Cannabidiol (CBD)

CBD Pharmacokinetics

Pharmacokinetics refers to what the body does to a drug, how the drug moves into, through, and out of the body: the time course of its absorption, bioavailability, distribution, metabolism, and excretion. Whereas pharacodynamics refers to the effects a drug has on the body, including desired, therapeutic effects as well as side effects.


Understanding the pharmacokinetics of CBD and other cannabis constituents allows for identifying the pros and cons of the different formulations of cannabis/cannabinoids available as well as avoiding unintended responses and adverse effects associated with taking cannabis/cannabinoid products.


Links to other Pertinent Educational Pages:

Links to ALL Marijuana Educational Pages


See also:

THC – Pharmacokinetics

CBD – Side Effects and Drug Interactions


Cannabidiol (CBD):


The medical information on this site is provided as a resource for information only, and is not to be used or relied upon for any diagnostic or treatment purposes and is not intended to create any patient-physician relationship.  Readers are advised to seek professional guidance regarding the diagnosis and treatment of their medical concerns.


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CBD (Cannabidiol) Pharmacokinetics

Understanding the pharmacokinetics of CBD (cannabidiol) is essential to understanding the onset, magnitude, and duration of its pharmacologic effects in order to maximize benefit and minimize side effects. CBD pharmacokinetics includes how CBD is absorbed into the body with different routes of administration and from different drug formulations, how CBD is distributed throughout the body, metabolized by the liver and other tissues, and eliminated in urine, feces and sweat. Pharmacokinetic processes can change over time and under different conditions and they may be affected by the frequency and magnitude of CBD exposure.


Botanical Cannabis and CBD

Fresh botanical marijuana (cannabis) plants contain little to no CBD but instead contain cannabidiolic acid (CBDA) , the precursor or pro-drug to CBD which, when exposed to light, heat, or aging is decarboxylated into CBD. Similarly, delta 9-tetrahydrocannabinol (THC) is formed from the corresponding THCA which has anti-inflammatory and strong anti-nausea effects with neuroprotective and anticonvulsant effects..


These acid cannabinoids have had much less research, but are known to possess pharmacological properties in their own right. CBDA is a powerful anti-anxiety agent (at least in rodents), and may offer benefits for skin. CBDA may have anti-inflammatory properties as well as the ability to reduce nausea through 5HT 1a receptor activation. CBDA pharmabiological understanding is incomplete, but it may have equal, if not better absorption when compared to CBD. THCA  also has anti-inflammatory and strong anti-nausea effects with neuroprotective and anticonvulsant effects.


Plant concentrations of CBD (and THC) depend on the species, strain, cultivation, and storage of the plant. The average concentrations in more than 30,000 cannabis preparations confiscated in the U.S. between 1980 and 1997 were 3.1% THC and only 0.3% CBD. Various strains and marijuana-based products are now available that contain substantially higher contents of these constituents, especially THC.

The exact functions of CBDA (and THCA) physiologically suggest similar therapeutic benefits to CBD that may have the potential to work synergistically with CBD. These synergistic properties may be the primary reason that lower dosing of CBD whole hemp extract which also contains CBDA  can be therapeutic when compared to purified CBD.



The “bioavailability” of a medication is the measure of how effectively administration of that medicine achieves blood levels. As a standard of definition, the bioavailability of a medication given directly intravenously is 100%. Other forms of administration, such as smoking, eating and application to skin, will be associated with less bioavailability. Bioavailability is generally described in terms of maximum time in the blood (Cmax) and maximum overall absorption into the blood (AUC – Area under the Curve). Tmax is the time necessary to reach the maximum blood concentration after administration of a medication.


Bioavailability is the degree and rate at which a substance is absorbed into the blood where it can be delivered to the organ systems necessary for therapeutic effects. The greater the bioavailability, the less product needs to be consumed to achieve a therapeutic effect. Bioavailability of cannabis products varies somewhat from individual to individual and is determined mostly by how it is consumed, including if it is ingested with food. It is also affected by the individual’s age, general health and the presence of gastrointestinal disorders. As a general guide based on method of use, the bioavailability of cannabis is:

  • Smoking: 25-31% bioavailability (Reports vary)
  • Vaporization: 30-60% bioavailability
  • Tinctures (sublingual): 40-50% bioavailability
  • Edibles: 5-12% bioavailability (Reports vary from 4-20%)
  • Intranasal:  34-46% bioavailability
  • Transdermal: variable, but may increased by 3.7-fold in the presence of enhancer


Smoking and Inhalation

Inhalation vs. Oral vs. Buccal (sublingual) Administration of CBD

The pharmacokinetics of CBD are very different depending on the method of use. Inhalation provides the most rapid onset, but the shortest duration of effect.  Oral ingestion provides the slowest onset but the longest duration of effect, whereas the sublingual route, holding the medicine under the tongue for 1-2 minutes to allow for buccal absorption  directly into the blood, is in-between inhalation and oral.

The bioavailability of CBD following smoking is on average @31% – in other words, only 31% of the CBD inhaled while smoking will make it into the blood. This compares with the bioavailability of CBD following oral ingestion which is very low (6–19%)  due to extensive first pass metabolism when it passes through the liver after being absorbed from the gut and before entering the blood.

After smoking or vaping CBD, maximum blood levels are achieved quickly, within 5 minutes or so but levels also substantially drop off quickly, within an hour. For example, after smoking a cigarette containing 19.2 mg of CBD, highest plasma concentrations have been reported as 110 ng/mL, 3 minutes post-dose, which drops to 10.2 ng/ml 1 hour later. In another study, using a nebulizer resulted in a Cmax of 9.5 ng/mL which occurred at 0.6 hours, whereas aerosol administration produced Cmax (2.6 ng/mL) at 2.35 hours . In a small study of infrequent cannabis smokers smoking a cigarette containing 2 mg of CBD, Cmax was 2.0 ng/mL at 0.25 hours but CBD was no longer detected in blood after 1.0 hour.

Sublingual/Buccal Use

Oromucosal spray, either buccal, sublingual, or oropharyngeal administration, result in mean Cmax between 2.5 and 3.3 ng/mL and mean Tmax between 1.64 and 4.2 hours. Sublingual drops result in similar Cmax of 2.05 and 2.58 ng/mL and Tmax of 2.17 and 1.67 hours, respectively. These levels are dose dependent.

CBD bioavailability is increased in fed vs. fasted states as reported in a study evaluating a single 10 mg dose of CBD administered through an oromucosal spray which also contained THC. Mean AUC and Cmax are 5- and 3- fold higher respectively during fed conditions compared to fasted. Tmax is also delayed under the fed state (4.0 vs. 1.4 hours).

In other words, blood levels of CBD after oromucosal spray will be higher and last longer when CBD is administered after eating.


Oral Use of CBD (Edibles)

Oral bioavailability of CBD is estimated to be only 6-19% due to significant first-pass metabolism of CBD in the liver.  Cmax and AUC following oral administration are also dose dependent. A dose of 10mg CBD has a mean Cmax of 2.5 ng/mL at 1.27 hours, and a dose of 400 or 800 mg has a mean Cmax of 181 ng/mL (at 3.0 hours) and 114 ng/mL (at 1.5 hours) for 400 mg, and 221 ng/mL (at 3.0 hours) and 157 ng/mL (at 4.0 hours) for 800 mg. A dose of 800 mg oral CBD in a small study reported a mean Cmax of 78 ng/mL and mean Tmax of 3.0 hours . Although, an increase in dose corresponds with an increase in Cmax, the Cmax between the higher doses of CBD does not greatly differ, suggesting a saturation effect between 400 and 800 mg.

In other words, there appears to be little benefit in exceeding single oral CBD doses of 400-800 mg.


In another study, one hour after oral capsule administration containing 5.4 mg CBD in males and females, mean Cmax was reported as 0.93 ng/mL (higher for female participants than male). In those who ate a standard breakfast meal 1 hour after the capsules, there was a slightly increased mean Cmax to 1.13 ng/mL. CBD remained detectable in the blood for 3–4 hours after administration. This is also demonstrated in animal studies; co-administration of lipids with oral CBD increased systemic availability by almost 3-fold in rats while  a pro-nanoliposphere self-emulsifying formulation formulation increased oral bioavailability by about 3- 6-fold.


Research evaluating the bioaccessibility of CBD with and without food  showed that lipase enzyme activity and fatty acid absorption increased
in the presence of bile salts. In the fed-state digestion revealed significantly higher micelle formation with CBD compared to the fasted state.  The increase in bioaccessibility of CBD with food can be explained by the fact that micelle formation from hydrolyzed lipids aid in bioaccessibility of hydrophobic molecules which depends on the food matrix and the presence of lipase and bile salts. This understanding has lead to the design of new formulations that enhance absorption of CBD and other lipophyllic compounds.

Improving Bioavailability

Thirty percent of top marketed drugs in the USA and 70% of all new drug candidates are lipophilic and exhibit poor water solubility. With theee physicochemical properties, the oral bioavailability of these compounds is very limited and extremely erratic. Different lipid-based formulations have been explored in the past few decades to improve the oral delivery of such compounds. In recent years, the most popular approach is their incorporation into self-emulsifying drug delivery systems (SEDDS), with particular emphasis on self-nano-emulsifying drug delivery systems (SNEDDS).


Because CBD oil is highly lipophilic and therefore very poorly soluble in water, it is not absorbed well with oral ingestion (80% or more of ingested CBD is not absorbed. Additionally, THC and CBD are prone to extensive first pass mechanisms, meaning that the liver metabozizes a very significant proportion of these compounds immediately upon absortion from the gut before entering the blood. These absorption factors result in low and erratic, variable oral bioavailability, only a small fraction – less than 10% – of orally ingested CBD  actually enter a cells where they exert their medical properties (true also for other cannabinoids and terpenes in marijuana).  Instead, CBD remains in the blood until it passes through the liver and is metabolized.


New formulations of CBD are appearing on the market that offer enhanced water solubility and absorption that provide greater bioavaiability. These products include liposomal formulations,  nano-sized formulations and self emulsifying formulations. Furthermore, some formulations supplement with compounds such as peperine that enhance bioavaliability with other mechanisms.


Liposomal CBD

Liposomal technology provides a method used to enable medications to be better absorbed from the gut and into cells. It is a technology commonly used in nutriceutical supplements, including products described elsewhere on this website (See: Meriva and Siliphos). Liposomes are small sacs with membranes made of phospholipids – the same type of membrane that encloses the cells in our bodies. Liposomal formulations involves enclosing individual drug molecules like CBD inside liposomes, which facilitates their entry into cells in the same way the body transports its own substances into and out of cells. Thus, liposomal CBD is more efficiently used by the body, estimated at possibly 4-5 times more efficiently.

Advantages of Liposomal CBDs

      1. Encapsulates the active ingredients and delivers them directly into the cell;
      2. Reduces the breakdown of the CBD (avoids first pass metabolism by the liver); and 
      3. It improves the percentage of bioavailable CBD, as the full concentration can be absorbed


Nano Formulations

In general, cells can absorb particles only up to 50 nanometers (billionths of a meter) in diameter. Because CBD is hydrophobic and fatty, it binds with itself to a certain extent, creating chains of CBD that are too large to be absorbed by cells. Recent technology sometimes referred to as nano-amplification allows for the separation of CBD molecules  from each other.  Individually, CBD molecules are about 10-15 nanometers in diameter so that nano-forms of CBD are better absorbed by cells with less wastage.


Self-Nano Emulsifying Drug Delivery Systems (SNEDDS)

Self-nano emulsifying drug delivery systems (SNEDDS) increase the oral bioavailability of poorly water-soluble drugs by multiple mechanisms in concert including:

      1. Improvement in drug’s solubility
      2. Reduced intra-enterocyte metabolism by CYP P450 enzymes
      3. Reduced P-glycoprotein (P-gp) efflux activity
      4. Reduced hepatic first-pass metabolism bypass via lymphatic absorption


Self-Nano Emulsifying Drug Delivery Systems (SNEDDS) of THC and CBD with Piperine

To overcome these limitations advanced pro-nanolipospheres (PNL) formulation have been devised to improve delivery systems. One such method is comprised of a medium chain triglyceride, surfactants, a co-solvent and the unique addition of a natural absorption enhancer, piperine, a substance derived from black pepper. Piperine inhibits both Phase I and Phase II metabolism of these cannabinoids in the liver. This combination of ingredients self emulsifies the cannabinoids into nano particles that entrap the cannabinoids and the piperine in their core which improve their solubility and inhibits their intestinal metabolism while being safe for human consumption.

In a trial of a THC-CBD-piperine-PNL formulation involving 9 healthy volunteers under fasted conditions, subjects received a THC-CBD (10.8mg, 10mg respectively) and piperine (20mg) in a PNL filled capsule. As a compartor, an equivalent dose of THC-CBD (the oromucosal spray Sativex®) was provided to the subjects.  Single oral administration of the piperine-PNL formulation resulted in a 3-fold increase in Cmax and a 1.5-fold increase in AUC for THC when compared to Sativex®. For CBD, a 4-fold increase in Cmax and a 2.2-fold increase in AUC was observed. To summariz, self-emulsifying formulations have increased bioavailability and increased Cmax within a shorter time compared to oromucosal spray, demonstrating the potential for self emulsifying formulation to improving oral bioavailability of lipophilic compounds.



Transdermal Route

The steady-state blood concentrations of transdermal CBD maintain throughout 48 hours of gel application, starting to decline at about 6 hours after gel removal, indicating a skin reservoir effect in guinea pigs. The skin reservoir property of CBD is because of the high lipophilic property of the drug that makes it easier to cross the stratum corneum but makes it difficult to traverse through the aqueous dermis.

Because THC is more lipophilic than CBD, the skin reservoir effect is higher with THC, but steady-state blood concentrations of THC are lower than those achieved with CBD. With the use of the enhancer, CBD is delivered up to 3.7 times better than without, suggesting this would be the case with transdermal THC.


Half-Life of CBD (T-1/2)

The “half-life” (T-1/2) of a medication is the time it takes for blood levels to go down to half of a maximum level. It depends on the dose and route of administration. The half-life is shorter for smoked/vaped use and longer for sublingual/buccal and oral use. The half-life of CBD has been reported as short as 1.1 hours following vaping and between 1.4 and 10.9 hours after oromucosal spray. With chronic oral use, the half-life may be as long as  2-5 days. Overall, there is considerable variation of these times in different individuals.


Tissue Distribution of CBD

Minimal evidence of plasma accumulation has been reported by chronic dosing studies over 5–9 days. Like THC, CBD is rapidly and widely distributed from the blood into tissues into well-vascularized organs (e.g. brain, liver, lung, heart), with subsequent equilibration into less vascularized tissue. Also like THC, CBD preferentially accumulates in adipose (fat) tissues due to its high lipophilicity. Subsequent release and redistribution (such as weight loss) may allow persistence of cannabinoid activity or preence in the urine for several weeks after administration..


CBD Metabolism

CBD Metabolism

CBD metabolism is similar to that of THC, with primary hydroxylation to 7-hydroxy cannabidiol (7-OH-CBD), the major pharmacologically active metabolite which is further converted to the inactive metabolite 7-COOH-CBD. After this step there is further liver metabolism and subsequent fecal, and, to a lesser extent, urinary, excretion of the additional metabolites. Little is known about the pharmacological activity of the metabolites of CBD in humans.   


CBD is reportedly metabolized primarily by the liver enzymes CYP2C19 and CYP3A4, and additionally CYP1A1, CYP1A2, CYP2C9 and CYP2D6. A 2021 study concluded that both CYP2C19 and CYP2C9 are involved in CBD metabolism to the active metabolite 7-OH-CBD.  CYP2C19 enzyme activity in the formation of 7-OH-CBD  is not associated with CYP2C19 genetic variants (genotypes) which is consistent with factors besides CYP2C19 polymorphism influence CYP2C19 activity and CBD 7-hydroxylation. While CYP3A provides the greatest contribution to overall CBD clearance through other oxidative pathways, CYP3A does not contribute significantly to production of 7-OH-CBD. Metabolism also occurs in extra-hepatic tissues that have CYP450 enzymes, including the small intestine and brain.


CBD is a reversible inhibitor of CYP2C9 and a time-dependent inhibitor of CYP2C19, CYP3A, and CYP1A2. These activities may lead to clinically significant drug-drug interactions, including  hydrocodone, tizanidine (Zanaflex) – see below.



Both CYP2C19 and CYP2C9 are involved in CBD metabolism to the active metabolite 7-OH-CBD, but although CYP3A4 is the major contributor to CBD metabolism, it does so through pathways other than 7-hydroxylation. 7-OH-CBD formation is associated with CYP2C19 activity, but not CYP2C19 genotype, and CYP2C9 contributes significantly to 7-OH-CBD generation. These findings have implications for patients taking CBD, who may be at risk for clinically important CYP-mediated drug interactions.



Elimination of CBD and Metabolites

CBD and its metabolites are mostly excreted via the kidneys.


CBD and THC Metabolism

 It has been reported that CBD  inhibits THC metabolism but it is believed that the pharmacokinetics of THC are not meaningfully affected by CBD, except for a slight slowing of the metabolism of 11-OH- THC to THC-COOH. Co-administration of CBD does not significantly affect the total clearance, volume of distribution, or terminal elimination half-lives of THC or its metabolites.


Effects of Eating vs. Fasting on Oral intake of CBD

It has been determined that when THC or CBD are ingested on an empty stomach, their absorption into the blood is markedly reduced compared to ingesting on a full stomach. This effect is more pronounced with CBD than THC, with CBD absorbed as much as 4 times greater when ingested after a fatty meal compared with fasting, while THC is absorbed up to 3 times greater.



Metabolic Interactions with Other Drugs

A systematic review in 2014 concluded that CBD generally has a low risk of clinically significant drug-interactions, however, consideration should be noted when co-administering with other drugs using the CYP3A4. The major cannabinoids, THC and CBD are both metabolized in the liver by the CYP450 enzymes 2C9 and 3A4. Drugs that inhibit these enzymes may enhance or prolong the effects of THC and CBD. Whether people with genetic variants of these enzymes may experience altered effects from cannabinoids is not fully known. 

Metabolic Effects of Medications on CBD

CYP3A4 Inhibitors Effect on CBD

Treatment with CYP3A4 inhibitors such as ketoconazole can produce an increase in Cmax and AUC of CBD, with the increase in Cmax and AUC of the primary active metabolite of CBD increased 2- and 2-fold, respectively. Therefore, if concomitant drug treatment with CYP3A4 inhibitors (e.g. itraconazole, ritonavir, clarithromycin) is started or stopped during treatment with CBD, a dose adjustment may be required.


CYP3A4 Inducers Effect on CBD

Treatment with CYP3A4 inducers such as rifampicin can reduce the Cmax and AUC of CBD by 50% and 60%, respectively. Therefore, concomitant treatment with strong enzyme inducers (e.g. rifampicin, carbamazepine, phenytoin, phenobarbital, St John’s Wort) should be avoided whenever possible. Also, if concomitant drug treatment with CYP3A4 inducers (e.g. rifampicin, carbamazepine, phenytoin, phenobarbital, St John’s Wort) are started or stopped during treatment with CBD, a dose adjustment may be required within two weeks of starting or stopping the inducer.


Metabolic Effects of Cannabinoids on other Medications


CBD has been identified as a potent inhibitor of CYP2D6 which may have significant impact on the metabolism of medications that are broken down by CYP2D6, including hydrocodone (Norc0, Vicodin, Zohydro, Hysingla) and other opioids including tramadol and codeine. As such, use of CBD with tramadol, codeine or hydrocodone may significantly reduce the analgesic effectiveness of these opioids. Other common medications that may be affected include antidepressants.



CBD is also a potent inhibitor of CYP3A enzymes, especially CYP3A5. While CYP3A4 is the dominant CYP3A isoform in the metabolism of most drugs, some drugs such as diltiazem (Cardizem), are more efficiently metabolized by CYP3A5 than by CYP3A4. Also, CYP3A5 is a major isoform of CYP3A found in extrahepatic tissues that plays an important role in the metabolism of endogenous and exogenous compounds in these tissues. Thus, the inhibition of CYP3A5 by CBD may cause interactions with other medications and may also disturb normal metabolism of endogenous compounds. CBD was  also observed to be a potent inhibitor of CYP2C19 enzymes.


Since CBD is readily distributed in various tissues due to a high lipophilicity, tissue concentrations of CBD may be even higher than the blood concentration, suggesting that the inhibition of human CYP3A by CBD might be caused during and/or after marijuana smoking.


UGT1A9 and UGT2B7

Caution is also advised with concomitant use of CBD and substrates of UDP-glucuronosyltransferases UGT1A9 and UGT2B7. (?)




National Academy of Sciences

  1. The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research



This website appears to be good resource for exploring medical marijuana.




Medical Marijuana – Driving

  1. Establishing legal limits for driving under the influence of marijuana – 2014
  2. Medical Marijuana and Driving – a Review – 2014


Medical Marijuana – Opioids

  1. Impact of co-administration of oxycodone and smoked cannabis on analgesia and abuse liability. – PubMed – NCBI
  2. Cannabinoid–Opioid Interaction in Chronic Pain
  3. Synergistic interactions between cannabinoid and opioid analgesics. – PubMed – NCBI
  4. FDA approves CBD drug – Epidiolex – The Washi
    ngton Post

Medical Marijuana – Opioid Drug Interactions

  1. The Effect of CYP2D6 Drug-Drug Interactions on Hydrocodone Effectiveness – 2014
  2. Cannabidiol, a Major Phytocannabinoid, As a Potent Atypical Inhibitor for CYP2D6 – 2011
  3. Potent inhibition of human cytochrome P450 3A isoforms by cannabidiol. – Role of phenolic hydroxyl groups in the resorcinol moiety – 2011
  4. Interindividual variation in the pharmacokinetics of Delta9-tetrahydrocannabinol as related to genetic polymorphisms in CYP2C9. – PubMed – NCBI

Medical Marijuana – Pharmacokinetics

  1. Human Cannabinoid Pharmacokinetics – 2007
  2. A tale of two cannabinoids: the therapeutic rationale for combining tetrahydrocannabinol and cannabidiol. – PubMed – NCBI
  3. Cannabis and cannabis extracts – greater than the sum of their parts? – 2001
  4. Cannabinoids and Cytochrome P450 Interactions. – PubMed – NCBI
  5. Pharmacogenetics of Cannabinoids – 2018
  6. Adverse effects of medical cannabinoids – a systematic review – 2008
  7. Cannabimimetic effects modulated by cholinergic compounds. – PubMed – NCBI
  8. Antagonism of marihuana effects by indomethacin in humans. – PubMed – NCBI
  9. Pharmacokinetics and pharmacodynamics of cannabinoids. – PubMed – NCBI
  10. Clinical Pharmacodynamics of Cannabinoids – 2004
  11. Quality Control of Traditional Cannabis Tinctures – Pattern, Markers, and Stability – 2016
  12. Exogenous cannabinoids as substrates, inhibitors, and inducers of human drug metabolizing enzymes: a systematic review. – PubMed – NCBI
  13. Pharmacology of Cannabinoids
  14. The Cannabis sativa Versus Cannabis indica Debate – An Interview with Ethan Russo, MD – 2016
  15. Human Metabolites of Cannabidiol – A Review on Their Formation, Biological Activity, and Relevance in Therapy 2016
  16.  A Comprehensive Review on Pharmacotherapeutics of Herbal Bioenhancers – 2012
  17. The effects of black pepper on the intestinal absorption and hepatic metabolism of drugs. – PubMed – NCBI – 2011
  18. Piperine-pro-nanolipospheres as a novel oral delivery system of cannabinoids: Pharmacokinetic evaluation in healthy volunteers in comparison to buc… – PubMed – NCBI – 2017
  19. A Systematic Review on the Pharmacokinetics of Cannabidiol in Humans
  20. Clinical_Pharmacokinetics_of_Cannabinoids
  21. Δ9-Tetrahydrocannabinol (THC), 11-Hydroxy-THC, and 11-Nor-9-carboxy-THC Plasma Pharmacokinetics during and after Continuous High-Dose Oral THC – 2009
  22. MARINOL® (Dronabinol) product info – 2017
  23. Pharmacokinetics and pharmacodynamics of cannabinoids. – 2018
  24. Cannabidiol bioavailability after nasal and transdermal application – effect of permeation enhancers – 2010
  25. Serum cannabidiol, tetrahydrocannabinol (THC), and their native acid derivatives after transdermal application of a low-THC Cannabis sativa extract in beagles – PubMed – 2020
  26. Human skin permeation of Delta8-tetrahydrocannabinol, cannabidiol and cannabinol – PubMed – 2004
  27. Human Pharmacokinetic Parameters of Orally Administered Δ 9-Tetrahydrocannabinol Capsules Are Altered by Fed Versus Fasted Conditions and Sex Differences – PubMed
  28. Heat exposure of Cannabis sativa extracts affects the pharmacokinetic and metabolic profile in healthy male subjects – PubMed – 2012
  29. Effect of food on the pharmacokinetics of dronabinol oral solution versus dronabinol capsules in healthy volunteers – 2017
  30. Cytochrome P450-Catalyzed Metabolism of Cannabidiol to the Active Metabolite 7-Hydroxy-Cannabidiol – 2020


Cannabidiol (CBD) – Pharmacokinetics

  1. Human Cannabinoid Pharmacokinetics – 2007
  2. A tale of two cannabinoids: the therapeutic rationale for combining tetrahydrocannabinol and cannabidiol. – PubMed – NCBI
  3. Human Metabolites of Cannabidiol – A Review on Their Formation, Biological Activity, and Relevance in Therapy 2016
  4.  A Comprehensive Review on Pharmacotherapeutics of Herbal Bioenhancers – 2012
  5. The effects of black pepper on the intestinal absorption and hepatic metabolism of drugs. – PubMed – NCBI – 2011
  6. Piperine-pro-nanolipospheres as a novel oral delivery system of cannabinoids: Pharmacokinetic evaluation in healthy volunteers in comparison to buc… – PubMed – NCBI – 2017
  7. A Systematic Review on the Pharmacokinetics of Cannabidiol in Humans
  8. Heat exposure of Cannabis sativa extracts affects the pharmacokinetic and metabolic profile in healthy male subjects – PubMed – 2012
  9. Serum cannabidiol, tetrahydrocannabinol (THC), and their native acid derivatives after transdermal application of a low-THC Cannabis sativa extract in beagles – PubMed – 2020
  10. Human skin permeation of Delta8-tetrahydrocannabinol, cannabidiol and cannabinol – PubMed – 2004
  11. Cytochrome P450-Catalyzed Metabolism of Cannabidiol to the Active Metabolite 7-Hydroxy-Cannabidiol – 2020
  12. Pharmacokinetics and pharmacodynamics of cannabinoids. – 2018
  13. Serum cannabidiol, tetrahydrocannabinol (THC), and their native acid derivatives after transdermal application of a low-THC Cannabis sativa extract in beagles – PubMed – 2020
  14. The effect of Pro NanoLipospheres (PNL) formulation containing natural absorption enhancers on the oral bioavailability of delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) – PubMed – 2017
  15. The Effects of Food on Cannabidiol Bioaccessibility – 2021



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