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  • RSHO-Gold™ HempMeds Px LLC


    DIETARY SUPPLEMENT

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    RSHO-Gold™
    HempMeds Px LLC

    CLASSES

    Dietary Supplement prepared from the industrial hemp oil.

    PRODUCT DESCRIPTION

    RSHO-Gold™ (manufactured and distributed by HempMeds Px LLC) also known as Pure-Gold™ (manufactured and distributed by affiliated company - Kannaway LLC) is a proprietary product made exclusively from industrial hemp oil. RSHO-Gold™ is rich in cannabidiol (CBD), other phyto-cannabinoids, terpenes and medium chain triglycerides (MCT).

    RSHO-Gold™ may be useful as an adjunctive supplement to support healthy immune response and homeostasis, promote and maintain healthy mood, energy, sleep, pain response possibly via the modulation of endocannabinoid system (ESC), which is known as a vital factor in the regulation of homeostasis, symptomatic relief and overall metabolic functions.

    Disclaimer: "This statement has not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease."

    COMMON BRAND NAMES

    • RSHO-Gold™ (manufactured and distributed by HempMeds Px LLC)
    • Pure-Gold™ (manufactured and distributed by affiliated company - Kannaway LLC).

    HOW SUPPLIED

    RSHO-Gold™ is an oil tincture for oral and sublingual Administration.

    RSHO-Gold™ is contained in an amber glass bottle covered with a polyethylene cap. Each bottle contains 118 mL of a clear, colorless to yellow solution of industrial hemp oil with a cannabidiol content at 8.5 to 9.0 mg/mL. The product doesn't contain any measurable amounts of psychotropic Δ9-tetra-hydro-cannabinol (THC).

    Non-medicinal ingredients: MCT coconut oil

    INGREDIENTS AND SUPPLEMENT FACTS

    Suggested Serving Size: ¾ tps
    Servings per container: Approx. 32
    Amount per Serving % DV
    % Daily Values are based on a 2,000 calorie diet
    *
    Daily Value not established
    Cannabidiol (CBD) from stalk of hemp plant 31 mg *
    Medium Chain Triglycerides 3 g *
    Sugar 0 mg 0%

    DOSE RECOMENDATION

    Dosing Considerations

    RSHO-Gold™ is for oral and/or sublingual use only. The dropper should be directed to below the tongue. It must not be applied into the nose. It is recommended to keep the administered sublingual dose in mouth (sublingual or buccal space) for 0.5 min or longer before the dose is swallowed.

    The dosage of RSHO-Gold™ will depend on the nature of the desired health benefit. As an antioxidant RSHO-Gold™ may be effective at any dose. In order to have measurable wellness and beneficial physiologic effects, the daily intake should be at least around 30 mg (calculated based on CBD content) and then increased gradually according to the tolerance and achieved beneficial effects.

    Dosage should be adjusted as needed and tolerated. Some individuals may require and may tolerate a higher number of doses. Individual should titrate to their optimal dosing regimen. They should be advised that it might take a few weeks to find the optimal dosing level.

    Treatment initiation and stabilization

    • Treatment should be started at 0.4-0.5 mg/kg (~30 mg total cannabidiol, i.e. one serving, for the subject with average body weight of 75 kg) on the first day of the first week.
    • On subsequent 2-3 weeks patient may gradually increase the dose as tolerated.
    • If unacceptable adverse reactions such as dizziness or other type reactions develop at any time, dosing should be suspended until symptoms are relieved.
    • Some individuals may be able to continue dosing at the dose reached by increasing the interval between doses; others may require their subsequent doses reduced. Individuals should then carefully re-titrate the dose to a tolerated dosage regimen.
    • Re-titration of RSHO-Gold™ dose upwards or downwards may be appropriate if there are any changes in the tolerability.

    Missed Dose

    Preferably, individual should control their daily doses of RSHO-Gold™. In case of missed dose, individuals should follow with the next dose in their dose regimen.

    Over dosage

    There is no recorded experience of deliberate overdose with RSHO-Gold™.

    CONSIDERATIONS AND PRECAUTIONS

    Despite of a good safety profile of CBD in humans [1-11, 15], RSHO-Gold™ should not be recommended for:

    • individuals with known or suspected allergy to cannabidiol or coconut oil
    • individuals with significant hepatic or renal impairment
    • pregnant or nursing women
    • Pediatrics: The safety and efficacy of RSHO-Gold™ has not been established in adolescents or children under 18 years of age. Therefore, parents and caregivers need to seek their doctor's advice whether RSHO-Gold™ can be consumed by adolescents or children.
    • Geriatrics: There are limited data available on the use of cannabidiol in elderly patients, therefore, RSHO-Gold™ should be recommended cautiously and carefully monitored in this patient population.

    STORAGE

    RSHO-Gold™ should not be used beyond its expiry date. RSHO-Gold™ should be stored upright in original container at room temperature (15°C-25°C), away from sources of heat and direct sunlight. Once opened, RSHO-Gold™ should be stored in a refrigerator (2°C-8°C).

    DRUG INTERACTIONS

    RSHO-Gold™ has been consumed by adult individuals taking conventional pharmaceutical medications at the same time. No information from spontaneous reporting is available on any interactions resulting from simultaneous intake of conventional medicines with RSHO-Gold™.

    However, since the cannabidiol (CBD) is the major ingredient of RSHO-Gold™ there may be minor drug-drug interactions due to well-known CBD driven CYP450 inhibition and induction. CBD showed to be a weak inhibitor of CYP1A2, CYP2C6, CYP2D6, CYP2C19 and CYP3A4 with an EC50 approximately two orders of magnitude greater than the plasma levels seen in clinical use [1, 2].

    In preclinical studies with P-gp, BCRP, and P-gp/BCRP knockout mice, where CBD at 10 mg/kg was injected subcutaneously, showed that CBD is not a substrate of these transporters itself.

    CBD is highly bound to human plasma proteins. Although this displacement has not been confirmed in vivo, the dosing should be carefully monitored when administering RSHO-Gold™ to patients who are receiving other drugs which are tightly protein-bound, such as warfarin and diclofenac [1, 2].

    FOOD AND HERB INTERACTIONS

    No interactions with food or herbs have been established.

    MECHANISM OF ACTION

    There are two main cannabinoid (CB) receptors, CB1 which is primarily located in the central nervous system with some expression in peripheral tissues and CB2 receptors, which can be found in the periphery on cells with immune function and in the gastrointestinal tract and at low densities in the central nervous system [2-5].

    CBD does not appear to act directly at CB1 receptors, with a number of studies reporting that there is no measurable response in binding assays. In studies examining potential agonist effects at CB1 receptors, most find no effect, with one report of a weak agonist and one of a weak antagonist effect, each at high concentrations (>10 µM). CBD also shows low affinity at CB2 receptors [2-10]. Across a range of measures in humans and animals, CBD had been shown to have very different effects from those of THC. In mice, CBD failed to produce the behavioral characteristics (e.g. suppression of locomotor activity, hypothermia, anti-nociception) associated with CB1 activation, whereas THC generated all of the effects which occur when CB1 is activated. Neuroimaging studies in humans and animals have shown that CBD has effects which are generally opposite to those of THC. In contrast to THC, CBD has no effect on heart rate or blood pressure under normal conditions, but in animal models of stress it reduces heart rate and blood pressure. Other differences between THC and CBD are discussed below [6-9, 11-10].

    Some studies have shown that CBD may reduce or antagonize some of the effects of THC. The mechanism for this is unclear, with some suggesting that it may be a weak CB1 antagonist. Recent evidence suggests that it may be a negative allosteric modulator of the CB1 receptor, thereby acting as a noncompetitive antagonist of the actions of THC and other CB1 agonists [2- 17].

    CBD may also interact with the endocannabinoid system through indirect mechanisms such as enhanced action of the endogenous cannabinoid ligand anandamide [17, 18]. This results from blockade of anandamide reuptake and the inhibition of its enzymatic degradation. CBD has been shown to modulate several non-endocannabinoid signaling systems. It is not clear which, if any, of these mechanisms are responsible for any of CBD's potential clinical or other effects. Some of these mechanisms include:

    • Inhibition of adenosine uptake, possibly resulting in indirect agonist activity at adenosine receptors.
    • Enhanced activity at the 5-HT1a receptor.
    • Enhanced activity at a glycine receptor subtype.
    • Enhanced activity at the peroxisome proliferator-activated receptor (PPAR)
    • Agonist at the transient receptor potential channel vanilloid receptor (TRPV1)
    • Blockade of the orphan G-protein-coupled receptor GPR55 [3-11, 17,18].

    The principal pharmacological effects of CBD include analgesic, anti-convulsant, muscle relaxant, anxiolytic, neuroprotective, anti-oxidant (US Patent 6,630,507 hold by NIH), anti-inflammatory and anti-psychotic activity. The mechanisms by which the biological actions of endogenous cannabinoids are terminated, have not been fully evaluated. However, it appears likely that they are removed from the extracellular space by tissue uptake and that intracellular metabolism via an enzyme system, fatty acid amide hydrolase (FAAH), is also involved [20-21].

    PHARMACOKINETICS IN HUMAN

    Although human pharmacokinetic studies with RSHO-Gold™ have not been performed yet, there exists sufficient published information on CBD (the major bio-active cannabinoid of RSHO-Gold™) to allow an assessment of the pharmacokinetic profile of RSHO-Gold™ in human.

    Limited single dose pharmacokinetic data obtained from the human healthy volunteers following a under the tongue administration of EPIDIOLEX®, an oral formulation containing CBD at 100 mg/mL.

    Absorption and Distribution

    Due to its poor aqueous solubility, the absorption of CBD from the gastrointestinal tract is erratic, and the resulting pharmacokinetic profile is variable. Bioavailability from oral delivery was estimated to be 6% due to significant first-pass metabolism. Bioavailability (%F) from oral-mucosal and sublingual routes are less variable, but similar to oral delivery.

    Following a daily administration of CBD 10 mg/kg in 15 neuroleptic-free patients for 6 weeks, a mean CBD plasma level ranging from 5.9–11 ng/ml. CBD is rapidly distributed into the tissues with a high volume of distribution of ~32 L/kg. It may preferentially accumulate in adipose tissues due to its high lipophilicity. It is highly bound to plasma proteins and red blood cells. The release of CBD from fatty tissue is responsible for the prolonged terminal elimination half-life [1,2, 12, 13, 19-21].

    Metabolism and Excretion

    CBD is extensively metabolized in the liver [7]. The primary route is hydroxylation to 7-OH-CBD which is then metabolized further resulting in a number of metabolites that are excreted in feces and urine. Seven human CYP450 enzymes were identified as capable of metabolizing CBD: CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5. The two main isoforms involved are CYP3A4 and CYP2C19. CBD undergoes CYP3A- and CYP2Cdependent phase I metabolism to 7-hydroxy-CBD, which is further metabolized into 7-COOH-CBD and its glucuronide conjugated phase II metabolites and excreted, more in feces and to a lesser extent in urine. In a number of studies, CBD has been shown to inhibit CYP isozymes in vitro, but it is not clear that this occurs at concentrations achieved with doses used clinically. CBD has an estimated terminal half-life of 18–32 hours and a clearance of 57.6–93.6 L/hour [1,2, 11, 12].

    MANUFACTURING INFORMATION

    Production and Control Information

    RSHO-Gold™ is made from the non-genetically modified (non-GMO) cultivars of hemp grown in Europe. Only certified seeds of approved low-THC fiber hemp of the EU variety list are used for the cultivation of hemp for the extraction of CBD enriched oil. The hemp is cultivated and comply with the high internal quality standards, required for the cultivation of the medicinal plants. Farming facilities hold a special permit for the cultivation of hemp, issued by the authorities.

    Botanical Raw Material

    The hemp plants originate exclusively from pesticide and chemical fertilizer free farming. Harvesting takes place at the time of the hemp plants' highest quality shortly before flowering, observing hygienic standards which are comparable to high requirements for medicinal plants. At the time of harvest a variety verification is conducted by the authority to ensure that the cultivated variety of hemp corresponds to the one registered at the authority. Only the high-quality plants are used for producing hemp oil. A comprehensive quality control of the harvest is carried out upon arrival at the extracting facility. The content of CBD and other cannabinoids as well as other plant substances is analyzed and thoroughly documented. In addition to that, each batch is tested for conceivable germ or contaminant loads and is only accepted if it meets the strict requirements. The dried harvest is stored in purpose-designed, modern warehouses in compliance with the storage of medicinal plants according to the principles of Good Manufacturing Practice (GMP). Temperature and humidity are constantly monitored.

    Manufacturing of Botanical Substance

    All extraction processes of the hemp oil meet the strict requirements of the GMP in the pharmaceutical industry. CBD oil is extracted from the grinded fibrous stalk parts of the hemp plant by supercritical CO2 fluid technique (SFT) utilizing liquefied CO2 as an extracting solvent. The extraction process parameters are optimized for the higher CBD yield. The extracted CBD oil is subjected to heat aided decarboxylation and filtering steps.

    Manufacturing of Finished Product RSHO-Gold™

    As a final formulation step, decarboxylated and filtered hemp oil was diluted with the medium chain triglyceride (MCT) coconut oil (vehicle) to achieve a predetermined final concentration of CBD and terpenes. The final formulation is subjected to the analytical testing to verify the concentration of CBD, other cannabinoids and terpenes, as well as the metals, pesticides, microbes and organic solvents by convergence chromatography, head-space gas chromatography, ISO/IEC-17025, Liquid chromatography with mass spectrometry, respectively. The analytical testing is performed by independent qualified and certified analytical laboratory. The analysis results are documented in a corresponding Certificate of Analysis.

    CLINICAL TRIALS

    The efficacy of RSHO-Gold™ was not evaluated in clinical trials yet.

    REFERENCES

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    Ujva´ry,I, Hanus,L. Human metabolites of cannabidiol: a review on their formation, biological activity and relevance in therapy. Cannabis and Cannabinoid Research. 2016, 1(1), 90-101.
    2.
    Fasinu, P.S.; Phillips, S.; El Sohly, M.A.; Walker, L.A. Current status and prospects for cannabidiol preparations as new therapeutic agents. Pharmacotherapy 2016, 36 (7), 781– 796.
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    Pertwee, R.G. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-Tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin. Br. J. Pharmacol. 2008, 153, 199–215.
    4.
    Ryberg, E.; Larsson, N.; Sjögren, S.; Hjorth, S.; Hermansson, N.O.; Leonova, J.; Elebring, T.; Nilsson, K.; Drmota, T.; Greasley, P.J. The orphan receptor GPR55 is a novel cannabinoid receptor. Br. J. Pharmacol. 2007, 152, 1092–1101.
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    Mechoulam R, Peters M, Murillo-Rodriguez E, Hanus L. Cannabidiol--recent advances. Chem Biodivers. 2007, 4(8):1678-92.
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    Ross, H.R.; Napier, I.; Connor, M. Inhibition of recombinant human T-type calcium channels by Delta9-tetrahydrocannabinol and cannabidiol. J. Biol. Chem. 2008, 283, 16124–16134.
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    Massi, P.; Valenti, M.; Vaccani, A.; Gasperi, V.; Perletti, G.; Marras, E.; Fezza, F.; Maccarrone, M.; Parolaro, D. 5-Lipoxygenase and anandamide hydrolase (FAAH) mediate the antitumor activity of cannabidiol, a non-psychoactive cannabinoid. J. Neurochem. 2008, 104, 1091– 1100.
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    de Petrocellis, L.; di Marzo, V. Non-CB1, non-CB2 receptors for endocannabinoids, plant cannabinoids, and synthetic cannabimimetics: Focus on G-protein-coupled receptors and transient receptor potential channels. J. Neuroimmune Pharmacol. 2010, 5, 103–121.
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    Hampson AJ1, Grimaldi M, Axelrod J, Wink D. Cannabidiol and (-) Delta9-tetrahydrocannabinol are neuroprotective antioxidants. Proc Natl Acad Sci. 1998, 7; 95(14), p.8268- 73.
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    Morales P., Hurst D.P., Reggio P.H. Molecular Targets of the Phytocannabinoids - A Complex Picture. Prog. Chem. Org. Nat Prod. 2017; 103: 103–131.
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    Cannabidiol (CBD). Pre-Review Report. Agenda Item 5.2 Expert Committee on Drug Dependence, Thirty-Ninth Meeting. World Health Organization, Geneva, 6-10 November 2017.
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    Iffland, K; Grotenhermen, F. An update on safety and side effects of cannabidiol: a review of clinical data and relevant animal studies. Cannabis and Cannabinoid Research. 2017, 2 (1), 139-154.
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    Cunha J, Carlini EA, Pereira AE, et al. Chronic administration of cannabidiol to healthy volunteers and epileptic patients. Pharmacology. 1980; 21:175–185.
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    Aguirre-Velázquez, C. Report from a Survey of Parents Regarding the Use of Cannabidiol (Medicinal cannabis) in Mexican Children with Refractory Epilepsy. Neurology Research International, 2017, Article ID 2985729, p. 1-5.
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    Garza-Morales, S., Benavides-Aguilar, O and Bastida-Mercado, E. Efficacy and tolerability of add-on cannabidiol (RSHO-X™) in patients with the refractory Lennox-Gastaut Syndrome epileptic seizures: An open label observational study. Seizure – Eur. J. Epilepsy. 2018. Submitted.
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    PRODUCT PHOTO

    NOTE: These photos can be used only for identification by shape, color, and imprint. They do not depict actual or relative size.

    The product samples shown here have been supplied by the manufacturer and reproduced in full color by PDR as a quick-reference identification aid. While every effort has been made to assure accurate reproduction, please remember that any visual identification should be considered preliminary. In cases of poisoning or suspected over dosage, the drug's identity should be verified by chemical analysis.

    Image from Drug Label Content

    Image from Drug Label Content