Tetrodotoxin Pufferfish Extract

Tetrodotoxin Pufferfish Extract


Tetrodotoxin Pufferfish Extract, a neurotoxin C11H17N3O8 that is found especially in pufferfishes and that blocks nerve conduction by suppressing permeability of the nerve fiber to sodium ions Tetrodotoxin Pufferfish Extract. Tetrodotoxin (TTX) is a potent neurotoxin. Its name derives from Tetraodontiformes, an order that includes pufferfish, porcupinefish, ocean sunfish, and triggerfish; several of these species carry the toxin. Although tetrodotoxin was discovered in these fish and found in several other animals (e.g., in blue-ringed octopuses, rough-skinned newts, and moon snails), it is actually produced by certain infecting or symbiotic bacteria like Pseudoalteromonas, Pseudomonas, and Vibrio as well as other species found in Tetrodotoxin (TTX) is a selective sodium channel blocker nonprotein toxin. The consumption of an organism containing TTX can cause neurological and gastrointestinal symptoms. TTX, widely distributed among marine as well as terrestrial animals, induces dangerous intoxication. This toxin is mainly isolated from the skin, viscera, ovaries, and liver of the pufferfish. The toxin is produced by various species of bacteria, and TTX-bearing animals absorb and accumulate it through the food chain. TTX is commonly used in many laboratories as a pharmacological tool because of its ability to selectively block the sodium channels on the nerve membrane. No antidote is available for clinical use. animals.

Tetrodotoxin Pufferfish Extract (TTX) is a potent neurotoxin responsible for many human intoxications and fatalities each year. The origin of TTX is unknown, but in the pufferfish, it seems to be produced by endosymbiotic bacteria that often seem to be passed down the food chain.

The ingestion of contaminated pufferfish, considered the most delicious fish in Japan, is the usual route of toxicity. This neurotoxin, reported as a threat to human health in Asian countries, has spread to the Pacific and Mediterranean, due to the increase of temperature waters worldwide. Tetrodotoxin Pufferfish Extract

Detection of body fluids

Tetrodotoxin may be quantified in serum, whole blood or urine to confirm a diagnosis of poisoning in hospitalized patients or to assist in the forensic investigation of a case of fatal overdosage. Most analytical techniques involve mass spectrometric detection following gas or liquid chromatographic separation

Tetrodotoxin. The pufferfish has an endosymbiotic (a form of symbiosis in which one organism lives inside the other) bacterium in its body that produces tetrodotoxin, a toxin that is selective for voltage-gated sodium channels. In fact, this bacterium can be found in a variety of marine and terrestrial species in which tetrodotoxin is also found, including the blue-ringed octopus (Bane et al., 2014; Magarlamov et al., 2017). Despite the presence of this dangerous toxin, pufferfish (“fugu”) is a delicacy in Japan. Specially trained chefs purposely leave some tetrodotoxin in the fish they prepare so the consumer can experience the desired side effects of the meal: a tingling sensation in their mouth and a sense of euphoria.

Tetrodotoxin Pufferfish Extract. TTX, for which there is no known antidote, inhibits sodium channel producing heart failure in many cases and consequently death. In Japan, a regulatory limit of 2 mg eq TTX/kg was established, although the restaurant preparation of “fugu” is strictly controlled by law and only chefs qualified are allowed to prepare the fish. Due to its paralysis effect, this neurotoxin could be used in the medical field as an analgesic to treat some cancer pains.Bromazolam for sale USA


TTX is extremely toxic. The Material Safety Data Sheet for TTX lists the oral median lethal dose (LD50) for mice as 334 μg per kg. For comparison, the oral LD50 of potassium cyanide for mice is 8.5 mg per kg,[40] demonstrating that even orally, TTX is more poisonous than cyanide. TTX is even more dangerous if administered intravenously; the amount needed to reach a lethal dose by injection is 8 μg per kg in mice. Tetrodotoxin Pufferfish Extract

The toxin can enter the body of a victim by ingestion, injection, inhalation, or through abraded skin.

Poisoning occurring as a consequence of the consumption of fish from the order Tetraodontiformes is extremely serious. The organs (e.g. liver) of the pufferfish can contain levels of tetrodotoxin sufficient to produce the described paralysis of the diaphragm and corresponding death due to respiratory failure. Toxicity varies between species and at different seasons and geographic localities, and the flesh of many pufferfish may not be dangerously toxic.

The mechanism of toxicity is through the blockage of fast voltage-gated sodium channels, which are required for the normal transmission of signals between the body and the brain. As a result, TTX causes loss of sensation, and paralysis of voluntary muscles including the diaphragm and intercostal muscles, stopping breathing.

Tetrodotoxin Pufferfish Extract

Tetrodotoxin is a sodium channel blocker. It inhibits the firing of action potentials in neurons by binding to the voltage-gated sodium channels in nerve cell membranes and blocking the passage of sodium ions (responsible for the rising phase of an action potential) into the neuron. This prevents the nervous system from carrying messages and thus muscles from contracting in response to nervous stimulation.

Its mechanism of action, selective blocking of the sodium channel, was shown definitively in 1964 by Toshio Narahashi and John W. Moore at Duke University, using the sucrose gap voltage clamp technique.

The association of bacterial species with the production of the toxin is unequivocal – Lago and coworkers state, “[e]ndocellular symbiotic bacteria have been proposed as a possible source of eukaryotic TTX by means of an exogenous pathway, and Chau and coworkers note that the “widespread occurrence of TTX in phylogenetically distinct organisms… strongly suggests that symbiotic bacteria play a role in TTX biosynthesis” – although the correlation has been extended to most but not all metazoans in which the toxin has been identified.


The therapeutic uses of puffer fish (tetraodon) eggs were mentioned in the first Chinese pharmacopoeia Pen-T’so Ching (The Book of Herbs, allegedly 2838–2698 BC by Shennong; but a later date is more likely), where they were classified as having “medium” toxicity, but could have a tonic effect when used at the correct dose. The principal use was “to arrest convulsive diseases”.

In the Pen-T’so Kang Mu (Index Herbacea or The Great Herbal by Li Shih-Chen, 1596) some types of the fish Ho-Tun (the current Chinese name for tetraodon) were also recognized as both toxic yet, at the right dose, use as part of a tonic. Increased toxicity in Ho-Tun was noted in fish caught at sea (rather than river) after the month of March.

It was recognized that the most poisonous parts were the liver and eggs, but that toxicity could be reduced by soaking the eggs, noting that tetrodotoxin is slightly water-soluble, and soluble at 1 mg/ml in slightly acidic solutions.

The German physician Engelbert Kaempfer, in his “A History of Japan” (translated and published in English in 1727), described how well known the toxic effects of the fish were, to the extent that it would be used for suicide and that the Emperor specifically decreed that soldiers were not permitted to eat it. There is also evidence from other sources that knowledge of such toxicity was widespread throughout Southeast Asia and India.

The first recorded cases of TTX poisoning affecting Westerners are from the logs of Captain James Cook from 7 September 1774. On that date Cook recorded his crew eating some local tropic fish (pufferfish), and then feeding the remains to the pigs kept on board.

The crew experienced numbness and shortness of breath, while the pigs were all found dead the next morning. In hindsight, it is clear that the crew survived a mild dose of tetrodotoxin, while the pigs ate the pufferfish body parts that contain most of the toxin, thus being fatally poisoned.

The toxin was first isolated and named in 1909 by Japanese scientist Dr. Yoshizumi Tahara. It was one of the agents studied by Japan’s Unit 731, which evaluated biological weapons on human subjects in the 1930s.

On the contrary, there has been a failure in a single case, that of newts (Taricha granulosa), to detect TTX-producing bacteria in the tissues with the highest toxin levels (skin, ovaries, muscle), using PCR methods, although technical concerns about the approach have been raised.

Critically for the general argument, Takifugu rubripes puffers captured and raised in a laboratory on controlled, TTX-free diets “lose toxicity over time,” while cultured, TTX-free Takifugu niphobles puffers fed on TTX-containing diets saw TTX in the livers of the fishes increase to toxic levels.

Hence, as bacterial species that produce TTX are broadly present in aquatic sediments, a strong case is made for ingestion of TTX and/or TTX-producing bacteria, with accumulation and possible subsequent colonization and production.

Nevertheless, without clear biosynthetic pathways (not yet found in metazoans, but shown for bacteria), it remains uncertain whether it is simply via bacteria that each metazoan accumulates TTX; the question remains as to whether the quantities can be sufficiently explained by ingestion, ingestion plus colonization, or some other mechanism.

Symptoms and treatment

The diagnosis of pufferfish poisoning is based on the observed symptomatology and recent dietary history. Symptoms typically develop within 30 minutes of ingestion, but may be delayed by up to four hours; however, if the dose is fatal, symptoms are usually present within 17 minutes of ingestion. Paresthesia of the lips and tongue is followed by developing paresthesia in the extremities, hypersalivation, sweating, headache, weakness, lethargy, incoordination, tremor, paralysis, cyanosis, aphonia, dysphagia, and seizures. The gastrointestinal symptoms are often severe and include nausea, vomiting, diarrhea, and abdominal pain; death is usually secondary to respiratory failure. There is increasing respiratory distress, speech is affected, and the victim usually exhibits dyspnea, mydriasis, and hypotension. Paralysis increases, and convulsions, mental impairment, and cardiac arrhythmia may occur. The victim, although completely paralyzed, may be conscious and in some cases completely lucid until shortly before death, which generally occurs within 4 to 6 hours (range ~20 minutes to ~8 hours). However, some victims enter a coma. If the patient survives 24 hours, recovery without any residual effects will usually occur over a few days. Therapy is supportive and based on symptoms, with aggressive early airway management. If ingested, treatment can consist of emptying the stomach, feeding the victim activated charcoal to bind the toxin, and taking standard life-support measures to keep the victim alive until the effect of the poison has worn off. Alpha adrenergic agonists are recommended in addition to intravenous fluids to combat hypotension; anticholinesterase agents “have been proposed as a treatment option but have not been tested adequately”. Toad vemom for sale No antidote has been developed and approved for human use, but a primary research report (preliminary result) indicates that a monoclonal antibody specific to tetrodotoxin is in development by USAMRIID that was effective, in one study, for reducing toxin lethality in tests on mice.


Potential medicinal use

The deathstalker’s powerful venom contains the 36-amino acid peptide chlorotoxin (ribbon diagram shown). This blocks small-conductance chloride channels, immobilizing its prey. Scorpion venom is a mixture of neurotoxins; most of these are peptides, and chains of amino acids.

Many of them interfere with membrane channels that transport sodium, potassium, calcium, or chloride ions. These channels are essential for nerve conduction, muscle contraction and many other biological processes. Some of these molecules may be useful in medical research and might lead to the development of new disease treatments.

Among their potential therapeutic uses are analgesic, anti-cancer, antibacterial, antifungal, antiviral, antiparasitic, bradykinin-potentiating, and immunosuppressive drugs. As of 2020, no scorpion toxin-based drug is on sale, though chlorotoxin is being trialled for use against glioma, a brain cancer. Tetrodotoxin Pufferfish Extract Tetrodotoxin Pufferfish Extract Tetrodotoxin Pufferfish Extract Tetrodotoxin Pufferfish Extract Tetrodotoxin Pufferfish Extract Tetrodotoxin Pufferfish Extract  Tetrodotoxin Pufferfish Extract Tetrodotoxin Pufferfish Extract Tetrodotoxin Pufferfish Extract Mode of action Tetrodotoxin causes paralysis by affecting the sodium ion transport in both the central and peripheral nervous systems. A low dose of tetrodotoxin produces tingling sensations and numbness around the mouth, fingers, and toes. Higher doses produce nausea, vomiting, respiratory failure, difficulty walking, extensive paralysis, and death. As little as 1–4 mg of the toxin can kill an adult. Saxitoxin has a very different chemical structure than tetrodotoxin, but it has similar effects on the transport of cellular sodium and produces similar neurological effects. Saxitoxin is less toxic than tetrodotoxin. Some people, particularly in Asia, consider puffer fish a fine delicacy if it is carefully prepared by experienced chefs. The trick is to get just a small dose to feel mild tingling effects, but not the more serious symptoms of tetrodotoxin poisoning. In the United States tetrodotoxin poisoning is rare, but a recent US report indicated several cases of people catching and consuming puffer fish containing elevated levels of these toxins and suffering the ill effects. Treatment Treatment is supportive and symptom-based. Activated charcoal may be helpful.

Synthetic Cathinones

Synthetic Cathinones

Synthetic Cathinones

Synthetic Cathinones. What are synthetic cathinones?

Synthetic cathinones, more commonly known as bath salts, are human-made stimulants chemically related to cathinone, a substance found in the khat plant. Khat is a shrub grown in East Africa and southern Arabia, where some people chew its leaves for their mild stimulant effects. Human-made versions of cathinone can be much stronger than the natural product and, in some cases, very dangerous.

Synthetic cathinones usually take the form of a white or brown crystal-like powder and are sold in small plastic or foil packages labelled “not for human consumption.” They can be labelled as bath salts, plant food, jewellery cleaner, or phone screen cleaner.

Synthetic cathinones are part of a group of drugs that concern public health officials called new psychoactive substances (NPS). NPS are unregulated psychoactive mind-altering substances with no legitimate medical use and are made to copy the effects of controlled substances.

They are introduced and reintroduced into the market in quick succession to dodge or hinder law enforcement efforts to address their manufacture and sale.

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Synthetic cathinones are marketed as cheap substitutes for other stimulants such as amphetamines and cocaine. Products sold as Molly often contain synthetic cathinones instead of MDMA (see Synthetic Cathinones and Molly (Ecstasy).

Synthetic cathinones (Bath salts, eutylone, Flakka M-Cat, Monkey Dust) are a large group of manufactured chemicals which mimic the effects of other substances.

They usually come as a pill, capsule, powder or crystal. They are often mis-sold as MDMA or cocaine, but they require a lower dose which greatly increases the risk of overdose.

The effects vary a lot, and while they often have similar effects to MDMA or methamphetamine, paranoia and anxiety are more common. Synthetic cathinones found in New Zealand include N-ethylpentalone, mephedrone, methylenedioxypyrovalerone (MDPV), methylone, mexedrone, and Alpha PVP.


Khat leaves are removed from the plant stalk and are kept in a ball in the cheek and chewed. Chewing releases juices from the leaves, which include the alkaloid cathinone. The absorption of cathinone has two phases: one in the buccal mucosa and one in the stomach and small intestine.

The stomach and small intestine are very important in the absorption of ingested alkaloids. At approximately 2.3 hours after chewing khat leaves, the maximum concentration of cathinone in blood plasma is reached.

The mean residence time is 5.2 ± 3.4 hours.[3] The elimination half-life of cathinone is 1.5 ± 0.8 hours. A two-compartment model for the absorption and elimination best describes this data.

However, at most, only 7% of the ingested cathinone is recovered in the urine. This indicates that the cathinone is being broken down in the body. Cathinone has been shown to selectively metabolize into R,S-(-)-norephedrine and cathine.

The reduction of the ketone group in cathinone will produce cathine. This reduction is catalyzed by enzymes in the liver. The spontaneous breakdown of cathinone is the reason it must be chewed fresh after cultivation

Synthetic Cathinones.

What are synthetic cathinones?
Synthetic cathinones is the name of a category of drugs related to the naturally occurring khat plant.1 They are stimulants, meaning that they speed up the messages between the brain and the body and have similar effects to amphetamines.

Synthetic cathinones are also part of a group of drugs known as New Psychoactive Substances (NPS). NPSs are a range of drugs that first appeared on the recreational drug market in the mid-2000s, that have been designed to mimic established illicit drugs, such as cannabis, cocaine, ecstasy and LSD. Between 2005 and 2014 more than 81 synthetic cathinone derivatives were reported to the EU Early Warning System.

Synthetic cathinones are mostly white or brown powders but also exist in the form of small, chunky crystals. They are sometimes found as capsules and less commonly as tablets.3

Types of cathinones commonly used
Mephedrone (4-MMC), M-CAT)
Alpha-Pyrrolidinovalerophenone (alpha-PVP)

Synthetic Cathinones.

How do synthetic cathinones affect the brain?
Much is still unknown about how synthetic cathinones affect the human brain. Researchers do know that synthetic cathinones are chemically similar to drugs like amphetamines, cocaine, and MDMA.

A study found that 3,4-methylenedioxypyrovalerone (MDPV), a common synthetic cathinone, affects the brain in a manner similar to cocaine, but is at least 10 times more powerful. MDPV is the most common synthetic cathinone found in the blood and urine of patients admitted to emergency departments after taking bath salts.2

Synthetic cathinones can produce effects that include:

paranoia—extreme and unreasonable distrust of others
hallucinations—experiencing sensations and images that seem real but are not
increased friendliness
increased sex drive
panic attacks
excited delirium—extreme agitation and violent behaviour.

Synthetic production

Cathinone can be synthetically produced from propiophenone through a Friedel-Crafts Acylation of propionic acid and benzene. The resulting propiophenone can be brominated, and the bromine can be substituted with ammonia to produce a racemic mixture of cathinone.

A different synthetic strategy must be employed to produce enantiomerically pure (S)-cathinone. This synthetic route starts out with the N-acetylation of the optically active amino acid, S-alanine.

Then, phosphorus pentachloride (PCl5) is used to chlorinate the carboxylic acid forming an acyl chloride. At the same time, a Friedel-Crafts acylation is performed on benzene with aluminum chloride catalyst. Finally, the acetyl protecting group is removed by heating with hydrochloric acid to form enantiomerically pure S-(-)-cathinone.

Using synthetic cathinones with other drugs
The effects of combining cathinones with other drugs – including over-the-counter or prescribed medications – can be unpredictable and dangerous. The following combinations could have the following effects:

Synthetic cathinones + ice, speed or ecstasy: increase the risk of cardiovascular (heart) problems and substance-induced psychosis.7
Synthetic cathinones + alcohol + cannabis: nausea and vomiting.

Health and Safety
If possible, find out the specific cathinone you are using so you know what to expect and what a common dose is. Synthetic cathinone harm reduction advice is partly based on what is known of related drugs like amphetamines and MDMA, as not enough research has been done on individual synthetic cathinones specifically.

The use of synthetic cathinone is likely to be more dangerous when

taken in combination with alcohol or other drugs, particularly stimulants such as crystal methamphetamine (‘ice’) or ecstasy
driving or operating heavy machinery
judgment or motor coordination is required
alone (in case medical assistance is required)
the person has a mental health problem
the person has an existing heart problem.

In Australia, poisons information centres and clinical toxicology units around Australia are often contacted for advice on poisonings from synthetic cathinones. Features of these poisonings include agitation, tachycardia (increased heart rate), hypertension and in severe cases delirium, aggressive behaviour, hallucinations, hyperthermia, cardiac dysrhythmia (irregular heart beat) and seizures. Deaths have occurred due to alpha-PVP toxicity.4

Injecting synthetic cathinones can cause soft tissue and vascular damage.4

Sharing needles may also transmit:

Hepatitis B
Hepatitis C
Dependence and tolerance
There is limited data regarding people seeking treatment for synthetic cathinone dependence, however, people who use synthetic cathinones have reported a strong compulsion to redose, as well dependence.

Synthetic Cathinones

Effects of synthetic cathinones
There is no safe level of drug use. The use of any drug always carries some risk. It’s important to be careful when taking any type of drug.

Synthetic cathinones affect everyone differently, based on:

the amount taken
a person’s size, weight and health
whether the person is used to taking it
whether other drugs are taken around the same time
the strength of the drug (which can vary from batch to batch).
The individual effects and toxicity of each cathinone are distinct and can vary greatly between each person using them.

Generally speaking, in small doses the following effects may be experienced and may last for approximately 2-4 hours:

the rush of intense pleasure
feeling happy, energetic and wanting to talk more
intense connection with music
restless sleep
muscle tension (face and jaw)
blurred vision
light-headedness, dizziness
distorted sense of time
enlarged (dilated) pupils, blurred vision
dry mouth, thirst
memory loss
reduced appetite.5
Higher doses may result in the following adverse effects:

nose bleeds from snorting the drug
stomach pains, nausea, vomiting
skin rashes
fast or irregular heartbeat
high blood pressure and hot flushes
strong urge to re-dose
chest pain
tremors, convulsions, death.

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New Cathinone

New Cathinone

New Cathinone

New Cathinone. Cathinone /ˈkæθɪnoʊn/ (also known as benzoylethanamine, or β-keto-amphetamine) is a monoamine alkaloid found in the shrub Catha edulis (khat) and is chemically similar to ephedrine, cathine, methcathinone and other amphetamines. It is probably the main contributor to the stimulant effect of Catha edulis, also known as khat.

Cathinone differs from many other amphetamines in that it has a ketone functional group. Other phenethylamines that share this structure include the stimulants methcathinone, MDPV, mephedrone and the antidepressant bupropion.

Khat is usually supplied as a bundle of leaves and fresh shoots wrapped in banana leaves. It is reported to have a sharp taste and an aromatic odour. Alcoholic extracts (tinctures) of khat have occasionally been reported, especially in ‘herbal high’ sales outlets and at music festivals.

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New Cathinone. Khat (also known as qat or chat) comprises the leaves and fresh shoots of Catha edulis Forsk, a flowering evergreen shrub cultivated in East Africa and the South-West Arabian Peninsula.

Khat leaves are typically wrapped as a bundle in banana leaves. The principal active components in khat are cathinone and cathine (norpseudoephedrine) (see also Drug profile on synthetic cathinones).

Chewing khat releases these substances into the saliva; they are rapidly absorbed and eliminated. Both cathinone and cathine are closely related to amphetamine, and the pharmacological effects of cathinone are qualitatively similar to those of amphetamine, although it is less potent.

Only fresh leaves are chewed because cathinone soon degrades into old or dry plant material. The analysis relies on the characteristic appearance of khat and the presence of cathinone and/or cathine. Khat is not under International control but is scheduled by some Member States. Cathinone and cathine are listed in the 1971 United Nations Convention on Psychotropic Substances under Schedules I and III respectively.

The principal active component in khat is S-cathinone, otherwise known as (-)-2-aminopropiophenone or, more formally, S-(-)-2-amino-1-phenyl-1-propanone. Cathinone is labile and is transformed within a few days of harvesting to a dimer (3,6-dimethyl-2,5-diphenylpyrazine).

It is for this reason that khat needs to be consumed while still fresh. Cathine (1S, 2S-norpseudoephedrine), a further psychoactive substance, arises from the metabolism of cathinone in the mature plant. Apart from common plant products such as tannins, terpenes, flavonoids and sterols, a number of other substances occur in khat including smaller amounts of 1R, 2S-norephedrine and a large number of cathedulins (polyhydroxylated sesquiterpenes).

Both cathinone and cathine are close chemical relatives of the phenethylamines. Thus cathinone is the β-keto analogue of amphetamine. A large number of synthetic cathinone derivatives have been produced, some of which have found use as active pharmaceutical agents.


Cathinone can be extracted from Catha edulis, or synthesized from α-bromopropiophenone (which is easily made from propiophenone). Because cathinone is both a primary amine and a ketone, it is very likely to dimerize, especially as a free base isolated from plant matter.

New Cathinone. The structure of cathinone is very similar to that of other molecules. By reducing the ketone, it becomes cathine if it retains its stereochemistry, or norephedrine if its stereochemistry is inverted. Cathine is a less potent version of cathinone and cathinone’s spontaneous reduction is the reason that older khat plants are not as stimulating as younger ones.

Cathinone and amphetamine are closely related in that amphetamine is only lacking the ketone C=O group. Cathinone is structurally related to methcathinone, in much the same way as amphetamine is related to methamphetamine. Cathinone differs from amphetamine by possessing a ketone oxygen atom (C=O) on the β (beta) position of the side chain.

The corresponding alcohol, cathine, is a less powerful stimulant. The biophysiological conversion from cathinone to cathine is to blame for the depotentiation of khat leaves over time. Fresh leaves have a greater ratio of cathinone to cathine than dried ones, therefore having more psychoactive effects.

There are many cathinone derivatives that include the addition of an R group to the amino end of the molecule. Some of these derivatives have medical uses as well. Bupropion is one of the most commonly prescribed antidepressants and its structure is Cathinone with a tertiary butyl group attached to the nitrogen and chlorine attached to the benzene ring meta- to the main carbon chain.

Other cathinone derivatives are strong psychoactive drugs. One such drug is methylone, a drug structurally similar to MDMA.

Effects on health
The first documentation of the khat plant being used in medicine was in a book published by an Arabian physician in the 10th century. It was used as an antidepressant because it led to feelings of happiness and excitement. Chronic khat chewing can also create drug dependence, as shown by animal studies. In such studies, monkeys were trained to push a lever to receive the drug reward. As the monkeys’ dependence increased, they pressed the lever at an increasing frequency.

New Cathinone. Khat chewing and the effects of cathinone on the body differ from person to person, but there is a general pattern of behavior that emerges after ingesting fresh cathinone:

Feelings of euphoria that last for one to two hours
Discussion of serious issues and increased irritability
The chewer’s imagination is very active
Depressive stage
Irritability, loss of appetite and insomnia
There are other effects not related to the CNS. The chewer can develop constipation and heartburn after a khat session. Long-term effects of cathinone can include gum disease or oral cancer, cardiovascular disease and depression. The withdrawal symptoms of cathinone include hot flashes, lethargy and a great urge to use the drug for at least the first two days.


New Cathinone. The synthesis of cathinone in khat begins with L-phenylalanine and the first step is carried out by L-phenylalanine ammonia lyase (PAL), which cleaves off an ammonia group and creates a carbon-carbon double bond, forming cinnamic acid.[15] After this, the molecule can either go through a beta-oxidative pathway or a non-beta-oxidative pathway.

The beta-oxidative pathway produces benzoyl-CoA while the non-beta-oxidative pathway produces benzoic acid. Both of these molecules can be converted to 1-phenylpropane-1,2-dione by a condensation reaction catalyzed by a ThDP-dependent enzyme (Thiamine diphosphate-dependent enzyme) with pyruvate and producing CO2.[15] 1-phenylpropane-1,2-dione goes through a transaminase reaction to replace a ketone with an ammonia group to form (S)-cathinone. (S)-Cathinone can then undergo a reduction reaction to produce the less potent but structurally similar cathine or norephedrine, which are also found in the plant.[15]

Aside from the beta- and non-beta-oxidative pathways, the biosynthesis of cathinone can proceed through a CoA-dependent pathway. The CoA-dependent pathway is actually a mix between the two main pathways as it starts like the beta-oxidative pathway and then when it loses CoA, it finishes the synthesis in the non-beta-oxidative pathway. In this pathway, the trans-cinnamic acid produced from L-phenylalanine is ligated to Coenzyme A (CoA), just like the beginning of the beta-oxidative pathway. It then undergoes hydration at the double bond.

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This product then loses the CoA to produce benzaldehyde, an intermediate of the non-beta-oxidative pathway. Benzaldehyde is converted into benzoic acid and proceeds through the rest of the synthesis. New Cathinone

Cannabinoids Information

Cannabinoids information

Cannabinoids Information

Cannabinoids Information. Cannabinoids are naturally occurring compounds found in the Cannabis sativa plant. Of over 480 different compounds present in the plant, only around 66 are termed cannabinoids.

Cannabinoids Information. The most well-known among these compounds is the delta-9-tetrahydrocannabinol (Δ9-THC), which is the main psychoactive ingredient in cannabis.

Cannabidiol (CBD) is another important component, which makes up about 40% of the plant resin extract.

Cannabinoids Information/ Classes of cannabinoids
The cannabinoids are separated into the following subclasses:

Cannabigerols (CBG)
Cannabichromenes (CBC)
Cannabidiol (CBD)
Tetrahydrocannabinol (THC)
Cannabinol (CBN)
Cannabinodiol (CBDL)
Other cannabinoids including cannabicyclol (CBL), cannabielsoin (CBE) and cannabitriol (CBT)

Cannabinoids (/kəˈnæbənɔɪdzˌ ˈkænəbənɔɪdz/) are several structural classes of compounds found in the cannabis plant primarily and most animal organisms (although insects lack such receptors) or as synthetic compounds. The most notable cannabinoid is the phytocannabinoid tetrahydrocannabinol (THC) (delta-9-THC), the primary intoxicating compound in cannabis.

Cannabinoids Information. Cannabidiol (CBD) is a major constituent of temperate Cannabis plants and a minor constituent in tropical varieties. At least 113 distinct phytocannabinoids have been isolated from cannabis, although only four (i.e., THCA, CBDA, CBCA and their common precursor CBGA) have been demonstrated to have a biogenetic origin.

It was reported in 2020 that phytocannabinoids can be found in other plants such as rhododendron, licorice and liverwort,[7] and earlier in Echinacea.

Phytocannabinoids are multi-ring phenolic compounds structurally related to THC,[8] but endocannabinoids are fatty acid derivatives. Nonclassical synthetic cannabinoids (cannabimimetics) include aminoalkylindoles, 1,5-diarylpyrazoles, quinolines, and arylsulfonamides as well as eicosanoids related to endocannabinoids.

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Cannabinoids Information

Cannabinoids have drawn increasing public attention with expanding legalization and accessibility. Cannabinoids are a group of compounds that are biologically and structurally similar to the chemical compounds of Cannabis sativa.46 There are three classes of cannabinoids: plant-derived cannabinoids (phytocannabinoids), endogenous cannabinoids (endocannabinoids), and synthetic cannabinoids. Cannabinoids Information

Phytocannabinoids are plant-derived cannabinoids that are historically derived from cannabis sativa.47 The most notable phytocannabinoids are Δ9-tetrahydrocannabinol (THC), which can have psychotropic effects, and cannabidiols (CBD), which are mostly non-psychotropic.

Endocannabinoids are endogenous lipids that function as ligands for cannabinoid receptors.46 Synthetic cannabinoids are developed in laboratories and mimic phytocannabinoids and endocannabinoids.

The effects of cannabinoids are mediated by cannabinoid receptors CB1 and CB2. CB1 is responsible for the psychoactive effects through the release of various neurotransmitters,48 while CB2 is presumed to mediate immunomodulation and the anti-inflammatory effects of cannabinoids.49 Generally, oral cannabinoids have been shown to target systemic symptoms such as anorexia, nausea, and pain, whereas topically applied cannabinoids often target localized pain and inflammation.50–54.

Cannabinoids Information

The pathogenesis of HS includes a complex relationship between pilosebaceous unit occlusion due to keratinocyte proliferation, sebaceous gland disruption, and an overlapping, autoinflammatory response.3,4,55,56 Cannabinoids have been shown to inhibit keratinocyte proliferation in vitro CBD, and other phytocannabinoids have also been shown to inhibit a number of inflammatory pathways, including the NF-κB pathway.57

Anandamide is a CB1 agonist that interacts with vanilloid receptors to transduce and regulate nociceptive signals (including pain and itch) to the peripheral nervous system.

Phytocannabinoids and cannabinoid agonists have demonstrated clinical improvements for patients with pain associated with chronic medical conditions.60–62 CB1 and CB2 agonists have been shown to reduce itch for patients with lichen simplex chronicus, uremic pruritus, atopic dermatitis (AD), and prurigo nodularis.63,64 In a study of acne patients, application of topical cannabis seed extract cream resulted in significant decreases in skin sebum and erythema.65 Cannabinoids may have an analgesic effect in HS due to inhibition of the release of calcitonin gene-related peptide, which is stored in sensory neurons and involved in the transmission of pain.66

Despite the growing interest in the therapeutic applications of cannabinoids, there remains a lack of high-quality randomized controlled trials that evaluate their effects in dermatology. Cannabinoids Information

In a recent HS CAM survey, marijuana and topical CBD oil were both among the more commonly used CAM methods by respondents. Most users reported them as helpful, with 57% reporting marijuana as helpful and 45% reporting topical CBD oil as helpful. Systemic toxicity can occur as a result of overstimulation of the endocannabinoid system from exogenous cannabinoid use through ingestion or inhalation.

67 Notable side effects of cannabinoid systemic toxicity include tachycardia (acute), bradycardia (chronic), decreased systemic vascular resistance, nystagmus, conjunctival injection, decreased intraocular pressure, lethargy, decreased concentration, and generalized psychomotor impairment.

Differences between cannabinoids

The main way in which the cannabinoids are differentiated is based on their degree of psychoactivity.

For example, CBG, CBC and CBD are not known to be psycholgically active agents whereas THC, CBN and CBDL along with some other cannabinoids are known to have varying degrees of psychoactivity.

The most abundant of the cannabinoids is CBD, which is thought to have anti-anxiety effects, possibly counteracting the psychoactive effects of THC.

When THC is exposed to the air, it becomes oxidized and forms CBN which also interacts with THC to lessen its impact.

This is why cannabis that has been left out unused will has less potent effects when smoked, due to the increased CBN to THC ratio.

Cannabinoid-based pharmaceuticals

Cannabinoids Information. Nabiximols (brand name Sativex) is an aerosolized mist for oral administration containing a near 1:1 ratio of CBD and THC.[50] Also included are minor cannabinoids and terpenoids, ethanol and propylene glycol excipients, and peppermint flavouring.

The drug, made by GW Pharmaceuticals, was first approved by Canadian authorities in 2005 to alleviate pain associated with multiple sclerosis, making it the first cannabis-based medicine. It is marketed by Bayer in Canada.

Sativex has been approved in 25 countries; clinical trials are underway in the United States to gain FDA approval. In 2007, it was approved for the treatment of cancer pain.In Phase III trials, the most common adverse effects were dizziness, drowsiness and disorientation; 12% of subjects stopped taking the drug because of the side effects.

Dronabinol (brand name Marinol) is a THC drug used to treat poor appetite, nausea, and sleep apnea.[55] It is approved by the FDA for treating HIV/AIDS-induced anorexia and chemotherapy-induced nausea and vomiting.[56][57][58]

The CBD drug Epidiolex has been approved by the Food and Drug Administration for the treatment of two rare and severe forms of epilepsy,[59] Dravet and Lennox-Gastaut syndromes.

Effects of cannabinoids

Cannabinoids exert their effects by interacting with specific cannabinoid receptors present on the surface of cells.

These receptors are found in different parts of the central nervous system and the two main types of cannabinoid receptors in the body are CB1 and CB2.

In 1992, a naturally occurring substance in the brain that binds to CB1 was discovered, called anandamide. This cannabinoid-like chemical and others that were later discovered are referred to as endocannabinoids.

The effects of cannabinoids depend on the brain area involved. Effects on the limbic system may alter memory, cognition and psychomotor performance; effects on the mesolimbic pathway may affect the reward and pleasure responses and pain perception may also be altered.

What to know about endocannabinoids and the endocannabinoid system

The endocannabinoid system is an active and complex cell signalling network. It involves a combination of endocannabinoids, enzymes, and cannabinoid receptors that help regulate several functions in the human body.

The discovery of the ECS is relatively new. In the early 1990s, a chemist isolated the first endocannabinoid in the human brain. Since that time, researchers have been learning more about this system and the role it plays in bodily functions.

Endocannabinoids are similar to the cannabinoids present in the cannabis sativa (C. sativa) plant. However, the human body naturally produces endocannabinoids. The term “endo” refers to “within,” as in within the body.

In this article, we will define the endocannabinoid system, and examine its function and potential therapeutic uses.

Endocannabinoid receptors

Cannabinoid receptors are on the surface of cells throughout the body. Endocannabinoids attach or bind to the receptors, which sends a message to the ECS to kick-start a response.

The two primary cannabinoid receptors are present throughout the body:

CB1 is mainly present in the central nervous system (CNS), which consists of the brain and spinal cord.
CB2 is mainly present in the peripheral nervous system (PNS) and in immune cells.
Experts think a third cannabinoid receptor may also exist, but research is not conclusive.

Endocannabinoids may attach to either type of receptor, causing different results depending on the location of the receptor in the body.

For example, endocannabinoids may target CB1 receptors in a spinal nerve to relieve pain or bind to a CB2 receptor in an immune cell, which signals that the body is experiencing inflammation. Cannabinoids Information

What are the therapeutic uses of cannabinoids?
Research indicates that the ECS may contain multiple promising therapeutic targets. While the body can produce endocannabinoids, there are also many cannabinoids present in the C.sativa plant which are of medical interest.

Two of the most well-known cannabinoids include tetrahydrocannabinol (THC) and cannabidiol (CBD). They can also bind to cannabinoid receptors and produce similar effects to endocannabinoids. THC is the cannabinoid that causes the “high” that people may associate with cannabis, whereas CBD does not produce this sensation.

Studies are ongoing to determine the therapeutic benefits of cannabinoids. For example, a 2016 study investigated the effect of CBD on joint inflammation in rats. The study suggests that applying a topical gel containing CBD decreased pain and joint swelling in rats without side effects.

Additional research indicates that cannabinoids may be helpful in treating a variety of conditions such as:

pain in adults
abnormal muscle tightness associated with multiple sclerosis
nausea and vomiting associated with chemotherapy
sleep disturbances
Research continues on how inhibiting or stimulating the endocannabinoid system could have medical and health benefits.

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Research Chemicals
CategoriesResearch Chemicals

Research Chemicals

Research Chemicals

Research chemicals are chemical substances used by scientists for medical and scientific research purposes. One characteristic of a research chemical is that it is for laboratory research use only; a research chemical is not intended for human or veterinary use. This distinction is required on the labels of research chemicals and is what exempts them from regulation.

Research chemicals are fundamental in the development of novel pharmacotherapies. The common medical laboratory uses include in vivo and animal testing to determine therapeutic value, toxicology testing by contract research organizations to determine drug safety and analysis by drug test and forensic toxicology labs for the purposes of evaluating human exposure.

Many pharmacologically active chemicals are sold online under the guise of “research chemicals,” when in reality they are untested designer drugs that are being sold for recreational use despite the compounds’ transitional or unclear legal status.

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Pharmaceutical industry

The pharmaceutical industry discovers, develops, produces, and markets drugs or pharmaceutical drugs for use as medications to be administered to patients (or self-administered), with the aim to cure them, vaccinate them, or alleviate symptoms. Pharmaceutical companies may deal in generic or brand medications and medical devices.

They are subject to a variety of laws and regulations that govern the patenting, testing, safety, efficacy using drug testing and marketing of drugs. The global pharmaceuticals market produced treatments worth $1,228.45 billion in 2020 and showed a compound annual growth rate (CAGR) of 1.8%.Research chemicals

Research agrochemicals are created and evaluated to select effective substances for use in commercial off-the-shelf end-user products. Many research agrochemicals are never publicly marketed. Agricultural research chemicals often use sequential code names.

This is a list of prices of chemical elements. Listed here are mainly average market prices for bulk trade of commodities. Data on elements’ abundance in Earth’s crust is added for comparison. Research chemicals

As of 2020, the most expensive non-synthetic element by both mass and volume is rhodium. It is followed by caesium, iridium and palladium by mass and iridium, gold and platinum by volume. Of those elements, rhodium, caesium and gold have only one stable isotope (133
Cs, 103
Rh and 197
Au respectively), iridium has two (191
Ir & 193
Ir) whereas palladium and platinum both have several. Carbon in the form of diamond can be more expensive than rhodium.

Per-kilogram prices of some synthetic radioisotopes range to trillions of dollars. While the difficulty of obtaining macroscopic samples of synthetic elements in part explains their high value, there has been interest in converting base metals to gold (Chrysopoeia) since ancient times, but only deeper understanding of nuclear physics has allowed the actual production of a tiny amount of gold from other elements for research purposes as demonstrated by Glenn Seaborg.

However, both this and other routes of synthesis of precious metals via nuclear reactions is orders of magnitude removed from economic viability.

Chlorine, sulfur and carbon (as coal) are cheapest by mass. Hydrogen, nitrogen, oxygen and chlorine are cheapest by volume at atmospheric pressure.

When there is no public data on the element in its pure form, price of a compound is used, per mass of element contained. This implicitly puts the value of compounds’ other constituents, and the cost of extraction of the element, at zero. For elements whose radiological properties are important, individual isotopes and isomers are listed. The price listing for radioisotopes is not exhaustive.

Experimental drug

An experimental drug is a medicinal product (a drug or vaccine) that has not yet received approval from governmental regulatory authorities for routine use in human or veterinary medicine.

A medicinal product may be approved for use in one disease or condition but still be considered experimental for other diseases or conditions. In 2018 the United States of America signed the legislation “Right to Try”, this allows individuals who fit into the criteria to try experimental drugs that are not yet deemed safe.

In the United States, the body responsible for approval is the U.S. Food and Drug Administration (FDA), which must grant the substance Investigational New Drug (IND) status before it can be tested in human clinical trials.

IND status requires the drug’s sponsor to submit an IND application that includes data from laboratory and animal testing for safety and efficacy. A drug that is made from a living organism or its products undergoes the same approval process but is called a biologics license application (BLA). Biological drugs include antibodies, interleukins, and vaccines.

In Canada, a Clinical Trial Application (CTA) must be filed with the Health Products and Food Branch (HPFB) of Health Canada before starting a clinical trial. If the clinical trial results show that therapeutic effect of the drug outweighs negative side effects then the sponsor can then to file a New Drug Submission.

Clinical trials in the European Union (EU) are regulated by the European Medicines Agency (EMA). Beginning in 2019 all applications for clinical trials must use a centralize EU portal and database. All clinical trial results will available to the public with the summary written in layperson’s language.

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Mid-1800s – 1945: From botanicals to the first synthetic drugs
The modern era of pharmaceutical industry began with local apothecaries that expanded from their traditional role of distributing botanical drugs such as morphine and quinine to wholesale manufacture in the mid-1800s, and from discoveries resulting from applied research.

Intentional drug discovery from plants began with the isolation between 1803 and 1805 of morphine – an analgesic and sleep-inducing agent – from opium by the German apothecary assistant Friedrich Sertürner, who named this compound after the Greek god of dreams, Morpheus.

By the late 1880s, German dye manufacturers had perfected the purification of individual organic compounds from tar and other mineral sources and had also established rudimentary methods in organic chemical synthesis.

The development of synthetic chemical methods allowed scientists to systematically vary the structure of chemical substances, and growth in the emerging science of pharmacology expanded their ability to evaluate the biological effects of these structural changes.

Epinephrine, norepinephrine, and amphetamine

By the 1890s, the profound effect of adrenal extracts on many different tissue types had been discovered, setting off a search both for the mechanism of chemical signalling and efforts to exploit these observations for the development of new drugs.

The blood pressure raising and vasoconstrictive effects of adrenal extracts were of particular interest to surgeons as hemostatic agents and as treatment for shock, and a number of companies developed products based on adrenal extracts containing varying purities of the active substance.

In 1897, John Abel of Johns Hopkins University identified the active principle as epinephrine, which he isolated in an impure state as the sulfate salt. Industrial chemist Jōkichi Takamine later developed a method for obtaining epinephrine in a pure state, and licensed the technology to Parke-Davis. Parke-Davis marketed epinephrine under the trade name Adrenalin.

Injected epinephrine proved to be especially efficacious for the acute treatment of asthma attacks, and an inhaled version was sold in the United States until 2011 (Primatene Mist). By 1929 epinephrine had been formulated into an inhaler for use in the treatment of nasal congestion.

While highly effective, the requirement for injection limited the use of epinephrine[clarification needed] and orally active derivatives were sought. A structurally similar compound, ephedrine, was identified by Japanese chemists in the Ma Huang plant and marketed by Eli Lilly as an oral treatment for asthma.

Following the work of Henry Dale and George Barger at Burroughs-Wellcome, academic chemist Gordon Alles synthesized amphetamine and tested it in asthma patients in 1929. The drug proved to have only modest anti-asthma effects but produced sensations of exhilaration and palpitations.

Amphetamine was developed by Smith, Kline and French as a nasal decongestant under the trade name Benzedrine Inhaler. Amphetamine was eventually developed for the treatment of narcolepsy, post-encephalitic parkinsonism, and mood elevation in depression and other psychiatric indications. It received approval as a New and Nonofficial Remedy from the American Medical Association for these uses in 1937, and remained in common use for depression until the development of tricyclic antidepressants in the 1960s.


Patents have been criticized in the developing world, as they are thought[who?] to reduce access to existing medicines.[152] Reconciling patents and universal access to medicine would require an efficient international policy of price discrimination. Moreover, under the TRIPS agreement of the World Trade Organization, countries must allow pharmaceutical products to be patented. In 2001, the WTO adopted the Doha Declaration, which indicates that the TRIPS agreement should be read with the goals of public health in mind, and allows some methods for circumventing pharmaceutical monopolies: via compulsory licensing or parallel imports, even before patent expiration.

In March 2001, 40 multi-national pharmaceutical companies brought litigation against South Africa for its Medicines Act, which allowed the generic production of antiretroviral drugs (ARVs) for treating HIV, despite the fact that these drugs were on-patent.

HIV was and is an epidemic in South Africa, and ARVs at the time cost between US$10,000 and US$15,000 per patient per year. This was unaffordable for most South African citizens, and so the South African government committed to providing ARVs at prices closer to what people could afford.

To do so, they would need to ignore the patents on drugs and produce generics within the country (using a compulsory license), or import them from abroad. After international protest in favour of public health rights (including the collection of 250,000 signatures by Médecins Sans Frontières), the governments of several developed countries (including The Netherlands, Germany, France, and later the US) backed the South African government, and the case was dropped in April of that year.

In 2016, GlaxoSmithKline (the world’s sixth largest pharmaceutical company) announced that it would be dropping its patents in poor countries so as to allow independent companies to make and sell versions of its drugs in those areas, thereby widening the public access to them.[156] GlaxoSmithKline published a list of 50 countries they would no longer hold patents in, affecting one billion people worldwide.


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