Science

The Cannabis sativa L. plant is the botanical source of se•d8™. Selected strains of this plant produce hemp, legally defined by the U.S.D.A. as crops of Cannabis sativa L. naturally containing less than 0.3% by dry weight of delta-9-tetrahydrocannabinol (THC), the psychoactive component of marijuana.

The breadth and depth of cannabis use is well-documented beginning in 2700 B.C. with many references since as to its well-tolerated use, few adverse effects and positive clinical history in the worldwide literature involving a multitude of different cultures.1 The endogenous cannabinoid system in animals and humans is of major physiological and pharmacological significance. Natural to us as is our endorphin µ-opioid receptors responsible for narcotic (opium poppy plant) clinical responses, the endocannabinoid receptors (Cannabis sativa L.) are more varied and differentiated than originally postulated not being limited only to the two (CB1 and CB2) endocannabinoid receptors as to their clinical effect.

CBD is NOT a Scheduled I-V drug under the DEA Controlled Substances Act (CSA). Drug placement on the federal Controlled Substances Act is based upon the substance’s medical use, potential for abuse, safety and/or risk of dependence. Examples of scheduled drugs include narcotics, benzodiazepines, barbiturates and dissociative anesthetic drugs such as ketamine.

There have been no recorded deaths from cannabis use in over 5000 years even at recreational dose levels.2 This safety margin for overdose error starkly contrasts with the list of DEA Controlled Substance Act (CSA) scheduled drugs including opioids, benzodiazepines and dissociative drugs.

CBD can act as a neurotransmitter (agonist) within the central nervous system specifically including the 5-HT (seratonin) and GABA (gamma-aminobutyric acid). This mechanism of action may explain the documented anxiolysis (calming) effect of CBD in the management of situational anxiety acting via the GABA receptors as do the benzodiazepines such as midazolam, a DEA CSA Scheduled IV drug.

The precise molecular mechanism of action(s) of CBD is not well understood. CBD affects appear multi-faceted being linked to the inhibition of fatty acid amide hydrolase, inhibition of the reuptake of adenosine, agonism of transient receptor potential channels, antagonism of the orphan G-protein-coupled receptor GPR55, facilitation of 5-HT1A mediated neurotransmission and inhibition of inflammatory cytokines via action at receptors such as peroxisome proliferator-activated receptor gamma.

Unlike the psychotomimetic (e.g., dissociative side effects including dysphoria, agitation, hallucinations or anxiety) and sympathomimetic (e.g., tachycardia, hypertension) effects of ketamine, a DEA CSA Schedule III drug, CBD has no psychoactive or cardiac side effects at proposed therapeutic dose levels.

The analgesic effect of non-THC cannabinoids was recently and elegantly demonstrated by a British anesthesiology article on a patient who clinically presented as perceiving little to no pain throughout her life. After a diagnostic workup at the University College of London, the woman was shown to have two gene mutations (FAAH and FAAH-OUT) which reduced the rate of the enzymatic breakdown of the natural endocannabinoid neurotransmitter, anandamide (arachidonoylethanolamide), which helps provide pain relief similar in effect to our natural endorphins acting on the µ-opioid receptors. As a result of persisting elevated levels of anandamide, the patient perceived minimal pain as did her daughter.

It is now widely accepted that THC concentrations between 0.3% and 1.0% by dry weight have no discernable clinical central nervous affect. JOS Pharmaceuticals nevertheless removes all naturally occurring THC less than the legally required 0.3% to non-detectable levels by standard laboratory measurement.

Although non-THC cannabinoids have been studied for years in the scientific literature, rigorous studies of the actual pharmacokinetics (PK) and pharmacodynamics (PD) as related to efficacy in humans have lagged historically because of the difficulty of obtaining cannabis biomass for research in the United States until very recently.

Academic review articles, however, have established the safety of non-THC cannabinoids in humans at doses of less than 150mg/day in an adult.3 The efficacy of CBD as to the management of pain and anxiety in humans has been widely confirmed in Europe, Israel and Canada in the academic, scientific and medical literature.4

It is estimated that 33% of U.S. adults have taken or are currently taking CBD for joint pain and discomfort. However, among these same individuals, many continue to be wary of the quality of marketed CBD product presently available to them. It is estimated that half of all adults currently taking CBD have increased their use during the COVID-19 pandemic presumably because of increased anxiety.

The se•d8™ wafer is a new and superior premedication for medical procedures performed under awake conscious sedation. The addiction, abuse, overdose deaths and criminal diversion of both opioids (often fentanyl, a DEA Schedule II drug) and benzodiazepines over the past two decades demand the immediate and concerted reduction in their prescriptive clinical use including as an anesthetic premedication. Furthermore, the clinical risk of the potential induction of an unintended, potentially harmful, dissociative mental state by ketamine used as a premedication should not be lightly dismissed.

Numerous advantages accrue as to the potential use of se•d8™ CBD as a prescription-only, anesthetic premedication including (1) cannabidiol is not a DEA CSA scheduled drug, (2) cannabidiol is a natural derivative of certified hemp and not a synthetic drug, (3) cannabidiol is not a cardiac stimulant raising heart rate and/or blood pressure (potentially dangerous in the older age groups) unlike ketamine, (4) cannabidiol is non-addictive at therapeutic doses, (5) cannabidiol is not a dissociative drug, (6) cannabidiol is an analgesic, (7) cannabidiol is an anxiolytic, (8) cannabidiol with Zydis™ wafer technology, allows efficient and accurate delivery, making it easily titratable for an individualized, rapid clinical effect, (9) cannabidiol is safe, (10) cannabidiol is an anti-inflammatory and (11) the projected patient cost should be much less than current anesthetic premedication including oral midazolam and/or ketamine.

In summary, CBD offers multiple potential opportunities for transformative therapeutic interventions for a variety of indications which only now are being explored and confirmed by new medical and pharmacology research.

1 Pertwee, Roger G., Handbook of Cannabis, (Oxford University Press, 2014), pages 23-29.
2 Ibid., page 424.
3 Australian TGA, Safety of Low Dose Cannabidiol, Version 1, April 2020.
4 Shannon, Scott et al, Cannabidiol for Anxiety and Sleep, A Large Case Study, PubMed 30624194.

Cannabis has been in use since 2700 B.C.

No recorded deaths from Cannabis use in over 5000 years.

No psychoactive or cardiac side effects.

Analgesia and Anxiolysis.

Anti-Emetic and Anti-Inflammatory.

Safe, Convenient and No I.V.

Cannabis has been in use since 2700 B.C.

The breadth and depth of cannabis use is well-documented beginning in 2700 B.C. with many references since as to its well-tolerated use, few adverse effects and positive clinical history in the worldwide literature involving a multitude of different cultures.1 The endogenous cannabinoid system in animals and humans is of major physiological and pharmacological significance. Natural to us as is our endorphin µ-opioid receptors responsible for narcotic (opium poppy plant) clinical responses, the endocannabinoid receptors (Cannabis sativa L.) are more varied and differentiated than originally postulated not being limited only to the two (CB1 and CB2) endocannabinoid receptors as to their clinical effect.

CBD is NOT a Scheduled I-V drug under the DEA Controlled Substances Act (CSA). Drug placement on the federal Controlled Substances Act is based upon the substance’s medical use, potential for abuse, safety and/or risk of dependence. Examples of scheduled drugs include narcotics, benzodiazepines, barbiturates and dissociative anesthetic drugs such as ketamine.

No recorded deaths from Cannabis use in over 5000 years.

There have been no recorded deaths from cannabis use in over 5000 years even at recreational dose levels.2 This safety margin for overdose error starkly contrasts with the list of DEA Controlled Substance Act (CSA) scheduled drugs including opioids, benzodiazepines and dissociative drugs.

Analgesia and Anxiolysis.

CBD can act as a neurotransmitter (agonist) within the central nervous system specifically including the 5-HT (seratonin) and GABA (gamma-aminobutyric acid). This mechanism of action may explain the documented anxiolysis (calming) effect of CBD in the management of situational anxiety acting via the GABA receptors as do the benzodiazepines such as midazolam, a DEA CSA Scheduled IV drug.

The precise molecular mechanism of action(s) of CBD is not well understood. CBD affects appear multi-faceted being linked to the inhibition of fatty acid amide hydrolase, inhibition of the reuptake of adenosine, agonism of transient receptor potential channels, antagonism of the orphan G-protein-coupled receptor GPR55, facilitation of 5-HT1A mediated neurotransmission and inhibition of inflammatory cytokines via action at receptors such as peroxisome proliferator-activated receptor gamma.

No psychoactive or cardiac side effects.

Unlike the psychotomimetic (e.g., dissociative side effects including dysphoria, agitation, hallucinations or anxiety) and sympathomimetic (e.g., tachycardia, hypertension) effects of ketamine, a DEA CSA Schedule III drug, CBD has no psychoactive or cardiac side effects at proposed therapeutic dose levels.

The analgesic effect of non-THC cannabinoids was recently and elegantly demonstrated by a British anesthesiology article on a patient who clinically presented as perceiving little to no pain throughout her life. After a diagnostic workup at the University College of London, the woman was shown to have two gene mutations (FAAH and FAAH-OUT) which reduced the rate of the enzymatic breakdown of the natural endocannabinoid neurotransmitter, anandamide (arachidonoylethanolamide), which helps provide pain relief similar in effect to our natural endorphins acting on the µ-opioid receptors. As a result of persisting elevated levels of anandamide, the patient perceived minimal pain as did her daughter.

It is now widely accepted that THC concentrations between 0.3% and 1.0% by dry weight have no discernable clinical central nervous affect. JOS Pharmaceuticals nevertheless removes all naturally occurring THC less than the legally required 0.3% to non-detectable levels by standard laboratory measurement.

Although non-THC cannabinoids have been studied for years in the scientific literature, rigorous studies of the actual pharmacokinetics (PK) and pharmacodynamics (PD) as related to efficacy in humans have lagged historically because of the difficulty of obtaining cannabis biomass for research in the United States until very recently.

Academic review articles, however, have established the safety of non-THC cannabinoids in humans at doses of less than 150mg/day in an adult.3 The efficacy of CBD as to the management of pain and anxiety in humans has been widely confirmed in Europe, Israel and Canada in the academic, scientific and medical literature.4

Anti-Emetic and Anti-Inflammatory.

It is estimated that 33% of U.S. adults have taken or are currently taking CBD for joint pain and discomfort. However, among these same individuals, many continue to be wary of the quality of marketed CBD product presently available to them. It is estimated that half of all adults currently taking CBD have increased their use during the COVID-19 pandemic presumably because of increased anxiety.

Safe, Convenient and no I.V.

The se•d8™ wafer is a new and superior premedication for medical procedures performed under awake conscious sedation. The addiction, abuse, overdose deaths and criminal diversion of both opioids (often fentanyl, a DEA Schedule II drug) and benzodiazepines over the past two decades demand the immediate and concerted reduction in their prescriptive clinical use including as an anesthetic premedication. Furthermore, the clinical risk of the potential induction of an unintended, potentially harmful, dissociative mental state by ketamine used as a premedication should not be lightly dismissed.

Numerous advantages accrue as to the potential use of se•d8™ CBD as a prescription-only, anesthetic premedication including (1) cannabidiol is not a DEA CSA scheduled drug, (2) cannabidiol is a natural derivative of certified hemp and not a synthetic drug, (3) cannabidiol is not a cardiac stimulant raising heart rate and/or blood pressure (potentially dangerous in the older age groups) unlike ketamine, (4) cannabidiol is non-addictive at therapeutic doses, (5) cannabidiol is not a dissociative drug, (6) cannabidiol is an analgesic, (7) cannabidiol is an anxiolytic, (8) cannabidiol with Zydis™ wafer technology, allows efficient and accurate delivery, making it easily titratable for an individualized, rapid clinical effect, (9) cannabidiol is safe, (10) cannabidiol is an anti-inflammatory and (11) the projected patient cost should be much less than current anesthetic premedication including oral midazolam and/or ketamine.

In summary, CBD offers multiple potential opportunities for transformative therapeutic interventions for a variety of indications which only now are being explored and confirmed by new medical and pharmacology research.

1 Pertwee, Roger G., Handbook of Cannabis, (Oxford University Press, 2014), pages 23-29.
2 Ibid., page 424.
3 Australian TGA, Safety of Low Dose Cannabidiol, Version 1, April 2020.
4 Shannon, Scott et al, Cannabidiol for Anxiety and Sleep, A Large Case Study, PubMed 30624194.