea plants in to meet growing demand in the industry. The biosynthesis of theacrine in plants occurs within the pathway, originating from where serves as the initial precursor. This compound undergoes sequential N-methylation by S-adenosyl-L-methionine-dependent methyltransferases, first forming 7-methylxanthine, then (3,7-dimethylxanthine), and subsequently (1,3,7-trimethylxanthine). In select species, such as Camellia kucha, is further transformed into theacrine (1,3,7,9-tetramethyluric acid) through a three-step process: oxidation at the C8 position to yield 1,3,7-trimethyluric acid as an intermediate, followed by N9-methylation catalyzed by the specific N9-methyltransferase CkTcS. Theacrine is chemically related to other purine alkaloids, sharing early biosynthetic steps with and but diverging through the additional oxidation and methylation at the N9 position of the backbone, which lacks. Unlike , which accumulates widely in species, theacrine forms as a downstream primarily in kucha and related variants, where the pathway enzymes exhibit substrate specificity for this extension. This structural kinship— differing by the absence of the 9-methyl group and C8 oxidation—underlies their similar pharmacological profiles while highlighting theacrine's unique occurrence in certain lineages. Levels of theacrine in vary due to environmental influences, including altitude and conditions, which modulate synthesis broadly in plants. Higher altitudes typically reduce accumulation through altered temperature, light, and nutrient availability, potentially affecting downstream theacrine production similarly, while nutrient imbalances, such as or deficiencies common in plantations, can suppress overall . The evolutionary role of theacrine, like other alkaloids, is hypothesized to involve plant defense, providing against herbivory by deterring feeding through bitter taste and , as well as mitigating environmental stresses such as UV via mechanisms. This across plant families underscores its adaptive significance in enhancing survival in native habitats.

Chemical properties

Molecular structure and formula

Theacrine is a characterized by the molecular formula C₉H₁₂N₄O₃. Its systematic IUPAC name is 1,3,7,9-tetramethyl-7,9-dihydro-1H-purine-2,6,8(3H)-trione, commonly referred to as 1,3,7,9-tetramethyl to reflect its relation to the core. The molecule consists of a fused imidazole-pyrimidine ring system typical of , with carbonyl groups at positions 2, 6, and 8, and methyl substituents on the atoms at positions 1, 3, 7, and 9; this configuration yields a dimethylated derivative. Unlike (1,3,7-trimethylxanthine), theacrine incorporates an additional N9-methyl group and an oxo functionality at C8, altering the ring's substitution pattern. No natural isomers of theacrine are known to occur in sources. Synthetic analogs, such as those modifying the pattern for research purposes, exist but are not detailed here as they fall outside natural variants.

Physical and chemical characteristics

Theacrine is a white to off-white crystalline powder possessing a bitter akin to , which contributes to the sensory profile of teas containing it. Its ranges from 227 to 228 °C, indicating thermal stability suitable for formulation processes. In terms of , theacrine exhibits moderate in , approximately 25 mg/mL at 20 °C, with increased in hot ; it is moderately soluble in but insoluble in , facilitating its extraction and purification from sources. This profile supports its use in aqueous-based supplements, though low room-temperature may require solubilization aids for optimal in formulations. Theacrine demonstrates stability under neutral conditions, as typical for alkaloids, but undergoes degradation in strongly acidic or alkaline environments, necessitating careful control during storage and processing. For analytical identification, theacrine shows a characteristic UV maximum at 274 nm, enabling straightforward detection; (HPLC) coupled with UV or diode array detection is routinely employed for purity assessment in dietary supplements, often achieving separation from related alkaloids like .

Pharmacology

Pharmacodynamics

Theacrine functions as an at adenosine A1 and receptors, thereby counteracting -mediated inhibition of neuronal activity and promoting in a manner analogous to . This antagonism attenuates motor depression induced by adenosine A1 agonist cyclopentyladenosine (CPA) and agonist CGS-21680 in models, confirming its blockade of these receptors. The compound also modulates dopaminergic neurotransmission, with its locomotor-activating effects in rats blocked by dopamine D1 receptor antagonist SCH23390 and D2 receptor antagonist eticlopride, indicating facilitation of D1 and D2 receptor signaling. Direct infusion of theacrine into the shell, a key region of the ventral , elicits locomotor , thereby enhancing dopaminergic tone. This modulation inhibits adenosine-induced sedation and contributes to psychostimulant-like activity. In comparison to , theacrine shares structural similarities that enable antagonism but demonstrates reduced tolerance development; chronic administration (48 mg/kg intraperitoneally for 7 days) in rats produces no locomotor or , unlike under similar conditions. Its dimethyluric acid backbone may confer greater metabolic stability, supporting sustained receptor interactions.

Pharmacokinetics

Theacrine is rapidly absorbed following , with peak plasma concentrations (C_max) typically achieved within 1 to 2 hours post-ingestion. In human studies using doses of 25 to 125 mg, theacrine demonstrates good oral absorption via intestinal pathways, though exact percentages have not been precisely quantified in humans; coadministration with enhances exposure by increasing C_max and area under the curve (AUC) by approximately 50%, likely through improved absorption. Theacrine distributes widely throughout the body, with an apparent (Vd/F) of approximately 35 to 51 L (roughly 0.5 to 0.7 L/kg in a 70 kg adult), indicating moderate tissue penetration. It efficiently crosses the blood-brain barrier, as evidenced by detectable levels in tissue following oral dosing in animal models. Protein binding data remain limited, but structural similarities to suggest low . Metabolism of theacrine is thought to occur primarily in the liver via enzymes, possibly involving CYP1A2-mediated demethylation analogous to 's primary pathway, though specific profiles in humans require further elucidation; coadministration with does not significantly alter theacrine's metabolic processing. Elimination of theacrine is characterized by a prolonged of 16 to 29 hours, substantially longer than 's typical 5 to 6 hours, supporting sustained effects with once-daily dosing. Oral clearance (CL/F) ranges from 1.2 to 2.0 L/h, and excretion is primarily renal, consistent with , with dose-linearity observed across 25 to 125 mg in healthy adults.

Biological effects and potential uses

Cognitive and mood enhancement

Theacrine has been investigated in clinical trials for its potential to enhance cognitive functions such as attention, reaction time, and . In a randomized, double-blind, placebo-controlled study involving young adults, acute ingestion of 200 mg theacrine improved subjective measures of focus and concentration without altering or , with activation occurring around 2 hours after intake, indicating a favorable profile for cognitive support. These effects suggest theacrine may bolster vigilance and executive function under demanding conditions, though larger studies are needed to confirm broader applicability. Regarding mood modulation, TeaCrine®, a branded form of theacrine, at doses of 200-300 mg has been shown to elevate subjective levels, reduce feelings of and , and maintain without inducing jitteriness associated with traditional stimulants, providing sustained energy and motivation without habituation or tolerance buildup. In a crossover study, TheaTrim (a supplement containing theacrine and 150 mg caffeine) acutely increased ratings of attentiveness, , and focus while decreasing grogginess compared to or caffeine alone. Additionally, over eight weeks of daily use at 200-300 mg, theacrine sustained these mood benefits without , keeping anxiety levels stable and preventing tolerance development. A November 2024 dose-response study (100-400 mg theacrine) found initial evidence of improved next-morning cognitive performance in aspects like and , without negatively impacting quality or duration. An August 2025 randomized in gamers showed that a combination of , theacrine, and enhanced psychomotor performance, reaction time, and accuracy in a first-person shooter scenario, with benefits on focus and reduced errors compared to . Animal studies provide mechanistic insights into these effects. In , theacrine at 48 mg/kg intraperitoneally increased locomotor activity and exploratory behavior, an effect mediated through in the and attenuated by D1 and D2 receptor antagonists. Separate research in stressed mice demonstrated antidepressant-like properties, with theacrine alleviating depression-related behaviors and promoting hippocampal neurogenesis via pathways that may indirectly involve dopamine modulation. Typical dosages for cognitive and mood benefits range from 100-300 mg, with evidence of sustained efficacy over eight weeks without , distinguishing theacrine from habit-forming stimulants. These findings position theacrine as a promising non-jittery option for mental enhancement, though its effects via antagonism warrant further exploration in cognitive contexts.

Physical performance and energy effects

Theacrine supplementation has been investigated for its potential to enhance subjective levels during . In a randomized crossover study involving healthy adults, a single 200 mg dose of theacrine increased self-reported on visual analog scales compared to , with effects observed over several hours and activation occurring around 2 hours after intake, without altering oxygen consumption or hemodynamic parameters. Regarding , evidence suggests modest benefits in specific protocols. A double-blind with high-level soccer players found that 275 mg of theacrine showed a non-significant trend toward extending time to exhaustion during a cycling-based test by approximately 27% compared to (from 194 seconds to 246 seconds; p = 0.052), with a trivial, non-significant effect on ratings of perceived exertion (RPE) scales (ES = -0.12, p = 0.282). However, a 2022 study using 200 mg in young athletes reported no improvement in aerobic during a 12-minute run test, highlighting variability across protocols. Studies on performance metrics in resistance training indicate limited ergogenic effects. In resistance-trained men, 300 mg of theacrine consumed 90 minutes before exercise did not enhance maximal strength (e.g., 1-repetition maximum or squat), muscular endurance (repetitions to failure at 70% 1RM), or power output (peak power or velocity) compared to . A 2022 randomized controlled trial with 200 mg daily over eight weeks in young male athletes similarly showed no gains in anaerobic capacity (e.g., 40-second run distance) or power (e.g., sextuple jump), with improvements attributable to training alone rather than supplementation. Recovery markers were not directly assessed in these trials, but no adverse impacts on training status (e.g., IGF-1 levels) were observed. Theacrine exhibits metabolic effects that may support energy utilization during exercise, primarily through preclinical evidence. In cell and mouse models, theacrine (10-20 mg/kg) activated the SIRT3/AMPK/ACC pathway, promoting fat oxidation by upregulating genes like LCAD and LPL while reducing hepatic accumulation and markers (e.g., FAS, ACC). These actions suggest potential for increased without excessive cardiovascular strain, as human studies report no elevations in resting . Additionally, theacrine demonstrates properties in tissues, inhibiting mediators like IL-6, TNF-α, and IL-1β via pathways such as TGF-β/SMAD, which could aid muscle recovery post-exercise, though direct human muscle data are lacking. Long-term supplementation with TeaCrine®, a commercial form of theacrine, maintains these effects without developing tolerance or habituation. An eight-week randomized with 200-300 mg daily in healthy adults found sustained subjective and levels, with no or observed across visual analog scale assessments, unlike typical responses. This non-habituating profile aligns with theacrine's longer , supporting prolonged provision.

Safety and regulatory status

Toxicology and adverse effects

Theacrine exhibits low in animal models, with an oral LD50 of 810.6 mg/kg (95% : 769.5–858.0 mg/kg) reported in mice, corresponding to an estimated equivalent dose of approximately 4 grams for a 76 kg individual without observed lethality. No acute toxicity data indicate lethality at doses up to 1000 mg, though higher doses may disrupt architecture, such as increased wake after sleep onset and reduced efficiency following 400 mg administered 12 hours prior to . In chronic exposure studies, a 90-day oral gavage in rats established a (NOAEL) of 180 mg/kg body weight per day, with adverse effects including centrilobular hepatocellular and reduced male reproductive organ weights observed only at higher doses (300–375 mg/kg/day). Human clinical trials support safety at therapeutic doses; an 8-week randomized, double-blind, placebo-controlled study in 60 healthy adults (ages 18–60) found no significant changes in liver enzymes (ALT, AST, ALP), kidney function (), , , or electrocardiogram parameters with daily doses of 200–300 mg. These trials reported no or , consistent with theacrine's profile. Adverse effects in humans are minimal at standard doses, with no clinically significant side effects noted in multiple trials up to 300 mg/day; however, doses exceeding 400 mg may cause mild subjective increases in perceived without broader hemodynamic impacts. Potential interactions include additive effects when combined with , though no adverse hemodynamic changes (e.g., elevated or ) were observed in studies using co-administration at 100–200 mg each. Caution is advised with agonists, as theacrine antagonizes their motor-depressant effects in preclinical models, potentially altering therapeutic outcomes. Data on vulnerable populations remain limited; no human studies exist for pregnant or lactating women, children, or adolescents, and animal assessments have not identified teratogenic effects, though comprehensive evaluations are lacking. As of 2025, no new clinical data have emerged for these groups. In the United States, theacrine is classified and marketed as a ingredient under the Dietary Supplement Health and Education Act (DSHEA) of 1994, which allows for the sale of such substances without pre-market FDA approval as long as they are not represented as . The branded form TeaCrine®, a nature-identical version of theacrine, received self-affirmed (GRAS) status in 2016 from an independent expert panel, based on toxicological and safety data supporting its use in foods and beverages at levels up to 300 mg per day. No formal FDA GRAS notification was filed for theacrine, distinguishing it from FDA-reviewed notices, and it has not received approval as a pharmaceutical . Internationally, theacrine is regarded as a in the under Regulation (EU) 2015/2283, requiring pre-market authorisation due to its limited history of significant consumption in the EU prior to 1997. As of November 2025, theacrine has not been authorised for placement on the market, with notifications through the Rapid Alert System for Food and Feed (RASFF)—such as a 2021 alert on unauthorised food supplements—indicating ongoing regulatory scrutiny. In sports contexts, theacrine is permitted and not listed on the (WADA) Prohibited List as of the 2026 list (effective January 2026), with TeaCrine® validated as compliant through third-party testing by Informed-Sport, confirming absence of prohibited substances. Labeling and purity standards for theacrine supplements emphasize compliance with current good manufacturing practices (cGMP) under DSHEA, including accurate declaration of ingredient content and avoidance of adulteration. Third-party testing by organizations like or USP is recommended to verify purity and potency, as unregulated markets have raised concerns about potential contamination or substitution with undeclared stimulants in products. Historical regulatory developments for theacrine began with its initial novelty as a , addressed through safety studies in the early that resolved concerns over and , leading to GRAS affirmation; however, ongoing monitoring persists for potential doping implications in athletic use, though no bans have been imposed.

References

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