Tetrahydrocannabihexol
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THCH (tetrahydrocannabihexol) — also known as parahexyl — is an emerging naturally-occurring cannabinoid of the dibenzopyran class. It sits between Δ9-THC and Δ9-THCP in potency, its six-carbon side chain conferring stronger CB1 binding than conventional THC.[1][2] THCH is a full agonist at the CB1 receptor, producing its effects by maximally activating the brain's primary cannabinoid signalling system.
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First synthesized by Roger Adams around 1941–1942 as "parahexyl," the compound was identified as a natural cannabis constituent only in 2020.[3] Semi-synthetic THCH products entered recreational markets in 2021–2022,[4] prompting emergency scheduling in Japan after documented hospitalisations.[5] It remains unscheduled in most jurisdictions and circulates through online cannabinoid vendors with minimal quality control.
Subjective effects include sedation, euphoria, appetite enhancement, and time alteration. The experience is presumed to resemble an intensified version of conventional cannabis — similar in character but with a steeper climb toward overwhelming effects, closer in risk profile to synthetic cannabinoids than to plant-derived THC. Anxiety, paranoia, cognitive impairment, and hallucinations are characteristic unsought effects.
Dependence liability is uncharacterised but presumed at least equivalent to Δ9-THC; no lethal dose or controlled toxicity data exist. As a full CB1 agonist, THCH can achieve receptor activation levels that Δ9-THC's partial agonism cannot reach, narrowing the margin between desired effects and severe adverse reactions including prolonged unconsciousness. THCH is among the least-studied psychoactive cannabinoids on consumer markets — current understanding rests on a single isolation paper, mouse metabolism data, and Japanese adverse event reports.
History[edit]
Discovery
Roger Adams and collaborators at the University of Illinois synthesized the compound they called parahexyl (also synhexyl) around 1941–1942, as part of systematic work to identify the active principles of cannabis.[6] Pharmacologist S. Loewe tested it in mice in 1946, observing catalepsy and motor impairment consistent with natural THC isolates.[7] The compound remained classified as a purely synthetic structural analog for nearly eighty years.
Natural isolation and market emergence
In 2020, Linciano and colleagues at the University of Modena and Reggio Emilia isolated Δ9-THCH from the FM2 medicinal cannabis variety, establishing it as a natural phytocannabinoid for the first time.[3] The discovery followed the same group's 2019 identification of Δ9-THCP (seven-carbon chain), filling the structural gap in the THC homologous series between the pentyl and heptyl members.[8]
Regulatory response
By 2021–2022, semi-synthetic THCH products appeared on online markets in Japan, Europe, and the United States.[9][4] Forensic analyses consistently revealed mislabelling — products frequently contained cannabinoids other than those advertised.[4] Japan designated both Δ8-THCH and Δ9-THCH as controlled substances in August 2023 following at least nine documented adverse events,[5] and the UK's Advisory Council on the Misuse of Drugs recommended Class B control in May 2025.[10]
The name parahexyl (and its variant synhexyl) dates to the Adams laboratory's naming conventions of the 1940s, reflecting the compound's hexyl side chain. The modern abbreviation THCH or THC-H follows the pattern established by THCP and THCB — appending a letter for the side-chain length. In online cannabinoid communities, THCH occupies an ambiguous commercial position: marketed as "stronger than THC" but without the notoriety of THCP, it is often bundled into multi-cannabinoid vape blends rather than sold as a standalone product.
Chemistry[edit]
Structural class
Tetrahydrocannabihexol belongs to the dibenzopyran family of classical cannabinoids — terpenophenolic compounds sharing a tricyclic ring system of a phenol ring, a cyclohexene ring, and a pyran ring. THCH is a homolog of Δ9-THC, differing only in its alkyl side chain at C-3: six carbons (hexyl) instead of five (pentyl).[3]
The THC homologous series runs from propyl (Δ9-THCV, 3 carbons) through butyl (Δ9-THCB), pentyl (Δ9-THC), hexyl (Δ9-THCH), to heptyl (Δ9-THCP). Each additional carbon increases CB1 potency and lipophilicity.[2] A corresponding Δ8 isomer (Δ8-THCH) exists, differing in double-bond position; both have been identified in commercial products.[9]
Molecular identity
| Molecular formula | C₂₂H₃₂O₂ |
| Molecular weight | 328.5 g/mol |
The Δ9 designation indicates the position of the double bond in the cyclohexene ring. The phenolic hydroxyl at C-1 and the hexyl chain at C-3 are the primary pharmacophoric elements: the hydroxyl participates in hydrogen bonding at the CB1 receptor, while the alkyl chain occupies a hydrophobic groove whose depth tolerance governs potency.[2]
Stereochemistry
THCH has two chirality centres at C-6a and C-10a. The naturally occurring active form adopts the (6aR,10aR) configuration, identical to natural Δ9-THC.[3] Linciano and colleagues confirmed this via stereoselective synthesis matched against the isolated natural product.[3]
Natural occurrence
Δ9-THCH was isolated from the FM2 Italian medicinal cannabis variety at trace concentrations.[3] It is classified as a minor phytocannabinoid.[11] Most commercially available THCH is produced semi-synthetically rather than extracted from plant material.
Pharmacology[edit]
Mechanism of action
THCH acts as a full agonist at the cannabinoid CB1. In a bioassay covering 30 THC variants, Janssens and colleagues found THCH among multiple homologs demonstrating higher CB1 activation potential than Δ9-THC.[1] No specific binding affinity or potency values have been published for the compound. safety citation needed
The enhanced potency follows directly from the longer side chain. In the THC homologous series, extending the C-3 alkyl chain increases lipophilicity and deepens engagement with a hydrophobic pocket in the CB1 receptor.[2][12] This relationship is well established: each additional carbon from five to seven generally strengthens binding.
As a full agonist, THCH can theoretically achieve maximal receptor activation — unlike Δ9-THC, which is a partial agonist with a ceiling on its effects.[13][1] This distinction places THCH pharmacologically closer to synthetic cannabinoids and Δ9-THCP than to conventional cannabis.
CB2 activity has not been characterised for THCH. By class inference, CB2 affinity is expected but likely lower than CB1 affinity.[2] inferred
Pharmacokinetics
No controlled human pharmacokinetic studies have been published for THCH. Bioavailability, time to peak plasma concentration, half-life, and protein binding are entirely unknown in humans.
The only metabolic data come from mice. Brown and Harvey (1988) administered both Δ8-THCH and Δ9-THCH intraperitoneally and identified hepatic metabolites.[14] Δ9-THCH yielded 16 metabolites, primarily through the same C-11 hydroxylation pathway that converts Δ9-THC to its active metabolite 11-OH-THC. Compared to THC, THCH metabolism shifted toward hydroxy metabolites rather than carboxylic acids.[14]
Consumer products are typically inhaled (vaped) or taken orally. By analogy with Δ9-THC, inhaled delivery likely produces rapid onset while oral ingestion delays onset but may extend duration. No route-specific data exist for THCH.
Neuroscience[edit]
Where it acts
CB1 receptors — the most abundant G-protein-coupled receptors in the brain — concentrate in the hippocampus, cerebellum, basal ganglia, and prefrontal cortex. As a full CB1 agonist,[1] THCH is expected to suppress neurotransmitter release at both excitatory and inhibitory synapses throughout these regions.
In the hippocampus, this disrupts memory formation. In the cerebellum, it impairs motor coordination. In the prefrontal cortex, it interferes with executive function. CB1 activation in the ventral tegmental area disinhibits dopamine release into the nucleus accumbens, underlying the compound's rewarding properties.
Why it matters
The critical distinction is full versus partial agonism. Δ9-THC hits a ceiling at moderate CB1 occupancy; THCH can drive receptor activation further, meaning effects that THC produces only at high doses — anxiety, paranoia, perceptual disturbance — become pharmacologically accessible at lower doses of THCH.
The endocannabinoid system normally maintains tonic signalling through endogenous ligands. Exogenous full agonists override this regulation, producing acute effects followed by compensatory downregulation that underlies tolerance development.
The most critical gap is the absence of measured binding affinity data — without published Ki or EC50 values, THCH's potency relative to Δ9-THC and Δ9-THCP remains interpolated rather than quantified. Whether THCH exhibits biased agonism (favouring G-protein over β-arrestin signalling or vice versa) is unknown and would significantly affect its risk profile.
Subjective Effects[edit]
The THCH experience is presumed to mirror cannabis in character — sedation, euphoria, sensory alteration, appetite enhancement — but amplified by the compound's full CB1 agonism and higher potency. The dose-response curve is expected to be steeper and less forgiving than Δ9-THC's: the margin between a comfortable experience and overwhelming effects narrows because full agonism unlocks receptor activation levels that THC's partial agonism cannot reach. Set, setting, and dose are primary modulators, but the reduced margin for error makes context sensitivity more consequential than with conventional cannabis.
THCH sits pharmacologically between Δ9-THC and Δ9-THCP in the cannabinoid potency series. Relative to conventional cannabis, the qualitative experience is expected to be similar but quantitatively more intense — closer in risk profile to synthetic cannabinoids than to plant-derived THC, despite sharing the classical dibenzopyran structure. No controlled human data confirm these characterisations; they are derived from pharmacological class inference and limited adverse event reports.
Effect Grid
At common doses, the full cannabimimetic profile manifests clearly: cognitive euphoria, pronounced sedation, significant thought deceleration, and marked time alteration. Memory suppression is notable — short-term recall becomes unreliable. Humor enhancement and immersion enhancement are prominent. Focus suppression and analysis suppression impair complex cognitive tasks.
Physically, body high intensifies with bodily heaviness and muscle relaxation. Appetite enhancement is strong. Dry mouth is reliable. Motor control impairment becomes apparent in fine movements. Abnormal heartbeat (tachycardia) may be noticed.
Significant functional impairment precludes productive activity. Duration of commitment is unknown — no published data confirm how long the experience lasts at any dose.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Color alteration · Depth perception distortion · Perspective distortion · Proprioceptive distortion · Sound sensitivity · Spatial disorientation · Touch enhancement · Vestibular distortion · Visual haze / noise · Olfactory enhancement · Brightness alteration · Light sensitivity · Visual acuity suppression · Visual processing suppression
Sound sensitivity · Spatial disorientation · Touch enhancement · Vestibular distortion · Visual haze / noise · Olfactory enhancement · Brightness alteration · Light sensitivity · Visual acuity suppression · Visual processing suppression
Sedation · Appetite enhancement · Body scan awareness · Bodily heaviness · Dizziness · Heart rate perception changes · Laughter fits · Pain suppression · Physical fatigue · Temperature dysregulation · Body schema distortion · Nausea suppression · Spontaneous body sensations · Tactile euphoria · Constipation · Nausea · Sexual arousal enhancement · Vomiting · Restlessness · Bodily dissociation
Bodily heaviness · Dizziness · Heart rate perception changes · Laughter fits · Pain suppression · Physical fatigue · Body schema distortion · Nausea suppression · Spontaneous body sensations · Tactile euphoria · Constipation · Nausea · Sexual arousal enhancement · Vomiting · Restlessness · Bodily dissociation
Information processing suppression · Memory fragmentation · Aesthetic enhancement · Analysis suppression · Cognitive euphoria · Immersion enhancement · Humor enhancement · Cognitive fatigue · Conceptual thinking · Confusion · Increased nature relatedness · Introspection enhancement · Language suppression · Motivation suppression · Multiple thought streams · Novelty enhancement · Openness enhancement · Suggestibility enhancement · Thought connectivity · Thought deceleration · Thought disorganization · Thought loops · Creativity enhancement · Memory replays · Cognitive dysphoria · Cognitive flexibility · Compulsive redosing urge · Pattern recognition enhancement · Thought acceleration · Amnesia
Analysis suppression · Cognitive euphoria · Immersion enhancement · Humor enhancement · Cognitive fatigue · Conceptual thinking · Confusion · Increased nature relatedness · Introspection enhancement · Language suppression · Motivation suppression · Multiple thought streams · Novelty enhancement · Openness enhancement · Thought connectivity · Thought deceleration · Thought disorganization · Thought loops · Creativity enhancement · Memory replays · Cognitive dysphoria · Cognitive flexibility · Compulsive redosing urge · Pattern recognition enhancement · Thought acceleration · Amnesia
Emotional enhancement · Simultaneous emotions · Anxiety suppression · Dysphoria · Empathy enhancement · Irritability
Empathy enhancement · Irritability
Emotional susceptibility · Sociability enhancement · Automaticity · Compulsive behavior reduction · Craving · Sociability suppression · Social connection · Social disconnection · Trust enhancement · Flow state · Cognitive disconnection · Boundary dissolution
Craving · Sociability suppression · Social connection · Social disconnection · Trust enhancement · Flow state · Cognitive disconnection · Boundary dissolution
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Low
- Withdrawal
- Moderate
- Tolerance buildup
- moderate
- Tolerance reset
- 21 days
- Physical
- Low
- Psychological
- Moderate
- Compulsive redosing
- Low
- Dose escalation
- Moderate
- Cross-tol.
- Δ9-THC · Δ8-THC · THCP
Toxicity
No lethal dose, therapeutic index, or controlled toxicity data exist for THCH in any species. safety citation needed
Documented adverse events
Japanese post-market surveillance documented at least nine safety incidents attributed to THCH products before the compound's scheduling in August 2023.[5] Reported symptoms included nausea, vomiting, hallucinations, facial and upper-body numbness, uncontrolled eye movements, severe dizziness, and loss of consciousness — in one case, unconsciousness lasting two days requiring ICU admission.
The severity of these events exceeds the typical adverse profile of Δ9-THC and is consistent with a more potent CB1 full agonist. No deaths were documented.
Cardiovascular risk
CB1 full agonism is expected to produce elevated heart rate via sympathetic activation, with potential cardiovascular strain in predisposed individuals. THCH's higher potency implies these effects may emerge at lower doses than with Δ9-THC. No substance-specific data exist. inferred
Vaping-specific risks
THCH products are frequently sold as vaping liquids.[4][9] THCH acetate (THCH-O), identified in commercial e-cigarette products,[4] shares structural features with acetylated cannabinoids that may generate ketene — a highly reactive lung toxicant — when heated. This risk parallels concerns raised during the EVALI crisis. No THCH-O-specific studies have been published. inferred
Detection limitations
Standard drug screening immunoassays show reduced sensitivity for extended-chain THC homologs including THCH.[15] Confirmed identification requires laboratory mass spectrometry (LC-MS/MS[16] or LC-QTOF-MS[17]) — instrumentation unavailable in most clinical settings. Standard workplace or hospital drug tests may fail to detect THCH use.
Psychological risks
No controlled studies of THCH's psychological effects exist. Risk assessment is derived from CB1 full agonist pharmacology and Japanese adverse event reports.
Anxiety and paranoia are dose-dependent and consistent with the biphasic nature of CB1 agonism — calming at low occupancy, distressing at high occupancy. Full agonists reach higher occupancy than Δ9-THC, making anxiogenic effects more accessible at moderate doses.
Confusion and cognitive impairment follow from CB1 activation in hippocampal and prefrontal circuits, disrupting working memory and executive function.
Hallucinations were documented in Japanese adverse event reports.[5] Psychosis risk is elevated relative to Δ9-THC, particularly in individuals with personal or family history of psychotic disorders. inferred
Prolonged unconsciousness — documented in at least one Japanese case — represents a severe event not typically associated with Δ9-THC at any dose.
Tolerance and dependence
No published tolerance or dependence data specific to THCH exist. By CB1 agonist pharmacology, repeated use produces downregulation via β-arrestin2-mediated internalisation.[1] Cross-tolerance with Δ9-THC and other CB1 agonists is expected.
THCH's full agonist status and higher potency suggest tolerance may develop more rapidly than with Δ9-THC and that abuse liability is at least equivalent. Withdrawal is expected to resemble cannabis withdrawal syndrome: irritability, insomnia, appetite disturbance, anxiety, and restlessness. inferred
Drug interactions
No published drug interaction studies exist for THCH. All interactions are inferred from Δ9-THC pharmacology. inferred
CNS depressants (alcohol, benzodiazepines, opioids): Additive sedation and, with opioids, increased risk of respiratory depression. THCH's higher potency narrows the margin between recreational dose and dangerous synergistic depression.
CYP2C9 inhibitors (e.g., fluconazole, amiodarone): Expected to increase THCH plasma levels and prolong effects by reducing liver metabolism.
CYP3A4 inducers (e.g., rifampicin, carbamazepine, St John's Wort): Expected to reduce THCH plasma levels and shorten duration.
Stimulants and sympathomimetics: Additive heart rate elevation.
Product contamination: Documented mislabelling of THCH products[4] means consumers may be unknowingly exposed to additional unlabelled cannabinoids, making individual interaction risk unpredictable.
Contraindications
No substance-specific contraindication studies exist. The following are derived from CB1 full agonist pharmacology. inferred
Absolute:
- Personal or family history of psychotic disorders — CB1 full agonism elevates risk of acute psychosis and may accelerate onset of schizophrenia-spectrum conditions
- Pregnancy and breastfeeding — CB1 receptors are expressed in fetal brain tissue; exogenous agonism disrupts neurodevelopmental signalling
Relative:
- Heart conditions — CB1-mediated heart rate elevation; amplified by full agonist ceiling
- Active or past cannabis use disorder — higher potency and full agonism increase reinforcement and dependence risk
- Concurrent CNS depressant use — additive sedation risk
- Liver impairment — expected reduced clearance
- Adolescence — endocannabinoid system is still developing; exogenous agonism may disrupt brain maturation
Harm Reduction[edit]
Forms & Identification
THCH enters consumer markets primarily as vape cartridges and oil tinctures, often blended with other semi-synthetic cannabinoids. Forensic analyses have consistently found that product labels do not reliably reflect actual contents[4] — a product labelled "THCH" may contain different cannabinoids, different concentrations, or acetylated variants like THCH-O.
Third-party certificates of analysis (COAs) should be verified against the testing laboratory's own records rather than accepted at face value from the vendor. The semi-synthetic cannabinoid market has minimal quality infrastructure; independent testing is the only reliable safeguard.
Guidelines
- Start extremely low. No established human dosing data exist. Begin well below what would be a threshold dose for Δ9-THC and wait for full onset before considering redosing
- Test your product. Given documented mislabelling in the THCH market, test with available reagent kits and verify any COA independently
- Avoid combinations. Do not combine with alcohol, benzodiazepines, opioids, or other CNS depressants — THCH's full agonism narrows the margin for safe combination use
- Do not drive or operate machinery. Cognitive and motor impairment may be more severe and longer-lasting than expected from cannabis experience
- Have a sober companion. Prolonged unconsciousness has been documented — someone should be present who can monitor responsiveness and call for help
- Avoid vaping acetylated products. THCH-O (THCH acetate) may generate toxic byproducts when heated
Set & Setting
THCH's higher potency and full agonist pharmacology make environment and mental state more consequential than with conventional cannabis. A familiar, comfortable environment with a sober companion present is strongly recommended, particularly for first use.
The steeper dose-response curve means an uncomfortable experience can escalate rapidly. A trusted person who can provide reassurance or summon help reduces the risk of a manageable situation becoming dangerous.
Aftercare & integration. Post-experience recovery from THCH follows the pattern of other potent cannabinoids. Residual grogginess, mild confusion, or low mood may persist for 12–24 hours. Prioritise hydration, easily digestible food, and sleep. Avoid driving or demanding cognitive tasks until fully baseline.
If the experience was distressing — particularly if it involved prolonged confusion, dissociation, or panic — allow several days before re-evaluating. Persistent anxiety, depersonalisation, or intrusive thoughts beyond 48 hours warrant consultation with a healthcare provider familiar with substance-related concerns.
Recovery & Support
Individuals who find themselves using THCH compulsively or escalating doses to maintain effects should consider that full CB1 agonists carry a dependence profile at least equivalent to conventional cannabis. Cannabis use disorder is a recognised clinical condition with effective treatments including cognitive-behavioural therapy and motivational enhancement.
Support resources include SAMHSA's National Helpline (1-800-662-4357), Marijuana Anonymous, and local addiction services. Healthcare providers can assist with managing withdrawal symptoms — irritability, insomnia, and appetite disruption — which may be more pronounced after sustained use of high-potency CB1 agonists.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognising an emergency: Uncomfortable anxiety and mild confusion during THCH use do not require medical intervention. Seek immediate help if any of the following occur: loss of consciousness or inability to be roused, seizure, chest pain or irregular heartbeat, difficulty breathing, extreme confusion with inability to recognise surroundings or people, or self-harm behaviour.
Immediate steps:
- Call emergency services if the person is unresponsive, seizing, or showing signs of cardiovascular distress
- Place an unconscious but breathing person in the recovery position (on their side, head tilted back)
- Do not leave an unconscious person alone — monitor breathing continuously
- Do not induce vomiting if the product was ingested
- Keep the person warm and in a quiet environment if conscious but distressed
What to tell the dispatcher: State what was taken (THCH or the specific product name), how much, when, the route of administration, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
Tetrahydrocannabihexol occupies a rapidly evolving regulatory landscape. As a naturally occurring THC homolog that reached consumer markets via semi-synthetic production, THCH has prompted targeted scheduling in several jurisdictions while remaining unaddressed in others.[18]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| Japan | Designated substance | Both Δ8-THCH and Δ9-THCH designated July 25, 2023; effective August 4, 2023. Manufacturing, import, sale, and non-medical possession prohibited[5][19] |
| United Kingdom | Recommended Class B / Schedule 1 | ACMD recommended control of semi-synthetic THC homologs in May 2025; government accepted recommendation. Consultation on generic cannabinoid text amendment underway as of May 2026.[10] citation needed |
| Czech Republic | Banned | THCH included among 11 additional HHC derivatives banned in July 2024. citation needed |
| France | Banned | THCH banned among cannabinoids structurally related to THC. citation needed |
| European Union | Monitored (EUDA Early Warning System) | Δ8-THCH formally notified to the EU Early Warning System in May 2024.[20] Individual member state scheduling varies |
| United States | Not specifically scheduled; ambiguous | Not scheduled under the Controlled Substances Act. Federal Analogue Act may apply if consumed by humans. Hemp-derived THCH occupies a legal grey zone under the 2018 Farm Bill if total Δ9-THC content remains below 0.3%.[18] citation needed |
| Canada | Not confirmed | Likely captured by generic THC/cannabinoid provisions under the CDSA. citation needed |
| Australia | Not confirmed | Likely captured by generic cannabinoid provisions under the TGA scheduling framework. citation needed |
Analog and prodrug considerations
In the United States, THCH's structural and pharmacological similarity to Δ9-THC (a Schedule I substance) may trigger the Federal Analogue Act, which treats substantially similar compounds as controlled substances when intended for human consumption. THCH's demonstrated CB1 full agonism — pharmacologically more potent than Δ9-THC — strengthens the analogy argument. No DEA enforcement action specifically naming THCH has been identified as of May 2026.
THCH acetate (THCH-O), identified in commercial vaping products,[4] functions as a prodrug that converts to THCH in the body. Regulatory treatment of acetylated cannabinoid prodrugs varies by jurisdiction and may be captured by analog provisions or require separate scheduling.
references
- [1] ^abcdeJanssens LK, Van Uytfanghe K, Williams JB, Hering KW, Iula DM, Stove CP (2024) Investigation of the intrinsic cannabinoid activity of hemp-derived and semisynthetic cannabinoids with β-arrestin2 recruitment assays - and how this matters for the harm potential of seized drugs — Archives of Toxicology doi:10.1007/s00204-024-03769-4
- [2]
- [3] ^abcdefLinciano P, Citti C, Russo F, Tolomeo F, Laganà A, Capriotti AL, Luongo L, Iannotta M, Belardo C, Maione S, Forni F, Vandelli MA, Gigli G, Cannazza G (2020) Identification of a new cannabidiol n-hexyl homolog in a medicinal cannabis variety with an antinociceptive activity in mice: cannabidihexol — Scientific Reports doi:10.1038/s41598-020-79042-2
- [4] ^abcdefghWatanabe S, Murakami T, Muratsu S, Fujiwara H, Nakanishi T, Seto Y (2025) Discrepancies between the stated contents and analytical findings for electronic cigarette liquid products: Identification of the new cannabinoid, Δ9-tetrahydrocannabihexol acetate — Drug Testing and Analysis doi:10.1002/dta.3777
- [5]
- [6]