Δ-10-Tetrahydrocannabinol

Sources

2 strong · 15 moderate · 3 weak

Studies and references cited across this article, graded by evidence strength.

Values approved

32/32 (100%)

Data points an editor reviewed and accepted for publication.

Value Provenance

Dosing

oraltrace

Field	Published	AI Proposed	Confidence
Threshold	—	—	low
Low	—	—	low
Common	—	—	low
Strong	—	—	low
Heavy	—	—	low
Editorial	No published human dose-response data exist for oral Δ10-THC. Same rationale as inhaled route: CB1 antagonist profile makes Δ9-THC dose analogy fundamentally inapplicable. Oral bioavailability projected at 4–12% from Δ9-THC analogy but not measured. No tier values proposed; flagged for editorial review.
	ReasoningReasoning No published human dose-response data exist for oral Δ10-THC. Same rationale as inhaled route: CB1 antagonist profile makes Δ9-THC dose analogy fundamentally inapplicable. Oral bioavailability projected at 4–12% from Δ9-THC analogy but not measured. No tier values proposed; flagged for editorial review. Evidence basis: structural_analogy

inhaledtrace

Field	Published	AI Proposed	Confidence
Threshold	—	—	low
Low	—	—	low
Common	—	—	low
Strong	—	—	low
Heavy	—	—	low
Editorial	No published human dose-response data exist for inhaled Δ10-THC. Work-notes explicitly instruct: DO NOT propose dose ranges. The CB1 antagonist profile (Haghdoost 2023) means Δ9-THC dose analogy may be fundamentally inapplicable — 14-fold weaker CB1 binding and qualitatively different functional pharmacology (antagonist vs partial agonist) invalidate simple potency scaling. Mouse drug discrimination required 100 mg/kg for partial effect (Wiley 2024), which is not translatable to human doses. No tier values proposed; flagged for editorial review.
	ReasoningReasoning No published human dose-response data exist for inhaled Δ10-THC. Work-notes explicitly instruct: DO NOT propose dose ranges. The CB1 antagonist profile (Haghdoost 2023) means Δ9-THC dose analogy may be fundamentally inapplicable — 14-fold weaker CB1 binding and qualitatively different functional pharmacology (antagonist vs partial agonist) invalidate simple potency scaling. Mouse drug discrimination required 100 mg/kg for partial effect (Wiley 2024), which is not translatable to human doses. No tier values proposed; flagged for editorial review. Evidence basis: structural_analogy

Duration

inhaled

Field	Published	AI Proposed	Confidence
Onsettrace	1–5 minutes	1–5 minutes	low
Editorial	Structural analog inference from Δ9-THC inhaled pharmacokinetics. Rapid pulmonary absorption expected to produce first effects within 1–5 minutes. No Δ10-THC-specific onset data exist.
	ReasoningReasoning Structural analog inference from Δ9-THC inhaled pharmacokinetics. Rapid pulmonary absorption expected to produce first effects within 1–5 minutes. No Δ10-THC-specific onset data exist. Evidence basis: structural_analogy
Peaktrace	15–30 minutes	15–30 minutes	low
Editorial	Structural analog inference from Δ9-THC inhaled peak duration. Work-notes specify 15–30 min peak for inhaled ROA based on Δ9-THC analogy.
	ReasoningReasoning Structural analog inference from Δ9-THC inhaled peak duration. Work-notes specify 15–30 min peak for inhaled ROA based on Δ9-THC analogy. Evidence basis: structural_analogy
Totaltrace	2–4 hours	2–4 hours	low
Editorial	Structural analog inference from Δ9-THC inhaled total duration. Work-notes specify 2–4 hours total for inhaled ROA based on Δ9-THC analogy.
	ReasoningReasoning Structural analog inference from Δ9-THC inhaled total duration. Work-notes specify 2–4 hours total for inhaled ROA based on Δ9-THC analogy. Evidence basis: structural_analogy

oral

Field	Published	AI Proposed	Confidence
Onsettrace	30–90 minutes	30–90 minutes	low
Editorial	Structural analog inference from Δ9-THC oral pharmacokinetics. Slow GI absorption delays onset to 30–90 minutes. No Δ10-THC-specific oral onset data exist.
	ReasoningReasoning Structural analog inference from Δ9-THC oral pharmacokinetics. Slow GI absorption delays onset to 30–90 minutes. No Δ10-THC-specific oral onset data exist. Evidence basis: structural_analogy
Peaktrace	2–4 hours	2–4 hours	low
Editorial	Structural analog inference from Δ9-THC oral peak duration. Work-notes specify 2–4 hours peak for oral ROA based on Δ9-THC analogy.
	ReasoningReasoning Structural analog inference from Δ9-THC oral peak duration. Work-notes specify 2–4 hours peak for oral ROA based on Δ9-THC analogy. Evidence basis: structural_analogy
Totaltrace	4–8 hours	4–8 hours	low
Editorial	Structural analog inference from Δ9-THC oral total duration. Work-notes specify 4–8 hours total for oral ROA based on Δ9-THC analogy.
	ReasoningReasoning Structural analog inference from Δ9-THC oral total duration. Work-notes specify 4–8 hours total for oral ROA based on Δ9-THC analogy. Evidence basis: structural_analogy

Safety

Toxicity Profiletrace

Field	Published	AI Proposed	Confidence
Acute	low	low	low
Chronic	—	—	low
Organs Affected	cardiovascular, central nervous system, pulmonary	cardiovascular, central nervous system, pulmonary	low
Editorial	Work-notes specify acute toxicity 'low' based on pooled poison center data (Burgess 2024) that is 98.1% Δ8-THC — Δ10-THC fraction not disaggregated. No LD50, no lethal cases, no Δ10-specific toxicity studies. Organs affected (cardiovascular, CNS, pulmonary) are from pooled adverse event data and vaping route inference. All values are class-extrapolated from predominantly Δ8-THC data; evidence discount applied by maintaining 'low' rather than upgrading despite serious outcome rates in pooled data.
	ReasoningReasoning Work-notes specify acute toxicity 'low' based on pooled poison center data (Burgess 2024) that is 98.1% Δ8-THC — Δ10-THC fraction not disaggregated. No LD50, no lethal cases, no Δ10-specific toxicity studies. Organs affected (cardiovascular, CNS, pulmonary) are from pooled adverse event data and vaping route inference. All values are class-extrapolated from predominantly Δ8-THC data; evidence discount applied by maintaining 'low' rather than upgrading despite serious outcome rates in pooled data. Evidence basis: structural_analogy

Dependence Profiletrace

Field	Published	AI Proposed	Confidence
Physical	low	low	low
Psychological	low	low	low
Compulsive Redosing	low	low	low
Dose Escalation	low	low	low
Editorial	No Δ10-THC-specific dependence data exist. Physical and psychological dependence rated 'low' by class analogy to Δ8-THC (Vanegas 2022 mouse dependence data) and cannabis class (Heal 2024). Compulsive redosing rated 'low' per work-notes inference that mild effects reduce compulsive potential. CB1 antagonist profile fundamentally complicates standard cannabinoid dependence prediction.
	ReasoningReasoning No Δ10-THC-specific dependence data exist. Physical and psychological dependence rated 'low' by class analogy to Δ8-THC (Vanegas 2022 mouse dependence data) and cannabis class (Heal 2024). Compulsive redosing rated 'low' per work-notes inference that mild effects reduce compulsive potential. CB1 antagonist profile fundamentally complicates standard cannabinoid dependence prediction. Evidence basis: structural_analogy

Withdrawal Profiletrace

Field	Published	AI Proposed	Confidence
Severity	mild	mild	low
Symptoms	Irritability, Sleep disruption, Appetite changes, Craving	Irritability, Sleep disruption, Appetite changes, Craving	low
Fatal	No	No	low
Medical Supervision	Not required	Not required	low
Editorial	No Δ10-THC-specific withdrawal data exist. Withdrawal parameters inferred from cannabis class data (Heal 2024): 2–6 day syndrome with irritability, sleep disruption, appetite changes, and craving. Whether Δ10-THC — a CB1 antagonist in vitro — would produce the same CB1-downregulation-mediated withdrawal as CB1 agonists is an open question. Proposed as class-level inference with low confidence.
	ReasoningReasoning No Δ10-THC-specific withdrawal data exist. Withdrawal parameters inferred from cannabis class data (Heal 2024): 2–6 day syndrome with irritability, sleep disruption, appetite changes, and craving. Whether Δ10-THC — a CB1 antagonist in vitro — would produce the same CB1-downregulation-mediated withdrawal as CB1 agonists is an open question. Proposed as class-level inference with low confidence. Evidence basis: structural_analogy

Tolerance Profiletrace

Field	Published	AI Proposed	Confidence
Buildup	moderate	moderate	low
Half-life	5 days	5 days	low
Full Reset	21 days	21 days	low
Cross-tolerances	Δ9-THC, Δ8-THC, other CB1 receptor agonists	Δ9-THC, Δ8-THC, other CB1 receptor agonists	low
Editorial	No Δ10-THC-specific tolerance data exist. All values inferred from Δ8-THC (Vanegas 2022 demonstrated CB1 downregulation and cross-tolerance in mice) and Δ9-THC class pharmacology. Work-notes flag that the standard CB1 downregulation mechanism may not apply to Δ10-THC given its antagonist profile. Cross-tolerances listed with uncertainty caveat.
	ReasoningReasoning No Δ10-THC-specific tolerance data exist. All values inferred from Δ8-THC (Vanegas 2022 demonstrated CB1 downregulation and cross-tolerance in mice) and Δ9-THC class pharmacology. Work-notes flag that the standard CB1 downregulation mechanism may not apply to Δ10-THC given its antagonist profile. Cross-tolerances listed with uncertainty caveat. Evidence basis: structural_analogy

Effects & Profile

Contraindications

Field	Published	AI Proposed	Confidence
pregnancy breastfeeding Pregnancy and breastfeedingtrace	absolute	absolute	low
Editorial	Class-level cannabinoid contraindication. No Δ10-specific data; inferred from Δ9-THC class pharmacology.
	ReasoningReasoning Class-level cannabinoid contraindication. No Δ10-specific data; inferred from Δ9-THC class pharmacology.
age Pediatric exposure risktrace	absolute	absolute	medium
Editorial	Burgess et al. 2024 pooled poison center data documents disproportionate pediatric exposure and serious outcomes. Data is predominantly Δ8-THC but Δ10-THC products share the same edible formats and packaging.
	ReasoningReasoning Burgess et al. 2024 pooled poison center data documents disproportionate pediatric exposure and serious outcomes. Data is predominantly Δ8-THC but Δ10-THC products share the same edible formats and packaging.
cardiovascular Pre-existing cardiovascular diseasetrace	relative	relative	low
Editorial	Pooled poison center tachycardia rate (23%) from Burgess 2024. Class-extrapolated from predominantly Δ8-THC data; no Δ10-specific cardiovascular studies.
	ReasoningReasoning Pooled poison center tachycardia rate (23%) from Burgess 2024. Class-extrapolated from predominantly Δ8-THC data; no Δ10-specific cardiovascular studies.
metabolic Concurrent warfarin or anticoagulant therapytrace	relative	relative	low
Editorial	CYP2C9 competition inferred from Δ9-THC class pharmacology. Cannabinoid-anticoagulant interactions resulting in elevated INR have been documented for Δ9-THC-containing products; the same risk is presumed but unverified for Δ10-THC.
	ReasoningReasoning CYP2C9 competition inferred from Δ9-THC class pharmacology. Cannabinoid-anticoagulant interactions resulting in elevated INR have been documented for Δ9-THC-containing products; the same risk is presumed but unverified for Δ10-THC.
psychiatric Depression, anxiety disorders, or suicidal ideation historytrace	relative	relative	low
Editorial	Theoretical risk based on CB1 antagonist class parallel with rimonabant (Haghdoost 2023 demonstrated CB1 antagonism). No substance-specific psychiatric data exist; this is a pharmacological class flag, not an observed effect.
	ReasoningReasoning Theoretical risk based on CB1 antagonist class parallel with rimonabant (Haghdoost 2023 demonstrated CB1 antagonism). No substance-specific psychiatric data exist; this is a pharmacological class flag, not an observed effect.
other Operating vehicles or machinerytrace	relative	relative	low
Editorial	Class-level cannabinoid psychomotor impairment risk. No Δ10-specific driving or impairment data. Drug test cross-reactivity documented by Wolf et al. 2023.
	ReasoningReasoning Class-level cannabinoid psychomotor impairment risk. No Δ10-specific driving or impairment data. Drug test cross-reactivity documented by Wolf et al. 2023.

Timeline Phases

inhaled

Field	Published	AI Proposed	Confidence
Onsettrace	60–300 sec(i=0.30)	60–300 sec(i=0.30)	low
Editorial	All timeline data inferred from Δ9-THC structural analogy. No pharmacokinetic or duration data have been published for Δ10-THC. The CB1 antagonist profile may alter the temporal dynamics relative to Δ9-THC, but in the absence of data, class analogy is the only available framework. Work-notes specify onset 1–5 min, peak 15–30 min, total 2–4 hours for inhaled ROA based on Δ9-THC analogy.
	ReasoningReasoning All timeline data inferred from Δ9-THC structural analogy. No pharmacokinetic or duration data have been published for Δ10-THC. The CB1 antagonist profile may alter the temporal dynamics relative to Δ9-THC, but in the absence of data, class analogy is the only available framework. Work-notes specify onset 1–5 min, peak 15–30 min, total 2–4 hours for inhaled ROA based on Δ9-THC analogy. Evidence basis: structural_analogy
Peaktrace	900–1800 sec(i=1.00)	900–1800 sec(i=1.00)	low
Editorial	All timeline data inferred from Δ9-THC structural analogy. No pharmacokinetic or duration data have been published for Δ10-THC. The CB1 antagonist profile may alter the temporal dynamics relative to Δ9-THC, but in the absence of data, class analogy is the only available framework. Work-notes specify onset 1–5 min, peak 15–30 min, total 2–4 hours for inhaled ROA based on Δ9-THC analogy.
	ReasoningReasoning All timeline data inferred from Δ9-THC structural analogy. No pharmacokinetic or duration data have been published for Δ10-THC. The CB1 antagonist profile may alter the temporal dynamics relative to Δ9-THC, but in the absence of data, class analogy is the only available framework. Work-notes specify onset 1–5 min, peak 15–30 min, total 2–4 hours for inhaled ROA based on Δ9-THC analogy. Evidence basis: structural_analogy
Resolutiontrace	3600–10800 sec(i=0.40)	3600–10800 sec(i=0.40)	low
Editorial	All timeline data inferred from Δ9-THC structural analogy. No pharmacokinetic or duration data have been published for Δ10-THC. The CB1 antagonist profile may alter the temporal dynamics relative to Δ9-THC, but in the absence of data, class analogy is the only available framework. Work-notes specify onset 1–5 min, peak 15–30 min, total 2–4 hours for inhaled ROA based on Δ9-THC analogy.
	ReasoningReasoning All timeline data inferred from Δ9-THC structural analogy. No pharmacokinetic or duration data have been published for Δ10-THC. The CB1 antagonist profile may alter the temporal dynamics relative to Δ9-THC, but in the absence of data, class analogy is the only available framework. Work-notes specify onset 1–5 min, peak 15–30 min, total 2–4 hours for inhaled ROA based on Δ9-THC analogy. Evidence basis: structural_analogy
Afterglowtrace	3600–10800 sec(i=0.15)	3600–10800 sec(i=0.15)	low
Editorial	All timeline data inferred from Δ9-THC structural analogy. No pharmacokinetic or duration data have been published for Δ10-THC. The CB1 antagonist profile may alter the temporal dynamics relative to Δ9-THC, but in the absence of data, class analogy is the only available framework. Work-notes specify onset 1–5 min, peak 15–30 min, total 2–4 hours for inhaled ROA based on Δ9-THC analogy.
	ReasoningReasoning All timeline data inferred from Δ9-THC structural analogy. No pharmacokinetic or duration data have been published for Δ10-THC. The CB1 antagonist profile may alter the temporal dynamics relative to Δ9-THC, but in the absence of data, class analogy is the only available framework. Work-notes specify onset 1–5 min, peak 15–30 min, total 2–4 hours for inhaled ROA based on Δ9-THC analogy. Evidence basis: structural_analogy

oral

Field	Published	AI Proposed	Confidence
Onsettrace	1800–5400 sec(i=0.20)	1800–5400 sec(i=0.20)	low
Editorial	All timeline data inferred from Δ9-THC oral pharmacokinetics. No Δ10-THC-specific duration or PK data exist. Work-notes specify onset 30–90 min, peak 2–4 hours, total 4–8 hours for oral ROA based on Δ9-THC structural analogy. Oral bioavailability projected at 4–12% from Δ9-THC class data.
	ReasoningReasoning All timeline data inferred from Δ9-THC oral pharmacokinetics. No Δ10-THC-specific duration or PK data exist. Work-notes specify onset 30–90 min, peak 2–4 hours, total 4–8 hours for oral ROA based on Δ9-THC structural analogy. Oral bioavailability projected at 4–12% from Δ9-THC class data. Evidence basis: structural_analogy
Come uptrace	3600–7200 sec(i=0.50)	3600–7200 sec(i=0.50)	low
Editorial	All timeline data inferred from Δ9-THC oral pharmacokinetics. No Δ10-THC-specific duration or PK data exist. Work-notes specify onset 30–90 min, peak 2–4 hours, total 4–8 hours for oral ROA based on Δ9-THC structural analogy. Oral bioavailability projected at 4–12% from Δ9-THC class data.
	ReasoningReasoning All timeline data inferred from Δ9-THC oral pharmacokinetics. No Δ10-THC-specific duration or PK data exist. Work-notes specify onset 30–90 min, peak 2–4 hours, total 4–8 hours for oral ROA based on Δ9-THC structural analogy. Oral bioavailability projected at 4–12% from Δ9-THC class data. Evidence basis: structural_analogy
Peaktrace	7200–14400 sec(i=1.00)	7200–14400 sec(i=1.00)	low
Editorial	All timeline data inferred from Δ9-THC oral pharmacokinetics. No Δ10-THC-specific duration or PK data exist. Work-notes specify onset 30–90 min, peak 2–4 hours, total 4–8 hours for oral ROA based on Δ9-THC structural analogy. Oral bioavailability projected at 4–12% from Δ9-THC class data.
	ReasoningReasoning All timeline data inferred from Δ9-THC oral pharmacokinetics. No Δ10-THC-specific duration or PK data exist. Work-notes specify onset 30–90 min, peak 2–4 hours, total 4–8 hours for oral ROA based on Δ9-THC structural analogy. Oral bioavailability projected at 4–12% from Δ9-THC class data. Evidence basis: structural_analogy
Resolutiontrace	7200–14400 sec(i=0.40)	7200–14400 sec(i=0.40)	low
Editorial	All timeline data inferred from Δ9-THC oral pharmacokinetics. No Δ10-THC-specific duration or PK data exist. Work-notes specify onset 30–90 min, peak 2–4 hours, total 4–8 hours for oral ROA based on Δ9-THC structural analogy. Oral bioavailability projected at 4–12% from Δ9-THC class data.
	ReasoningReasoning All timeline data inferred from Δ9-THC oral pharmacokinetics. No Δ10-THC-specific duration or PK data exist. Work-notes specify onset 30–90 min, peak 2–4 hours, total 4–8 hours for oral ROA based on Δ9-THC structural analogy. Oral bioavailability projected at 4–12% from Δ9-THC class data. Evidence basis: structural_analogy
Afterglowtrace	7200–14400 sec(i=0.10)	7200–14400 sec(i=0.10)	low
Editorial	All timeline data inferred from Δ9-THC oral pharmacokinetics. No Δ10-THC-specific duration or PK data exist. Work-notes specify onset 30–90 min, peak 2–4 hours, total 4–8 hours for oral ROA based on Δ9-THC structural analogy. Oral bioavailability projected at 4–12% from Δ9-THC class data.
	ReasoningReasoning All timeline data inferred from Δ9-THC oral pharmacokinetics. No Δ10-THC-specific duration or PK data exist. Work-notes specify onset 30–90 min, peak 2–4 hours, total 4–8 hours for oral ROA based on Δ9-THC structural analogy. Oral bioavailability projected at 4–12% from Δ9-THC class data. Evidence basis: structural_analogy

Dose Tier Summaries

thresholdtrace

low

No published human dose-response data exist for Δ-10-THC, and no threshold dose has been established for any route of administration. The compound's CB1 antagonist profile in vitro means that the threshold for classical cannabinoid effects — if they occur at all through this mechanism — cannot be predicted from Δ9-THC or Δ8-THC dose data. Users of commercial Δ10-THC products may perceive threshold effects at doses below those required for other THC isomers, but whether these reflect genuine Δ10-THC pharmacology, placebo expectancy, or co-formulated cannabinoids in blended products is unknown. Any perceived threshold effect should be treated as uncharacterized.

Editorial

No published human dose-response data exist. Work-notes specify insufficient data to characterize. CB1 antagonist profile makes Δ9-THC dose analogy fundamentally inapplicable per Phase 1 notes.

Reasoning

No published human dose-response data exist. Work-notes specify insufficient data to characterize. CB1 antagonist profile makes Δ9-THC dose analogy fundamentally inapplicable per Phase 1 notes.

Evidence basis: structural_analogy

lighttrace

low

No controlled data define a light dose range for Δ-10-THC. Anecdotal user reports describe mild stimulating euphoria at sub-Δ9-THC-equivalent doses, with a clear-headed quality and reduced anxiety compared to conventional THC products. Physical effects at this level are reported as minimal — slight dry mouth and mild body awareness without pronounced sedation or heaviness. These reports cannot be attributed to Δ10-THC specifically, as most commercial products contain blends of multiple cannabinoids. The energizing, sativa-like character described by users is consistent with the compound's weak or absent CB1 agonism but remains unverified.

Editorial

Anecdotal user reports only; no controlled human data. Work-notes flag that products frequently blend Δ10-THC with other cannabinoids, confounding dose attribution.

Reasoning

Anecdotal user reports only; no controlled human data. Work-notes flag that products frequently blend Δ10-THC with other cannabinoids, confounding dose attribution.

Evidence basis: structural_analogy

commontrace

low

No established common dose range exists for Δ-10-THC. Users report clear-headed, mild cannabinoid effects at what they consider standard doses, including cognitive euphoria, gentle stimulation, and subtle time alteration. The experience is consistently described as milder than both Δ9-THC and Δ8-THC, with less cognitive impairment and reduced paranoia. Physical effects at reported common doses include dry mouth, mild appetite changes, and occasional tachycardia. Sedation is described as less pronounced than with other THC isomers. No dosing standards have been established, and product potency varies widely due to unregulated manufacturing.

Editorial

No controlled human dose data. Anecdotal reports provide qualitative texture only. Work-notes note no dosing standards established. Product variability makes community dose estimates unreliable.

Reasoning

No controlled human dose data. Anecdotal reports provide qualitative texture only. Work-notes note no dosing standards established. Product variability makes community dose estimates unreliable.

Evidence basis: structural_analogy

strongtrace

low

No data define a strong dose range for Δ-10-THC. Higher doses may produce more pronounced cannabinoid-like effects — increased euphoria, more noticeable time alteration, deeper cognitive shifts, and greater motor control impairment — but the dose-response relationship is entirely uncharacterized. The mechanism by which stronger effects would emerge is unclear given the compound's CB1 antagonist profile. Physical effects at higher doses may include more pronounced tachycardia, deeper sedation, and greater appetite disruption. The 23% tachycardia rate in pooled poison center data (predominantly Δ8-THC) suggests cardiovascular effects become clinically relevant at higher doses across this class.

Editorial

No controlled human data at any dose level. Work-notes flag mechanism unclear given CB1 antagonism. Tachycardia rate from Burgess 2024 pooled data provides the only quantitative safety signal.

Reasoning

No controlled human data at any dose level. Work-notes flag mechanism unclear given CB1 antagonism. Tachycardia rate from Burgess 2024 pooled data provides the only quantitative safety signal.

Evidence basis: structural_analogy

heavytrace

low

No human data define a heavy dose range for Δ-10-THC. Mouse drug discrimination studies required 100 mg/kg for even partial Δ9-THC-like responding — an extreme dose that also significantly depressed response rates, suggesting non-specific behavioral suppression rather than clean pharmacological effect. Translation of this dose to humans is not valid. Heavy doses carry elevated risk of CNS depression (25% in pooled adverse events), pronounced tachycardia, agitation, and serious medical outcomes (38.4% in pooled data). Product contamination risk compounds dose-dependent toxicity, as uncharacterized isomerization byproducts may have independent dose-response profiles. This is uncharted pharmacological territory.

Editorial

Mouse data (Wiley 2024) at 100 mg/kg is the only quantitative dose reference but is not translatable to humans. Work-notes explicitly flag extreme doses required. Adverse event rates from Burgess 2024 pooled data.

Reasoning

Evidence basis: structural_analogy

History

current version

published Oct 2, 2026system—

versions

2 total · since previous: +0 / −0 citations

publication ledger

publish Oct 2, 2026 · by agent-psx

backfill Jun 4, 2026

Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.

full version history suggest a correction contact@psychedex.org

Sources

2 strong · 15 moderate · 3 weak

[1]
moderate
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moderate
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weak
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Burgess A, Hays HL, Badeti J, Spiller HA, Rine NI, Gaw CE, Ding K, Smith GA · 2024 · Clinical Toxicology
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Delta-8 Tetrahydrocannabinol Product Impurities
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moderate
Delta-8 tetrahydrocannabinol: a scoping review and commentary
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weak
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linkno claims checked
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strong
Chemistry and Pharmacology of Delta-8-Tetrahydrocannabinol
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moderate
Mechanisms of Action and Pharmacokinetics of Cannabis
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moderate
The cross-reactivity of cannabinoid analogs (delta-8-THC, delta-10-THC and CBD), their metabolites and chiral carboxy HHC metabolites in urine of six commercially available homogeneous immunoassays
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moderate
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moderate
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Comprehensive cannabinoid profiling of acid-treated CBD samples and Δ8-THC-infused edibles
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[20]
moderate
Closing the Loophole on Hemp-Derived Cannabis Products
Harlow AF, Leventhal AM, Barrington-Trimis JL · 2022 · JAMA
doi.org/10.1001/jama.2022.20620 pubmed 36331491no claims checked

Claim Verification

No claim verification has run for this version.

Coverage & Gaps

No auxiliary datasets (effect links, interactions, receptor bindings, detection windows) recorded for this substance.

Δ-10-Tetrahydrocannabinol

Value Provenance

Dosing

oraltrace →

inhaledtrace →

Duration

inhaled

oral

Safety

Toxicity Profiletrace →

Dependence Profiletrace →

Withdrawal Profiletrace →

Tolerance Profiletrace →

Effects & Profile

Contraindications

Timeline Phases

inhaled

oral

Dose Tier Summaries

History

Sources

Claim Verification

Coverage & Gaps

oraltrace

inhaledtrace

Toxicity Profiletrace

Dependence Profiletrace

Withdrawal Profiletrace

Tolerance Profiletrace