Tetrahydrocannabiphorol

Sources

11 strong · 14 moderate

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

Values approved

185/185 (100%)

Data points an editor reviewed and accepted for publication.

Value Provenance

Dosing

oraltrace

Field	Published	AI Proposed	Confidence
Threshold	0.15 mg	0.15 mg	low
Low	0.15–0.5 mg	0.15–0.5 mg	low
Common	0.5–1.5 mg	0.5–1.5 mg	low
Strong	1.5–3 mg	1.5–3 mg	low
Heavy	5+ mg	5+ mg	low
Editorial	No controlled THCP oral dose data exist. Values derived by structural analog inference from Δ9-THC oral dose ranges (threshold ~2.5 mg, light 2.5–5 mg, common 5–15 mg, strong 15–30 mg, heavy 30+ mg) divided by ~33x CB1 potency ratio, with ranges widened to account for variable oral bioavailability and first-pass metabolism uncertainty. An unverified web report mentions psychotic symptoms at 8 mg oral in a regular cannabis user, which would place that dose well above the 'heavy' threshold proposed here. All values are speculative and flagged for editorial review. SAFETY_DATA_UNVERIFIED.
	ReasoningReasoning No controlled THCP oral dose data exist. Values derived by structural analog inference from Δ9-THC oral dose ranges (threshold ~2.5 mg, light 2.5–5 mg, common 5–15 mg, strong 15–30 mg, heavy 30+ mg) divided by ~33x CB1 potency ratio, with ranges widened to account for variable oral bioavailability and first-pass metabolism uncertainty. An unverified web report mentions psychotic symptoms at 8 mg oral in a regular cannabis user, which would place that dose well above the 'heavy' threshold proposed here. All values are speculative and flagged for editorial review. SAFETY_DATA_UNVERIFIED. Evidence basis: structural_analogy

vaporizedtrace

Field	Published	AI Proposed	Confidence
Threshold	0.1 mg	0.1 mg	low
Low	0.1–0.3 mg	0.1–0.3 mg	low
Common	0.3–0.75 mg	0.3–0.75 mg	low
Strong	0.75–1.5 mg	0.75–1.5 mg	low
Heavy	2+ mg	2+ mg	low
Editorial	No controlled THCP dose-response data exist. Values derived by structural analog inference from Δ9-THC vaporized dose ranges (threshold ~2–3 mg, light 3–5 mg, common 5–10 mg, strong 10–25 mg, heavy 25+ mg) divided by the ~33x CB1 potency ratio, with ranges widened conservatively to account for uncertainty. Research output cross-reference notes linear extrapolation would suggest threshold ~0.05–0.15 mg. All values are speculative and flagged for editorial review. SAFETY_DATA_UNVERIFIED.
	ReasoningReasoning No controlled THCP dose-response data exist. Values derived by structural analog inference from Δ9-THC vaporized dose ranges (threshold ~2–3 mg, light 3–5 mg, common 5–10 mg, strong 10–25 mg, heavy 25+ mg) divided by the ~33x CB1 potency ratio, with ranges widened conservatively to account for uncertainty. Research output cross-reference notes linear extrapolation would suggest threshold ~0.05–0.15 mg. All values are speculative and flagged for editorial review. SAFETY_DATA_UNVERIFIED. Evidence basis: structural_analogy

Duration

vaporized

Field	Published	AI Proposed	Confidence
Onsettrace	1–5 minutes	1–5 minutes	low
Editorial	Inferred from Δ9-THC smoked/vaporized onset (1–5 min). THCP's higher CB1 affinity may produce perceptible effects slightly faster, but onset kinetics are primarily absorption-dependent rather than affinity-dependent.
	ReasoningReasoning Inferred from Δ9-THC smoked/vaporized onset (1–5 min). THCP's higher CB1 affinity may produce perceptible effects slightly faster, but onset kinetics are primarily absorption-dependent rather than affinity-dependent. Evidence basis: structural_analogy
Come uptrace	5–15 minutes	5–15 minutes	low
Editorial	Inferred from Δ9-THC vaporized come-up (~5–15 min). Full agonism may steepen the come-up curve but total phase duration likely similar.
	ReasoningReasoning Inferred from Δ9-THC vaporized come-up (~5–15 min). Full agonism may steepen the come-up curve but total phase duration likely similar. Evidence basis: structural_analogy
Peaktrace	30–90 minutes	30–90 minutes	low
Editorial	Inferred from Δ9-THC vaporized peak (~20–40 min), widened to 30–90 min to account for THCP's higher receptor affinity and consumer reports suggesting longer duration than THC.
	ReasoningReasoning Inferred from Δ9-THC vaporized peak (~20–40 min), widened to 30–90 min to account for THCP's higher receptor affinity and consumer reports suggesting longer duration than THC. Evidence basis: structural_analogy
Offsettrace	1–3 hours	1–3 hours	low
Editorial	Inferred from Δ9-THC class. Higher receptor affinity and lipophilicity predict prolonged offset relative to THC.
	ReasoningReasoning Inferred from Δ9-THC class. Higher receptor affinity and lipophilicity predict prolonged offset relative to THC. Evidence basis: structural_analogy
Totaltrace	2–6 hours	2–6 hours	low
Editorial	Inferred from Δ9-THC vaporized total (2–4 h), extended to 2–6 h based on consumer reports suggesting THCP effects are more prolonged than THC and higher receptor affinity predicting slower dissociation.
	ReasoningReasoning Inferred from Δ9-THC vaporized total (2–4 h), extended to 2–6 h based on consumer reports suggesting THCP effects are more prolonged than THC and higher receptor affinity predicting slower dissociation. Evidence basis: structural_analogy
After effectstrace	2–12 hours	2–12 hours	low
Editorial	Inferred from Δ9-THC class aftereffects. Greater lipophilicity and tissue sequestration predict prolonged residual effects.
	ReasoningReasoning Inferred from Δ9-THC class aftereffects. Greater lipophilicity and tissue sequestration predict prolonged residual effects. Evidence basis: structural_analogy

oral

Field	Published	AI Proposed	Confidence
Onsettrace	30–90 minutes	30–90 minutes	low
Editorial	Inferred from Δ9-THC oral onset (30–90 min). Oral absorption kinetics are primarily GI-dependent rather than receptor-affinity-dependent.
	ReasoningReasoning Inferred from Δ9-THC oral onset (30–90 min). Oral absorption kinetics are primarily GI-dependent rather than receptor-affinity-dependent. Evidence basis: structural_analogy
Come uptrace	30–60 minutes	30–60 minutes	low
Editorial	Inferred from Δ9-THC oral come-up. First-pass metabolism produces 11-OH metabolite (by analogy) which may contribute to gradual intensification.
	ReasoningReasoning Inferred from Δ9-THC oral come-up. First-pass metabolism produces 11-OH metabolite (by analogy) which may contribute to gradual intensification. Evidence basis: structural_analogy
Peaktrace	1–3 hours	1–3 hours	low
Editorial	Inferred from Δ9-THC oral peak (1–3 h). Timeline notes suggest oral peak may be more intense than vaporized due to first-pass 11-OH metabolite formation.
	ReasoningReasoning Inferred from Δ9-THC oral peak (1–3 h). Timeline notes suggest oral peak may be more intense than vaporized due to first-pass 11-OH metabolite formation. Evidence basis: structural_analogy
Offsettrace	2–4 hours	2–4 hours	low
Editorial	Inferred from Δ9-THC oral offset. Extended relative to vaporized route due to sustained absorption and metabolite activity.
	ReasoningReasoning Inferred from Δ9-THC oral offset. Extended relative to vaporized route due to sustained absorption and metabolite activity. Evidence basis: structural_analogy
Totaltrace	4–10 hours	4–10 hours	low
Editorial	Inferred from Δ9-THC oral total (4–8 h), extended to 4–10 h based on THCP's higher receptor affinity and greater lipophilicity predicting prolonged effect duration.
	ReasoningReasoning Inferred from Δ9-THC oral total (4–8 h), extended to 4–10 h based on THCP's higher receptor affinity and greater lipophilicity predicting prolonged effect duration. Evidence basis: structural_analogy
After effectstrace	4–24 hours	4–24 hours	low
Editorial	Inferred from Δ9-THC oral aftereffects. Greater lipophilicity and tissue accumulation predict prolonged residual sedation and cognitive haze. Next-day effects possible.
	ReasoningReasoning Inferred from Δ9-THC oral aftereffects. Greater lipophilicity and tissue accumulation predict prolonged residual sedation and cognitive haze. Next-day effects possible. Evidence basis: structural_analogy

Safety

Toxicity Profiletrace

Field	Published	AI Proposed	Confidence
Acute	moderate	moderate	low
Chronic	moderate	moderate	low
Organs Affected	neuropsychiatric, cardiovascular	neuropsychiatric, cardiovascular	low
Editorial	All toxicity assessment is class-level inference from synthetic cannabinoid literature and THC pharmacology. No THCP-specific toxicity data exist. THC itself has extremely high therapeutic index, but THCP's full agonism removes the efficacy ceiling that limits THC's adverse effects, warranting 'moderate' acute and chronic ratings. Evidence discount applied: structural analogy from Δ9-THC and synthetic cannabinoid class (CP55940, JWH series).
	ReasoningReasoning All toxicity assessment is class-level inference from synthetic cannabinoid literature and THC pharmacology. No THCP-specific toxicity data exist. THC itself has extremely high therapeutic index, but THCP's full agonism removes the efficacy ceiling that limits THC's adverse effects, warranting 'moderate' acute and chronic ratings. Evidence discount applied: structural analogy from Δ9-THC and synthetic cannabinoid class (CP55940, JWH series). Evidence basis: structural_analogy

Dependence Profiletrace

Field	Published	AI Proposed	Confidence
Physical	moderate	moderate	low
Psychological	moderate	moderate	low
Compulsive Redosing	moderate	moderate	low
Dose Escalation	moderate	moderate	low
Editorial	All values inferred from cannabis use disorder epidemiology and synthetic cannabinoid class pharmacology. No THCP-specific dependence studies exist. Work-notes specify 'moderate-high' psychological dependence; schema enum lacks this granularity so 'moderate' is used as conservative mapping. Reference compounds: Δ9-THC (CUD data) and synthetic CB1 full agonists (potency-dependence relationship).
	ReasoningReasoning All values inferred from cannabis use disorder epidemiology and synthetic cannabinoid class pharmacology. No THCP-specific dependence studies exist. Work-notes specify 'moderate-high' psychological dependence; schema enum lacks this granularity so 'moderate' is used as conservative mapping. Reference compounds: Δ9-THC (CUD data) and synthetic CB1 full agonists (potency-dependence relationship). Evidence basis: structural_analogy

Withdrawal Profiletrace

Field	Published	AI Proposed	Confidence
Severity	moderate	moderate	low
Symptoms	irritability, anxiety, sleep disturbance, decreased appetite, restlessness, dysphoric mood	irritability, anxiety, sleep disturbance, decreased appetite, restlessness, dysphoric mood	low
Fatal	No	No	low
Medical Supervision	Not required	Not required	low
Editorial	Inferred from cannabis withdrawal syndrome (CWS) characterization. Symptoms begin 1–3 days after cessation, peak days 2–6, resolve within 2–4 weeks. No THCP-specific withdrawal data. Work-notes specify mild-moderate severity; 'moderate' chosen as conservative upper bound given full agonism may produce more severe withdrawal than partial-agonist THC.
	ReasoningReasoning Inferred from cannabis withdrawal syndrome (CWS) characterization. Symptoms begin 1–3 days after cessation, peak days 2–6, resolve within 2–4 weeks. No THCP-specific withdrawal data. Work-notes specify mild-moderate severity; 'moderate' chosen as conservative upper bound given full agonism may produce more severe withdrawal than partial-agonist THC. Evidence basis: structural_analogy

Tolerance Profiletrace

Field	Published	AI Proposed	Confidence
Buildup	moderate	moderate	low
Half-life	5 days	5 days	low
Full Reset	3 weeks	3 weeks	low
Cross-tolerances	Δ9-THC, Δ8-THC, HHC, HHCP, synthetic cannabinoids	Δ9-THC, Δ8-THC, HHC, HHCP, synthetic cannabinoids	low
Editorial	Entirely class-inferred from CB1 receptor downregulation mechanisms characterized for Δ9-THC and synthetic cannabinoids. Work-notes specify 3–7 day half-life and 2–4 week reset from THC class; midpoints (5 days, 3 weeks) proposed. No THCP-specific tolerance data.
	ReasoningReasoning Entirely class-inferred from CB1 receptor downregulation mechanisms characterized for Δ9-THC and synthetic cannabinoids. Work-notes specify 3–7 day half-life and 2–4 week reset from THC class; midpoints (5 days, 3 weeks) proposed. No THCP-specific tolerance data. Evidence basis: structural_analogy

Effects & Profile

Contraindications

Field	Published	AI Proposed	Confidence
psychiatric Personal or family history of psychotic disorders (schizophrenia, schizoaffective disorder)trace	absolute	absolute	low
Editorial	Class inference from high-potency CB1 full agonist pharmacology and cannabis-associated psychosis epidemiology (Schoeler et al. 2022). No THCP-specific data.
	ReasoningReasoning Class inference from high-potency CB1 full agonist pharmacology and cannabis-associated psychosis epidemiology (Schoeler et al. 2022). No THCP-specific data.
cardiovascular Unstable cardiovascular diseasetrace	absolute	absolute	low
Editorial	Class inference from synthetic cannabinoid adverse event literature and THC cardiovascular pharmacology. No THCP-specific cardiovascular data.
	ReasoningReasoning Class inference from synthetic cannabinoid adverse event literature and THC cardiovascular pharmacology. No THCP-specific cardiovascular data.
psychiatric Bipolar disordertrace	relative	relative	low
Editorial	Class inference from cannabis-bipolar disorder literature. No THCP-specific psychiatric outcome data.
	ReasoningReasoning Class inference from cannabis-bipolar disorder literature. No THCP-specific psychiatric outcome data.
pregnancy breastfeeding Pregnancy and lactationtrace	relative	relative	low
Editorial	Class inference from THC reproductive pharmacology. No THCP-specific reproductive data.
	ReasoningReasoning Class inference from THC reproductive pharmacology. No THCP-specific reproductive data.
age Adolescence (under 25)trace	relative	relative	low
Editorial	Class inference supported by Hines 2020 epidemiological data on high-potency cannabis and adolescent mental health. No THCP-specific developmental data.
	ReasoningReasoning Class inference supported by Hines 2020 epidemiological data on high-potency cannabis and adolescent mental health. No THCP-specific developmental data.
other Concurrent narrow-TI CYP2C9/CYP3A4 substrates (warfarin, tacrolimus, cyclosporine)trace	relative	relative	low
Editorial	Class inference from THC CYP pharmacology (Stout & Cimino 2014; Qian et al. 2019). No THCP-specific interaction data.
	ReasoningReasoning Class inference from THC CYP pharmacology (Stout & Cimino 2014; Qian et al. 2019). No THCP-specific interaction data.
psychiatric History of cannabis use disordertrace	relative	relative	low
Editorial	Class inference from CUD epidemiology and synthetic cannabinoid reinforcement pharmacology. No THCP-specific dependence data.
	ReasoningReasoning Class inference from CUD epidemiology and synthetic cannabinoid reinforcement pharmacology. No THCP-specific dependence data.
hepatic Hepatic impairmenttrace	relative	relative	low
Editorial	Class inference from THC hepatic metabolism. No THCP-specific hepatic impairment data.
	ReasoningReasoning Class inference from THC hepatic metabolism. No THCP-specific hepatic impairment data.

Timeline Phases

vaporized

Field	Published	AI Proposed	Confidence
Onsettrace	60–300 sec(i=0.20)	60–300 sec(i=0.20)	low
Editorial	All timeline phases inferred from Δ9-THC vaporized pharmacokinetics with adjustments for THCP's ~33x higher CB1 affinity and consumer reports suggesting longer duration. No controlled THCP duration data exist. Peak phase widened (30–90 min) relative to THC to reflect higher receptor affinity and reported prolonged effects. Reference compound: Δ9-THC (vaporized).
	ReasoningReasoning All timeline phases inferred from Δ9-THC vaporized pharmacokinetics with adjustments for THCP's ~33x higher CB1 affinity and consumer reports suggesting longer duration. No controlled THCP duration data exist. Peak phase widened (30–90 min) relative to THC to reflect higher receptor affinity and reported prolonged effects. Reference compound: Δ9-THC (vaporized). Evidence basis: structural_analogy
Come uptrace	300–900 sec(i=0.50)	300–900 sec(i=0.50)	low
Editorial	All timeline phases inferred from Δ9-THC vaporized pharmacokinetics with adjustments for THCP's ~33x higher CB1 affinity and consumer reports suggesting longer duration. No controlled THCP duration data exist. Peak phase widened (30–90 min) relative to THC to reflect higher receptor affinity and reported prolonged effects. Reference compound: Δ9-THC (vaporized).
	ReasoningReasoning All timeline phases inferred from Δ9-THC vaporized pharmacokinetics with adjustments for THCP's ~33x higher CB1 affinity and consumer reports suggesting longer duration. No controlled THCP duration data exist. Peak phase widened (30–90 min) relative to THC to reflect higher receptor affinity and reported prolonged effects. Reference compound: Δ9-THC (vaporized). Evidence basis: structural_analogy
Peaktrace	1800–5400 sec(i=1.00)	1800–5400 sec(i=1.00)	low
Editorial	All timeline phases inferred from Δ9-THC vaporized pharmacokinetics with adjustments for THCP's ~33x higher CB1 affinity and consumer reports suggesting longer duration. No controlled THCP duration data exist. Peak phase widened (30–90 min) relative to THC to reflect higher receptor affinity and reported prolonged effects. Reference compound: Δ9-THC (vaporized).
	ReasoningReasoning All timeline phases inferred from Δ9-THC vaporized pharmacokinetics with adjustments for THCP's ~33x higher CB1 affinity and consumer reports suggesting longer duration. No controlled THCP duration data exist. Peak phase widened (30–90 min) relative to THC to reflect higher receptor affinity and reported prolonged effects. Reference compound: Δ9-THC (vaporized). Evidence basis: structural_analogy
Plateautrace	1800–3600 sec(i=0.70)	1800–3600 sec(i=0.70)	low
Editorial	All timeline phases inferred from Δ9-THC vaporized pharmacokinetics with adjustments for THCP's ~33x higher CB1 affinity and consumer reports suggesting longer duration. No controlled THCP duration data exist. Peak phase widened (30–90 min) relative to THC to reflect higher receptor affinity and reported prolonged effects. Reference compound: Δ9-THC (vaporized).
	ReasoningReasoning All timeline phases inferred from Δ9-THC vaporized pharmacokinetics with adjustments for THCP's ~33x higher CB1 affinity and consumer reports suggesting longer duration. No controlled THCP duration data exist. Peak phase widened (30–90 min) relative to THC to reflect higher receptor affinity and reported prolonged effects. Reference compound: Δ9-THC (vaporized). Evidence basis: structural_analogy
Resolutiontrace	3600–10800 sec(i=0.30)	3600–10800 sec(i=0.30)	low
Editorial	All timeline phases inferred from Δ9-THC vaporized pharmacokinetics with adjustments for THCP's ~33x higher CB1 affinity and consumer reports suggesting longer duration. No controlled THCP duration data exist. Peak phase widened (30–90 min) relative to THC to reflect higher receptor affinity and reported prolonged effects. Reference compound: Δ9-THC (vaporized).
	ReasoningReasoning All timeline phases inferred from Δ9-THC vaporized pharmacokinetics with adjustments for THCP's ~33x higher CB1 affinity and consumer reports suggesting longer duration. No controlled THCP duration data exist. Peak phase widened (30–90 min) relative to THC to reflect higher receptor affinity and reported prolonged effects. Reference compound: Δ9-THC (vaporized). Evidence basis: structural_analogy
Afterglowtrace	7200–43200 sec(i=0.10)	7200–43200 sec(i=0.10)	low
Editorial	All timeline phases inferred from Δ9-THC vaporized pharmacokinetics with adjustments for THCP's ~33x higher CB1 affinity and consumer reports suggesting longer duration. No controlled THCP duration data exist. Peak phase widened (30–90 min) relative to THC to reflect higher receptor affinity and reported prolonged effects. Reference compound: Δ9-THC (vaporized).
	ReasoningReasoning All timeline phases inferred from Δ9-THC vaporized pharmacokinetics with adjustments for THCP's ~33x higher CB1 affinity and consumer reports suggesting longer duration. No controlled THCP duration data exist. Peak phase widened (30–90 min) relative to THC to reflect higher receptor affinity and reported prolonged effects. Reference compound: Δ9-THC (vaporized). Evidence basis: structural_analogy

oral

Field	Published	AI Proposed	Confidence
Onsettrace	1800–5400 sec(i=0.10)	1800–5400 sec(i=0.10)	low
Editorial	All timeline phases inferred from Δ9-THC oral pharmacokinetics. Oral route introduces first-pass metabolism variability and delayed onset, increasing both duration and overdose risk from impatient redosing. THCP's greater lipophilicity and higher receptor affinity predict prolonged plateau and resolution relative to THC. No controlled THCP oral duration data exist. Reference compound: Δ9-THC (oral).
	ReasoningReasoning All timeline phases inferred from Δ9-THC oral pharmacokinetics. Oral route introduces first-pass metabolism variability and delayed onset, increasing both duration and overdose risk from impatient redosing. THCP's greater lipophilicity and higher receptor affinity predict prolonged plateau and resolution relative to THC. No controlled THCP oral duration data exist. Reference compound: Δ9-THC (oral). Evidence basis: structural_analogy
Come uptrace	1800–3600 sec(i=0.40)	1800–3600 sec(i=0.40)	low
Editorial	All timeline phases inferred from Δ9-THC oral pharmacokinetics. Oral route introduces first-pass metabolism variability and delayed onset, increasing both duration and overdose risk from impatient redosing. THCP's greater lipophilicity and higher receptor affinity predict prolonged plateau and resolution relative to THC. No controlled THCP oral duration data exist. Reference compound: Δ9-THC (oral).
	ReasoningReasoning All timeline phases inferred from Δ9-THC oral pharmacokinetics. Oral route introduces first-pass metabolism variability and delayed onset, increasing both duration and overdose risk from impatient redosing. THCP's greater lipophilicity and higher receptor affinity predict prolonged plateau and resolution relative to THC. No controlled THCP oral duration data exist. Reference compound: Δ9-THC (oral). Evidence basis: structural_analogy
Peaktrace	3600–10800 sec(i=1.00)	3600–10800 sec(i=1.00)	low
Editorial	All timeline phases inferred from Δ9-THC oral pharmacokinetics. Oral route introduces first-pass metabolism variability and delayed onset, increasing both duration and overdose risk from impatient redosing. THCP's greater lipophilicity and higher receptor affinity predict prolonged plateau and resolution relative to THC. No controlled THCP oral duration data exist. Reference compound: Δ9-THC (oral).
	ReasoningReasoning All timeline phases inferred from Δ9-THC oral pharmacokinetics. Oral route introduces first-pass metabolism variability and delayed onset, increasing both duration and overdose risk from impatient redosing. THCP's greater lipophilicity and higher receptor affinity predict prolonged plateau and resolution relative to THC. No controlled THCP oral duration data exist. Reference compound: Δ9-THC (oral). Evidence basis: structural_analogy
Plateautrace	3600–7200 sec(i=0.80)	3600–7200 sec(i=0.80)	low
Editorial	All timeline phases inferred from Δ9-THC oral pharmacokinetics. Oral route introduces first-pass metabolism variability and delayed onset, increasing both duration and overdose risk from impatient redosing. THCP's greater lipophilicity and higher receptor affinity predict prolonged plateau and resolution relative to THC. No controlled THCP oral duration data exist. Reference compound: Δ9-THC (oral).
	ReasoningReasoning All timeline phases inferred from Δ9-THC oral pharmacokinetics. Oral route introduces first-pass metabolism variability and delayed onset, increasing both duration and overdose risk from impatient redosing. THCP's greater lipophilicity and higher receptor affinity predict prolonged plateau and resolution relative to THC. No controlled THCP oral duration data exist. Reference compound: Δ9-THC (oral). Evidence basis: structural_analogy
Resolutiontrace	7200–14400 sec(i=0.40)	7200–14400 sec(i=0.40)	low
Editorial	All timeline phases inferred from Δ9-THC oral pharmacokinetics. Oral route introduces first-pass metabolism variability and delayed onset, increasing both duration and overdose risk from impatient redosing. THCP's greater lipophilicity and higher receptor affinity predict prolonged plateau and resolution relative to THC. No controlled THCP oral duration data exist. Reference compound: Δ9-THC (oral).
	ReasoningReasoning All timeline phases inferred from Δ9-THC oral pharmacokinetics. Oral route introduces first-pass metabolism variability and delayed onset, increasing both duration and overdose risk from impatient redosing. THCP's greater lipophilicity and higher receptor affinity predict prolonged plateau and resolution relative to THC. No controlled THCP oral duration data exist. Reference compound: Δ9-THC (oral). Evidence basis: structural_analogy
Afterglowtrace	14400–86400 sec(i=0.15)	14400–86400 sec(i=0.15)	low
Editorial	All timeline phases inferred from Δ9-THC oral pharmacokinetics. Oral route introduces first-pass metabolism variability and delayed onset, increasing both duration and overdose risk from impatient redosing. THCP's greater lipophilicity and higher receptor affinity predict prolonged plateau and resolution relative to THC. No controlled THCP oral duration data exist. Reference compound: Δ9-THC (oral).
	ReasoningReasoning All timeline phases inferred from Δ9-THC oral pharmacokinetics. Oral route introduces first-pass metabolism variability and delayed onset, increasing both duration and overdose risk from impatient redosing. THCP's greater lipophilicity and higher receptor affinity predict prolonged plateau and resolution relative to THC. No controlled THCP oral duration data exist. Reference compound: Δ9-THC (oral). Evidence basis: structural_analogy

Dose Tier Summaries

thresholdtrace

low

Minimal perceptible alteration in baseline consciousness. A subtle mood shift — faint warmth or lightness — and a vague awareness that something has changed. Cognitive function remains largely intact, and the experience may be difficult to distinguish from placebo in individuals without prior cannabinoid experience. Physically, a slight relaxation of muscle tension may be noticed. Appetite is unaffected or negligibly increased. Dry mouth is unlikely at this level. Due to THCP's extreme potency relative to Δ9-THC, threshold doses are a small fraction of typical THC thresholds. The margin between threshold and light effects is narrow — precise dosing equipment is advisable.

Editorial

Entirely inferred from Δ9-THC threshold profile scaled by ~33x CB1 potency ratio. No controlled THCP dose-response data exist. Consumer reports confirm activity at doses far below THC equivalents.

Reasoning

Entirely inferred from Δ9-THC threshold profile scaled by ~33x CB1 potency ratio. No controlled THCP dose-response data exist. Consumer reports confirm activity at doses far below THC equivalents.

Evidence basis: structural_analogy

lighttrace

low

Mild euphoria emerges alongside gentle relaxation and a perceptible slowing of thought tempo. Appetite stimulation begins — food becomes more appealing. Time perception is subtly altered, with moments feeling slightly stretched. A light body high develops as warmth or pleasant heaviness in the limbs. Physically, mild muscle relaxation is noticeable. Dry mouth may appear. Heart rate may be slightly elevated but typically not perceived as concerning. Motor coordination is minimally impaired. Anxiety is unlikely at this tier in most individuals. Functional impairment is mild — simple tasks remain manageable, though complex cognitive work may feel less efficient.

Editorial

Inferred from Δ9-THC light-dose profile with adjustments for full CB1 agonism. Consumer reports of THCP describe cannabis-like effects at very low doses. No controlled data.

Reasoning

Inferred from Δ9-THC light-dose profile with adjustments for full CB1 agonism. Consumer reports of THCP describe cannabis-like effects at very low doses. No controlled data.

Evidence basis: structural_analogy

commontrace

low

Pronounced euphoria and sedation define the common-dose experience. Cognitive impairment becomes clear — short-term memory is disrupted, focus is suppressed, and thought tempo decelerates noticeably. Time distortion is prominent, with minutes feeling substantially elongated. Appetite enhancement is strong. Emotional responses are heightened, and humor enhancement is typical. Body heaviness and muscle relaxation are substantial. Dry mouth is likely. Heart rate perception changes may be noticed. Motor control is meaningfully impaired — coordination tasks become clumsy. A warm, spreading body high pervades. Anxiety is possible in predisposed individuals or unfamiliar settings. Functional impairment is significant — driving and complex tasks are unsafe. Duration of commitment is several hours.

Editorial

Inferred from Δ9-THC common-dose profile scaled for THCP's full CB1 agonism. Consumer self-reports (Caprari et al. 2024) describe intense sedation, euphoria, and cognitive impairment consistent with this tier.

Reasoning

Evidence basis: structural_analogy

strongtrace

low

Intense sedation and heavy body load dominate. Cognitive impairment is marked — thought disorganization, decision impairment, and near-complete short-term memory suppression. Time distortion is severe, with temporal disorientation common. Visual haze or noise may appear. Internal experience may feel dreamlike or disconnected. Physically, body heaviness approaches immobilization in comfortable settings. Motor control is significantly impaired. Tachycardia may become perceptible and anxiety-provoking. Dizziness is possible with position changes. Anxiety and paranoia become substantially more likely at this tier. The transition from common to strong effects may be steeper than with THC due to full agonism — the dose-response curve lacks THC's partial-agonist ceiling. Redosing is particularly risky.

Editorial

Inferred from Δ9-THC strong-dose profile with upward adjustment for full CB1 agonism removing the efficacy ceiling. Work-notes flag steeper dose-response transition at this tier.

Reasoning

Inferred from Δ9-THC strong-dose profile with upward adjustment for full CB1 agonism removing the efficacy ceiling. Work-notes flag steeper dose-response transition at this tier.

Evidence basis: structural_analogy

heavytrace

low

Overwhelming intoxication approaching incapacitation. Severe cognitive impairment with thought disorganization, confusion, and near-complete memory suppression for the duration. Derealization and depersonalization may occur. Intense paranoia and anxiety are common. The experience may feel uncontrollable and frightening. Physically, profound sedation renders most activity impossible. Motor control is severely impaired. Nausea and dizziness are possible. Tachycardia may be pronounced. Physical fatigue is heavy. Risk of acute psychotic symptoms is elevated, particularly in individuals with psychiatric vulnerability. THCP's full agonism means effects at this tier can exceed the ceiling of any typical cannabis experience, entering territory associated with synthetic cannabinoid adverse events. Emergency support should be accessible.

Editorial

Inferred from high-dose THC and synthetic cannabinoid adverse event profiles. Full CB1 agonism removes the partial-agonist efficacy ceiling, allowing effects to escalate beyond typical cannabis limits. One unverified report describes psychotic symptoms at 8 mg oral THCP.

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

11 strong · 14 moderate

[1]
strong
A novel phytocannabinoid isolated from Cannabis sativa L. with an in vivo cannabimimetic activity higher than Δ9-tetrahydrocannabinol: Δ9-Tetrahydrocannabiphorol
Citti C, Linciano P, Russo F, Luongo L, Iannotta M, Maione S, Laganà A, Capriotti AL, Forni F, Vandelli MA, Gigli G, Cannazza G · 2019 · Scientific Reports
doi.org/10.1038/s41598-019-56785-1 pubmed 31889124no claims checked
[2]
moderate
An emerging trend in Novel Psychoactive Substances (NPSs): designer THC
Caprari C, Ferri E, Vandelli MA, Citti C, Cannazza G · 2024 · Journal of Cannabis Research
doi.org/10.1186/s42238-024-00226-y pubmed 38702834no claims checked
[3]
strong
The Identification of Synthetic Impurities in a Vape Pen Containing Δ9-Tetrahydrocannabiphorol Using Gas Chromatography Coupled with Mass Spectrometry
Schirmer W, Schürch S, Weinmann W · 2024 · Psychoactives
doi.org/10.3390/psychoactives3040030no claims checked
[4]
moderate
Beyond THC: The New Generation of Cannabinoid Designer Drugs
Fattore L, Fratta W · 2011 · Frontiers in Behavioral Neuroscience
doi.org/10.3389/fnbeh.2011.00060 pubmed 22007163no claims checked
[5]
moderate
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
Janssens LK, Van Uytfanghe K, Williams JB, Hering KW, Iula DM, Stove CP · 2024 · Archives of Toxicology
doi.org/10.1007/s00204-024-03769-4 pubmed 38735004no claims checked
[6]
moderate
Marijuana Use and Its Impact on Outpatient Anesthesia.
Mann DK, Portnof J, Adlesic E · 2026 · Anesthesia Progress
doi.org/10.2344/25-0009 pubmed 41791719no claims checked
[7]
strong
Identification of a new cannabidiol n-hexyl homolog in a medicinal cannabis variety with an antinociceptive activity in mice: cannabidihexol
Linciano 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 · Scientific Reports
doi.org/10.1038/s41598-020-79042-2 pubmed 33328530no claims checked
[8]
strong
Single trichome phytocannabinomics of two different cannabis varieties
Ferri E, Cerrato A, Caprari C, Russo F, Laganà A, Capriotti AL, Faggiana G, Moro A, Citti C, Cannazza G · 2025 · Journal of Pharmaceutical and Biomedical Analysis
doi.org/10.1016/j.jpba.2025.116836 pubmed 40139041no claims checked
[9]
moderate
Appearance of hexahydrocannabinols as recreational drugs and implications for cannabis drug testing - focus on HHC, HHC-P, HHC-O and HHC-H
Helander A, Johansson M, Villén T, Andersson A · 2024 · Scandinavian Journal of Clinical and Laboratory Investigation
doi.org/10.1080/00365513.2024.2340039 pubmed 38619215no claims checked
[10]
moderate
Emergence of semi-synthetic cannabinoids in cannabis products seized in Eastern Denmark over a 6-year period
Jørgensen CF, Rasmussen BS, Línnet K, Thomsen R · 2024 · Journal of Forensic Sciences
doi.org/10.1111/1556-4029.15631 pubmed 39301976no claims checked
[11]
moderate
Cannabidiol-Derived Cannabinoids: The Unregulated Designer Drug Market Following the 2018 Farm Bill
Zawatsky CN, Mills-Huffnagle S, Augusto CM, Vrana KE, Nyland JE · 2024 · Medical Cannabis and Cannabinoids
doi.org/10.1159/000536339 pubmed 38352661no claims checked
[12]
strong
Enantioseparation of chiral phytocannabinoids in medicinal cannabis
Russo F, Tolomeo F, Vandelli MA, Biagini G, Laganà A, Capriotti AL, Cerrato A, Carbone L, Perrone E, Cavazzini A, Maiorano V, Gigli G, Cannazza G, Citti C · 2023 · Journal of Chromatography B
doi.org/10.1016/j.jchromb.2023.123682 pubmed 36965450no claims checked
[13]
moderate
Phytocannabinoids: Origins and Biosynthesis
Gülck T, Møller BL · 2020 · Trends in Plant Science
doi.org/10.1016/j.tplants.2020.05.005 pubmed 32646718no claims checked
[14]
strong
Exogenous cannabinoids as substrates, inhibitors, and inducers of human drug metabolizing enzymes: a systematic review.
Stout SM, Cimino NM · 2014 · Drug metabolism reviews
doi.org/10.3109/03602532.2013.849268 pubmed 24160757no claims checked
[15]
moderate
Human metabolism of the semi-synthetic cannabinoids hexahydrocannabinol, hexahydrocannabiphorol and their acetates using hepatocytes and urine samples
Lindbom K, Norman C, Baginski S, Krebs L, Stalberga D, Rautio T, Wu X, Kronstrand R, Grén H · 2025 · Drug Testing and Analysis
doi.org/10.1002/dta.3740 pubmed 38804224no claims checked
[16]
moderate
Identification of Hexahydrocannabiphorol Metabolites in Human Urine
Schirmer W, Schürch S, Weinmann W · 2025 · Drug Testing and Analysis
doi.org/10.1002/dta.3871 pubmed 39981602no claims checked
[17]
moderate
Association of High-Potency Cannabis Use With Mental Health and Substance Use in Adolescence
Hines LA, Freeman TP, Gage SH, Zammit S, Hickman M, Cannon M, Munafo M, MacLeod J, Heron J · 2020 · JAMA Psychiatry
doi.org/10.1001/jamapsychiatry.2020.1035 pubmed 32459328no claims checked
[18]
strong
CBD Versus CBDP: Comparing In Vitro Receptor-Binding Activities
Haghdoost M, Young S, Holloway AK, Roberts M, Zvorsky I, Bonn-Miller MO · 2024 · International Journal of Molecular Sciences
doi.org/10.3390/ijms25147724 pubmed 39062976no claims checked
[19]
strong
Cross-reactivity of 24 cannabinoids and metabolites in blood using the Immunalysis Cannabinoids Direct enzyme-linked immunosorbent assay
Patton AL, Pacheco IC, Seither JZ, Brown JT, Walterscheid JP, Karschner EL · 2024 · Journal of Analytical Toxicology
doi.org/10.1093/jat/bkae036 pubmed 38648393no claims checked
[20]
moderate
Comprehensive LC-MS-MS analysis of THC isomers, analogs, homologs, and metabolites in blood and urine
Muir LS, Doumit SE, Seither JZ, Knittel JL, Walterscheid JP, Karschner EL · 2025 · Journal of Analytical Toxicology
doi.org/10.1093/jat/bkaf023 pubmed 40098275no claims checked
[21]
strong
Rapid LC-QTOF-MS screening method for semi-synthetic cannabinoids in whole blood
Schirmer W, Walton SE, Weinmann W, Schürch S, Logan BK · 2025 · Journal of Analytical Toxicology
doi.org/10.1093/jat/bkaf095 pubmed 41117773no claims checked
[22]
moderate
The Potential for Pharmacokinetic Interactions Between Cannabis Products and Conventional Medications
Qian Y et al. · 2019 · Journal of Clinical Psychopharmacology
doi.org/10.1097/jcp.0000000000001089 pubmed 31433338no claims checked
[23]
moderate
Rates and correlates of cannabis-associated psychotic symptoms in over 230,000 people who use cannabis
Schoeler T, Ferris J, Winstock AR · 2022 · Translational Psychiatry
doi.org/10.1038/s41398-022-02112-8 pubmed 36068202no claims checked
[24]
strong
Evidence-based consensus guidelines for the pharmacological management of substance dependence: Recommendations from the British Association for Psychopharmacology
Sinclair JM, Kalk NJ, Kaar SJ, et al. · 2026 · Journal of psychopharmacology
doi.org/10.1177/02698811251399593 pubmed 41731947no claims checked
[25]
strong
In vitro activation of the CB1 receptor by the semi-synthetic cannabinoids hexahydrocannabinol (HHC), hexahydrocannabinol acetate (HHC-O) and hexahydrocannabiphorol (HHC-P)
Persson M, Kronstrand R, Evans-Brown M, Green H · 2025 · Drug Testing and Analysis
doi.org/10.1002/dta.3750 pubmed 38894658no claims checked

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Coverage & Gaps

effect links

142 links · 142 approved · 0 audited0/142 with evidence basis

Tetrahydrocannabiphorol

Value Provenance

Dosing

oraltrace →

vaporizedtrace →

Duration

vaporized

oral

Safety

Toxicity Profiletrace →

Dependence Profiletrace →

Withdrawal Profiletrace →

Tolerance Profiletrace →

Effects & Profile

Contraindications

Timeline Phases

vaporized

oral

Dose Tier Summaries

History

Sources

Claim Verification

Coverage & Gaps

oraltrace

vaporizedtrace

Toxicity Profiletrace

Dependence Profiletrace

Withdrawal Profiletrace

Tolerance Profiletrace