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2003 The on 7, holds Government CBD Oct the US patent

Panther
30.05.2018

Content:

  • 2003 The on 7, holds Government CBD Oct the US patent
  • US6630507B1 - Cannabinoids as antioxidants and neuroprotectants - Google Patents
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  • 6,, Why the U.S. government holds a patent on cannabis plant compounds PUBLISHED: August 28, at am | UPDATED: October 2, at pm 6,,, granted in to the U.S. Department of Health and Human Services and covering the potential use of non-psychoactive cannabinoids to. Some of the research on these antagonists has focused on cannabinoids, U.S. Pat. No. 5,, (3S,4S-deltatetrahydrocannabinoloic acids), U.S. Pat. The Government Of The United States Of America As. On the other, the government actually holds patents for the medical use of the plant. By Michael Billy Jul 7, in Politics. On the Just check out US Patent titled "Cannabinoids as The patent was obtained in October of

    2003 The on 7, holds Government CBD Oct the US patent

    Hence in spite of its potential use in treating glaucoma and seizures, cannabidiol has not been considered a neuroprotective agent that could be used to prevent glutamate induced damage in the central nervous system. It is an object of this invention to provide a new class of antioxidant drugs, that have particular application as neuroprotectants, although they are generally useful in the treatment of many oxidation associated diseases.

    Yet another object of the invention is to provide a subset of such drugs that can be substantially free of psychoactive or psychotoxic effects, are substantially non-toxic even at very high doses, and have good tissue penetration, for example crossing the blood brain barrier. It has surprisingly been found that cannabidiol and other cannabinoids can function as neuroprotectants, even though they lack NMDA receptor antagonist activity.

    This discovery was made possible because of the inventor's recognition of a previously unanticipated antioxidant property of the cannabinoids in general and cannabidiol in particular that functions completely independently of antagonism at the NMDA, AMPA and kainate receptors. Hence the present invention includes methods of preventing or treating diseases caused by oxidative stress, such as neuronal hypoxia, by administering a prophylactic or therapeutically effective amount of a cannabinoid to a subject who has a disease caused by oxidative stress.

    The cannabinoid may be a cannabinoid other than THC, HU, or other potent cannabinoid receptor agonists. The cannabinoid may also be other than HU or any other NMDA receptor antagonist that has previously been reported. A potent cannabinoid receptor agonist is one that has an EC 50 at the cannabinoid receptor of 50 nM or less, but in more particular embodiments nM or nM or less.

    In disclosed embodiments the cannabinoid is not psychoactive, and is not psychotoxic even at high doses. In some particularly disclosed embodiments, the cannabinoid is selected from the group: In other embodiments, the cannabinoid is one of the following: The C ring is aromatic, and the B ring can be a pyran.

    Particular embodiments are dibenzo pyrans and cyclohexenyl benzenediols. This high lipid solubility enhances penetration of the drug into the CNS, as reflected by its volume of distribution V d of 1. Particular embodiments may also be highly water soluble derivatives that are able to penetrate the CNS, for example carboxyl derivatives. R are independently selected from the group of H, substituted or unsubstituted alkyl, especially lower alkyl, for example unsubstituted C 1 -C 3 alkyl, hydroxyl, alkoxy, especially lower alkoxy such as methoxy or ethoxy, substituted or unsubstituted alcohol, and unsubstituted or substituted carboxyl, for example COOH or COCH 3.

    In other embodiments R can also be substituted or unsubstituted amino, and halogen. In other particular embodiments, the cannabinoids are one of the following: In yet other embodiments of the invention, the cannabinoids are. Particular examples of nonpsychoactive cannabinoids that fall within this definition are cannabidiol and. In more particular embodiments, the cannabinoid is used to prevent or treat an ischemic or neurodegenerative disease in the central nervous system of a subject, by administering to the subject a therapeutically effective amount of a cannabinoid to protect against oxidative injury to the central nervous system.

    The cannabinoid may be any of the compounds set forth above, or more specifically. The invention also includes an assay for selecting a cannabinoid to use in treating a neurological disease by determining whether the cannabinoid is an antioxidant.

    Once it has been determined that the cannabinoid is an antioxidant, an antioxidant effective amount of the cannabinoid is administered to treat the neurological disease, such as a vascular ischemic event in the central nervous system, for example the type caused by a neurovascular thromboembolism. Similarly, the method of the present invention includes determining whether a disease is caused by oxidative stress, and if the disease is caused by oxidative stress, administering the cannabinoid in a therapeutically effective antioxidant amount.

    The invention also includes identifying and administering antioxidant and neuroprotective compounds such as cannabidiol which selectively inhibit the enzyme activity of both 5- and lipoxygenase more than the enzyme activity of lipoxygenase. In addition, such compounds posses low NMDA antagonist activity and low cannabinoid receptor activity.

    Assays for selecting compounds with the desired effect on lipoxygenase enzymes, and methods for using identified compounds to treat neurological or ischemic diseases are also provided. Such diseases may include a vascular ischemic event in the central nervous system, for example a thromboembolism in the brain, or a vascular ischemic event in the myocardium. Useful administration of the compounds involves administration both during and after an ischemic injury.

    These and other objects of the invention will be understood more clearly by reference to the following detailed description and drawings.

    The voltage at which initial peaks occur is an indication of antioxidant activity. This invention provides antioxidant compounds and compositions, such as pharmaceutical compositions, that include cannabinoids that act as free radical scavengers for use in prophylaxis and treatment of disease. The invention also includes methods for using the antioxidants in prevention and treatment of pathological conditions such as ischemia tissue hypoxia , and in subjects who have been exposed to oxidant inducing agents such as cancer chemotherapy, toxins, radiation, or other sources of oxidative stress.

    The compositions and methods described herein are also used for preventing oxidative damage in transplanted organs, for inhibiting reoxygenation injury following reperfusion of ischemic tissues for example in heart disease , and for any other condition that is mediated by oxidative or free radical mechanisms of injury.

    In particular embodiments of the invention, the compounds and compositions are used in the treatment of ischemic cardiovascular and neurovascular conditions, and neurodegenerative diseases. However the present invention can also be used as an antioxidant treatment in non-neurological diseases. Molecular oxygen is essential for aerobic organisms, where it participates in many biochemical reactions, including its role as the terminal electron acceptor in oxidative phosphorylation.

    However excessive concentrations of various forms of reactive oxygen species and other free radicals can have serious adverse biological consequences, including the peroxidation of membrane lipids, hydroxylation of nucleic acid bases, and the oxidation of sulfhydryl groups and other protein moieties. Biological antioxidants include tocopherols and tocotrieneols, carotenoids, quinones, bilirubin, ascorbic acid, uric acid, and metal binding proteins.

    However these endogenous antioxidant systems are often overwhelmed by pathological processes that allow permanent oxidative damage to occur to tissue. Free radicals are atoms, ions or molecules that contain an unpaired electron, are usually unstable, and exhibit short half-lives.

    Reactive oxygen species ROS is a collective term, designating the oxygen radicals e. The hydroxyl radical sets off chain reactions and can interact with nucleic acids. Increased production of these poisonous metabolites in certain pathological conditions is believed to cause cellular damage through the action of the highly reactive molecules on proteins, lipids and DNA. In particular, ROS are believed to accumulate when tissues are subjected to ischemia, particularly when followed by reperfusion.

    It is evident to those of skill in the art that most pathological conditions are multifactorial, and that assigning or identifying the predominant causal factors for any particular condition is frequently difficult. Oxidative associated diseases include, without limitation, free radical associated diseases, such as ischemia, ischemic reperfusion injury, inflammatory diseases, systemic lupus erythematosis, myocardial ischemia or infarction, cerebrovascular accidents such as a thromboembolic or hemorrhagic stroke that can lead to ischemia or an infarct in the brain, operative ischemia, traumatic hemorrhage for example a hypovolemic stroke that can lead to CNS hypoxia or anoxia , spinal cord trauma, Down's syndrome, Crohn's disease, autoimmune diseases e.

    The present invention is believed to be particularly beneficial in the treatment of oxidative associated diseases of the CNS, because of the ability of the cannabinoids to cross the blood brain barrier and exert their antioxidant effects in the brain. In particular embodiments, the pharmaceutical composition of the present invention is used for preventing, arresting, or treating neurological damage in Parkinson's disease, Alzheimer's disease and HIV dementia; autoimmune neurodegeneration of the type that can occur in encephalitis, and hypoxic or anoxic neuronal damage that can result from apnea, respiratory arrest or cardiac arrest, and anoxia caused by drowning, brain surgery or trauma such as concussion or spinal cord shock.

    Antioxidants can act by scavenging biologically important reactive free radicals or other reactive oxygen species. OH, HOCl, ferryl, peroxyl, peroxynitrite, and alkoxyl , or by preventing their formation, or by catalytically converting the free radical or other reactive oxygen species to a less reactive species. Relative antioxidant activity can be measured by cyclic voltametry studies of the type disclosed in Example 5 and FIG.

    The voltage at which the first peak occurs is an indication of the voltage at which an electron is donated, which in turn is an index of antioxidant activity. Since oxidative damage is generally cumulative, there is no minimum threshold level or dose with respect to efficacy.

    However, minimum doses for producing a detectable therapeutic or prophylactic effect for particular disease states can be established. Cannabinoids also include compounds that have a characteristic dibenzopyran ring structure of the type seen in THC and cannabinoids which do not possess a pyran ring such as cannabidiol.

    Many other cannabinoids are similarly disclosed in Agurell et al. Psychoactivity is not meant to include non-cannabinoid receptor mediated effects such as the anxiolytic effect of CBD. In the presence of a sufficient concentration of antagonist, an agonist cannot activate its receptor. When the receptor is activated for a longer than normal period of time, this may cause neurotoxicity, as in the case of NMDA, AMPA and kainate receptors see Examples 3 and 4.

    This term is further exemplified by groups such as methyl, ethyl, n-propyl, isobutyl, t-butyl, pentyl, pivalyl, heptyl, adamantyl, and cyclopentyl. Alkyl groups can either be unsubstituted or substituted with one or more substituents, e. This term is further exemplified by such radicals as methyl, ethyl, n-propyl, i-propyl, n-butyl, t-butyl, i-butyl or 2-methylpropyl , cyclopropylmethyl, i-amyl, n-amyl, hexyl and heptyl.

    Lower alkyl groups can also be unsubstituted or substituted, where a specific example of a substituted alkyl is 1,1-dimethyl heptyl.

    An alcohol may be either linear or branched, such as isopropyl alcohol. In an unsubstituted alkoxy, the R is an unsubstituted alkyl. Arylalkoxys are a subset of substituted alkoxys. Examples of useful substituted alkoxy groups are: A particular aryloxy group is phenoxy.

    HetAr is a heteroaryl group, and R is a straight-chain or branched chain aliphatic group. Example of arylaklyl groups include benzyl and furfuryl. Arylalkyl groups can optionally be unsubstituted or substituted with, e. A particular amino group is —NH 2.

    The following examples show that both nonpsychoactive cannabidiol, and psychoactive cannabinoids such as THC, can protect neurons from glutamate induced death, by a mechanism independent of cannabinoid receptors.

    Cannabinoids are also be shown to be potent antioxidants capable of preventing ROS toxicity in neurons. Dihydrorhodamine was supplied by Molecular Probes Eugene, Oreg. T-butyl hydroperoxide, tetraethylammonium chloride, ferric citrate and sodium dithionite were all purchased from Aldrich WI. Solutions of cannabinoids, cyclothiazide and other lipophiles were prepared by evaporating a 10 mM ethanolic solution under a stream of nitrogen in a siliconized microcentrifuge tube.

    Dimethyl sulfoxide DMSO, less than 0. After evaporation, 1 ml of culture media was added and the drug was dispersed using a high power sonic probe. Special attention was used to ensure the solution did not overheat or generate foam. Following dispersal, all solutions were made up to their final volume in siliconized glass tubes by mixing with an appropriate quantity of culture media.

    Primary neuronal cultures were prepared according to the method of Ventra et al. Fetuses were extracted by Cesarian section from a 17 day pregnant Wistar rat, and the feral brains were placed into phosphate buffered saline. Cells were counted, tested for vitality using the trypan blue exclusion test and seeded onto poly-D-lysine coated 24 multiwell plates.

    This protocol resulted in a highly neuron-enriched culture. Media was conditioned by 24 hour treatment over a confluent layer of type I astrocytes, prepared from two day old Wistar rat pups. Cortices were dissected, cut into small pieces, and enzymatically digested with 0. Tissue was then dissociated by passage through a fire polished Pasteur pipette and the cell suspension plated into untreated 75 cm 2 T-flasks.

    After 24 hours the media was replaced and unattached cells removed. Once astrocytes achieved confluence, cells were divided into four flasks. Astrocyte cultures were used to condition DMEM for no longer than two months. Following exposure, cells were washed twice with saline, and incubated for 18 hours in conditioned DMEM.

    The level of lactate dehydrogenase LDH in the media was used as an index of cell injury. Specific AMPA and kainate receptor ligands were also used to separately examine the effects of cannabinoids on AMPA and kainate receptor mediated events. When specifically examining kainate receptor activity, cyclothiazide was replaced with 0.

    Comparable results were obtained with either the AMPA receptor ligand, fluorowillardiine or the kainate receptor specific ligand, 4-methyl-glutamate data not shown. Unlike cannabidiol, THC is a ligand and agonist for the brain cannabinoid receptor. See Mansbach et al. To investigate whether cannabinoids protect neurons against glutamate damage by reacting with ROS, the antioxidant properties of cannabidiol and other cannabinoids were assessed.

    Cyclic voltametry, a procedure that measures the ability of a compound to accept or donate electrons under a variable voltage potential, was used to measure the oxidation potentials of several natural and synthetic cannabinoids. Tetraethylammonium chloride in acetonitrile 0.

    Anandamide, a cannabinoid receptor ligand without a cannabinoid like structure, was used as a non-responsive control. Each experiment was repeated twice with essentially the same results. Anandamide arachidonyl ethanolamide did not undergo oxidation at these potentials FIG.

    Several other natural and synthetic cannabinoids, including cannabidiol, nabilone, and levanantrodol were also tested, and they too exhibited oxidation profiles similar to cannabidiol and THC data not shown.

    The ability of cannabinoids to be readily oxidized, as illustrated in Example 5, indicated they possess antioxidant properties comparable to BHT. Cannabidiol CBD and tetrahydrocannabinol THC were evaluated for their ability to prevent oxidation of dihydrorhodamine to the fluorescent compound rhodamine.

    Oxidant was generated by ferrous catalysis diothionite reduced ferric citrate of t-butyl hydroperoxide in a Various concentrations of cannabinoids and BHT were included to examine their ability to prevent dihydrorhodiamine oxidation. To confirm that cannabinoids act as antioxidants in the intact cell, neurons were also incubated with the oxidant t-butyl hydroperoxide and varying concentrations of cannabidiol FIG. The t-butyl hydroperoxide oxidant was chosen for its solubility in both aqueous and organic solvents, which facilitates oxidation in both cytosolic and membrane cell compartments.

    Cell toxicity was assessed hours after insult by measuring lactate dehydrogenase LDH release into the culture media. All experiments were conducted with triple or quadruple values at each point and all plates contained positive glutamate alone and baseline controls.

    The assay was validated by comparison with an XTT based metabolic activity assay. As shown in FIG. The middle cerebral artery of chloral hydrate anesthetized rats was occluded by insertion of suture thread into it.

    The animals were allowed to recover from the anesthetic and move freely for a period of two hours. After this time the suture was removed under mild anesthetic and the animals allowed to recover for 48 hours.

    Then the animals were tested for neurological deficits, sacrificed, and the infarct volume calculated. To examine the infarct volume, animals were anesthetized, ex-sanguinated, and a metabolically active dye 3-phenyl tetrazolium chloride was pumped throughout the body. All living tissues were stained pink by the dye, while morbid regions of infarcted tissue remained white. Brains were then fixed for 24 hours in formaldehyde, sliced and the infarct volumes measured. Control animals received injections of vehicle without drug.

    IV doses would be expected to be times less because of reduction of first pass metabolism. This data shows that infarct size was approximately halved in the animals treated with cannabidiol, which was also accompanied by a substantial improvement in the neurological status of the animal. These studies with the nonpsychotropic marijuana constituent, cannabidiol, demonstrate that protection can be achieved against both glutamate neurotoxicity and free radical induced cell death.

    THC, the psychoactive principle of cannabis, also blocked glutamate neurotoxicity with a potency similar to cannabidiol. In both cases, neuroprotection is unaffected by the presence of a cannabinoid receptor antagonist. These results therefore surprisingly demonstrate that cannabinoids can have useful therapeutic effects that are not mediated by cannabinoid receptors, and therefore are not necessarily accompanied by psychoactive side effects. Cannabidiol also acts as an anti-epileptic and anxiolytic, which makes it particularly useful in the treatment of neurological diseases in which neuroanatomic defects can predispose to seizures e.

    A particular advantage of the cannabinoid compounds of the present invention is that they are highly lipophilic, and have good penetration into the central nervous system. The volume of distribution of some of these compounds is at least L in a 70 kg person 1. The lipophilicity of particular compounds is also about as great as that of THC, cannabidiol or other compounds that have excellent penetration into the brain and other portions of the CNS.

    Hormones and neurotransmitters controls almost every aspect of your central nervous system. They could see the huge impact cannabinoids would make on mental and physical health in the future.

    They applied for this patent under the umbrella of the Department of Health and Human Services and got it. Therefore, it took about 11 years for the United States government to patent potent natural bioactive compounds that would affect this system. The reason this is important is cannabinoids have little or no side effects and have been shown to be extremely safe, even in high doses. They knew science had not caught up with these discoveries and were betting that when it did, public opinion would change, and people would be looking at these safe, natural healing compounds for their beneficial health effects.

    Their bet is starting to pay off 15 years later. Sort of strange, huh? Why would the US government want to patent pot? Let me see if I can shed some light on this story. Related Posts Real Life Wellness: Back in the Day — Feb.

    US6630507B1 - Cannabinoids as antioxidants and neuroprotectants - Google Patents

    6,, Why the U.S. government holds a patent on cannabis plant compounds Published: Aug 22, , am • Updated: Mar 9, , pm of non-psychoactive cannabinoids — chemical compounds found within the 6,, was granted to the U.S. Department of Health and Human Services in Patent , titled “Cannabinoids as antioxidants and neuroprotectants,” was issued on Oct. 7, issued to the United States as. On Oct. 7, , the US government issued Patent No. 6,,, you see, is for cannabinoids as antioxidants and neuroprotectants. this is the same US government that has been fighting the use of marijuana as a drug.

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