Thiamphenicol (also known as thiophenicol and dextrosulphenidol) is an antibiotic.[1] It is the methyl-sulfonyl analogue of chloramphenicol and has a similar spectrum of activity, but is 2.5 to 5 times as potent. Like chloramphenicol, it is insoluble in water, but highly soluble in lipids. It is used in many countries as a veterinary antibiotic, but is available in China, Morocco and Italy for use in humans. Its main advantage over chloramphenicol is that it has never been associated with aplastic anaemia.
Thiamphenicol is also widely used in Brazil, particularly for the treatment of sexually transmitted infections and pelvic inflammatory disease.[2]
Unlike chloramphenicol, thiamphenicol is not readily metabolized in cattle, poultry, sheep, or humans, but is predominantly excreted unchanged. In pigs and rats the drug is excreted both as parent drug and as thiamphenicol glucuronate (FAO, 1997).
https://en.wikipedia.org/wiki/Thiamphenicol
Buphedrone, also known as α-methylamino-butyrophenone (MABP), is a stimulant of the phenethylamine and cathinone chemical classes that was first synthesized in 1928.[1] It is legal in most countries as a research chemical, as long as it is not intended for human consumption.
https://en.wikipedia.org/wiki/Buphedrone
Sulfites or sulphites are compounds that contain the sulfite ion (or the sulfate(IV) ion, from its correct systematic name), SO2−
3. The sulfite ion is the conjugate base of bisulfite. Although its acid (sulfurous acid) is elusive,[1] its salts are widely used.
Sulfites are substances that naturally occur in some foods and the human body. They are also used as regulated food additives.[2] When in food or drink, sulfites are often lumped together with sulfur dioxide.[3]
https://en.wikipedia.org/wiki/Sulfite
Sulfur trioxide (alternative spelling sulphur trioxide, also known as nisso sulfan) is the chemical compound with the formula SO3. It has been described as "unquestionably the most important economically" sulfur oxide.[1] It is prepared on an industrial scale as a precursor to sulfuric acid.
Sulfur trioxide exists in several forms - gaseous monomer, crystalline trimer, and solid polymer. Sulfur trioxide is a solid at just below room temperature with a relatively narrow liquid range. Gaseous SO3 is the primary precursor to acid rain.[6]
https://en.wikipedia.org/wiki/Sulfur_trioxide
Trimethylamine (TMA) is an organic compound with the formula N(CH3)3. It is a colorless, hygroscopic, and flammable tertiary amine. It is a gas at room temperature but is usually sold as a 40% solution in water. (It is also sold in pressurized gas cylinders.) TMA is a nitrogenous base and can be readily protonated to give the trimethylammonium cation. Trimethylammonium chloride is a hygroscopic colorless solid prepared from hydrochloric acid. Trimethylamine is a good nucleophile, and this reaction is the basis of most of its applications. TMA is widely used in industry: it is used in the synthesis of choline, tetramethylammonium hydroxide, plant growth regulators or herbicides, strongly basic anion exchange resins, dye leveling agents, and a number of basic dyes.[5][6] At higher concentrations it has an ammonia-like odor, and can cause necrosis of mucous membranes on contact.[7] At lower concentrations, it has a "fishy" odor, the odor associated with rotting fish.
In humans, ingestion of certain plant and animal (e.g., red meat, egg yolk) food containing lecithin, choline and L-carnitine provides certain gut microbiota with the substrate to synthesize TMA, which is then absorbed into the bloodstream.[8][9] High levels of trimethylamine in the body are associated with the development of trimethylaminuria, or fish odor syndrome, caused by a genetic defect in the enzyme which degrades TMA; or by taking large doses of supplements containing choline or L-carnitine.[8][9] TMA is metabolized by the liver to trimethylamine N-oxide (TMAO); TMAO is being investigated as a possible proatherogenic substance which may accelerate atherosclerosis in those eating foods with a high content of TMA precursors.[9] TMA also causes the odor of some human infections, bad breath, and bacterial vaginosis.
Trimethylamine is a full agonist of human TAAR5,[10][11][12] a trace amine-associated receptor that is expressed in the olfactory epithelium and functions as an olfactory receptor for tertiary amines.[12][13] One or more additional odorant receptors appear to be involved in trimethylamine olfaction in humans as well.[13]
https://en.wikipedia.org/wiki/Trimethylamine
An ion-exchange resin or ion-exchange polymer is a resin or polymer that acts as a medium for ion exchange. It is an insoluble matrix (or support structure) normally in the form of small (0.25–0.5 mm radius) microbeads, usually white or yellowish, fabricated from an organic polymer substrate. The beads are typically porous, providing a large surface area on and inside them the trapping of ions occurs along with the accompanying release of other ions, and thus the process is called ion exchange. There are multiple types of ion-exchange resin. Most commercial resins are made of polystyrene sulfonate.[1]
Ion-exchange resins are widely used in different separation, purification, and decontamination processes. The most common examples are water softening and water purification. In many cases ion-exchange resins were introduced in such processes as a more flexible alternative to the use of natural or artificial zeolites. Also, ion-exchange resins are highly effective in the biodiesel filtration process.
https://en.wikipedia.org/wiki/Ion-exchange_resin
Unsymmetrical dimethylhydrazine (UDMH; 1,1-dimethylhydrazine ; НДМГ) is a chemical compound with the formula H2NN(CH3)2 that is used as a rocket propellant. It is a colorless liquid, with a sharp, fishy, ammonia-like smell typical for organic amines. Samples turn yellowish on exposure to air and absorb oxygen and carbon dioxide. It is miscible with water, ethanol, and kerosene. In concentration between 2.5% and 95% in air, its vapors are flammable. It is not sensitive to shock. Symmetrical dimethylhydrazine, 1,2-dimethylhydrazine is also known but is not as useful.[4]
https://en.wikipedia.org/wiki/Unsymmetrical_dimethylhydrazine
3-Iodothyronamine (T1AM) is an endogenous thyronamine. T1AM is a high-affinity ligand for the trace amine-associated receptor TAAR1 (TAR1, TA1), a recently discovered G protein-coupled receptor.[1][2] T1AM is the most potent endogenous TAAR1 agonist yet discovered.[3] Activation of TAAR1 by T1AM results in the production of large amounts of cAMP. This effect is coupled with decreased body temperature and cardiac output.[4] Wu et al. have pointed out that this relationship is not typical of the endocrine system, indicating that TAAR1 activity may not be coupled to G-proteins in some tissues, or that T1AM may interact with other receptor subtypes.[3]
T1AM may be part of a signaling pathway to modulate cardiac function, as the compound can induce negative inotropic effects and decrease cardiac output.[5]
https://en.wikipedia.org/wiki/3-Iodothyronamine
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 ketonefunctional group. Other phenethylamines that share this structure include the stimulants methcathinone, MDPV, mephedrone and the antidepressant bupropion.
https://en.wikipedia.org/wiki/Cathinone
Phenylisobutylamine, also known as α-ethylphenethylamine, Butanphenamine, B or AEPEA,[1] is a stimulant drug of the phenethylamine class. It is a higher homologue of amphetamine, differing from amphetamine's molecular structure only by the substitution of the methyl group at the alpha position of the side chain with an ethyl group. Compared to amphetamine, phenylisobutylamine has strongly reduced dopaminergic effects, and instead acts as a selective norepinephrine releasing agent.[citation needed] The dextroisomer of phenylisobutylamine partially substitutes for dextroamphetamine in rats.[1]
A number of derivatives of phenylisobutylamine are known, including BDB, MBDB, EBDB, butylone (bk-MBDB), eutylone (bk-EBDB), Ariadne (α-Et-DOM), 4-CAB, and 4-MAB.
"Phenylisobutylamine" is in fact a chemical misnomer because isobutylamine itself contains a branched chain. The correct name after this style for this class of compound would be "phenylsecbutylamine".
https://en.wikipedia.org/wiki/Phenylisobutylamine
1-(2-Phenylethyl)pyrrolidine (PEP) is a chemical compound. It is an analogue of 2-phenylethylamine where the amine has been replaced by a pyrrolidine ring.
It is the base chemical structure for a series of stimulant drugs, including:
All of these compounds differ from PEP in that the alpha carbon is extended and a ketone is attached to the beta carbon (with the exception of prolintane), among other modifications.
It is unknown whether PEP itself has any stimulant properties, but it can be considered likely.[citation needed]
See also[edit]
Prolintane (Catovit, Katovit, Promotil, Villescon) is a stimulant[1] and norepinephrine-dopamine reuptake inhibitor developed in the 1950s.[2] It is the member of amphetamine and derivatives. It is closely related in chemical structure to other drugs such as pyrovalerone, MDPV, and propylhexedrine and it has a similar mechanism of action.[3] Many cases of prolintane abuse have been reported.[4]
Under the trade-name "Katovit", prolintane was commercialized by the Spanish pharmaceutical company, FHER. Katovit was sold until 2001, and was most often used by students and workers as a stimulant to provide energy, promote alertness and concentration.
See also[edit]
- α-PVP (β-ketone-prolintane, prolintanone)
- Methylenedioxypyrovalerone (MDPV)
- Pyrovalerone (Centroton, Thymergix)
- Phenylpropylaminopentane
4'-Methyl-α-pyrrolidinopropiophenone (4-MePPP, MPPP or MαPPP) is a stimulant drug and substituted cathinone. It is structurally very similar to α-PPP, with only one added methyl group in the para position on the phenyl ring. 4-MePPP was sold in Germany as a designer drug in the late 1990s and early 2000s,[2][3][4] along with a number of other pyrrolidinophenone derivatives.[5][6] Although it has never achieved the same international popularity as its better-known relations α-PPP and MDPV, 4-MePPP is still sometimes found as an ingredient of grey-market "bath salt" blends[7] such as "NRG-3".[7]
Methamnetamine (also known as methylnaphetamine, MNA, MNT and PAL-1046) is a triple monoamine releasing agent and N-methyl analog of the non-neurotoxicexperimental drug naphthylaminopropane and the naphthalene analog of methamphetamine.[1][2][3] It has been sold online as a designer drug.[4][5]
It acts as a releasing agent of serotonin, norepinephrine, and dopamine, with EC50values of 13 nM, 34 nM, and 10 nM, respectively.[1]
https://en.wikipedia.org/wiki/Methamnetamine
Amphetamine[note 2] (contracted from alpha-methylphenethylamine) is a central nervous system (CNS) stimulant that is used in the treatment of attention deficit hyperactivity disorder (ADHD), narcolepsy, and obesity. Amphetamine was discovered in 1887 and exists as two enantiomers:[note 3]levoamphetamine and dextroamphetamine. Amphetamine properly refers to a specific chemical, the racemic free base, which is equal parts of the two enantiomers, levoamphetamine and dextroamphetamine, in their pure amine forms. The term is frequently used informally to refer to any combination of the enantiomers, or to either of them alone. Historically, it has been used to treat nasal congestion and depression. Amphetamine is also used as an athletic performance enhancer and cognitive enhancer, and recreationally as an aphrodisiac and euphoriant. It is a prescription drug in many countries, and unauthorized possession and distribution of amphetamine are often tightly controlled due to the significant health risks associated with recreational use.[sources 1]
The first amphetamine pharmaceutical was Benzedrine, a brand which was used to treat a variety of conditions. Currently, pharmaceutical amphetamineis prescribed as racemic amphetamine, Adderall,[note 4] dextroamphetamine, or the inactive prodrug lisdexamfetamine. Amphetamine increases monoamine and excitatory neurotransmission in the brain, with its most pronounced effects targeting the norepinephrine and dopamineneurotransmitter systems.[sources 2]
At therapeutic doses, amphetamine causes emotional and cognitive effects such as euphoria, change in desire for sex, increased wakefulness, and improved cognitive control. It induces physical effects such as improved reaction time, fatigue resistance, and increased muscle strength. Larger doses of amphetamine may impair cognitive function and induce rapid muscle breakdown. Addiction is a serious risk with heavy recreational amphetamine use, but is unlikely to occur from long-term medical use at therapeutic doses. Very high doses can result in psychosis (e.g., delusions and paranoia) which rarely occurs at therapeutic doses even during long-term use. Recreational doses are generally much larger than prescribed therapeutic doses and carry a far greater risk of serious side effects.[sources 3]
Amphetamine belongs to the phenethylamine class. It is also the parent compound of its own structural class, the substituted amphetamines,[note 5]which includes prominent substances such as bupropion, cathinone, MDMA, and methamphetamine. As a member of the phenethylamine class, amphetamine is also chemically related to the naturally occurring trace amineneuromodulators, specifically phenethylamine and N-methylphenethylamine, both of which are produced within the human body. Phenethylamine is the parent compound of amphetamine, while N-methylphenethylamine is a positional isomer of amphetamine that differs only in the placement of the methyl group.[sources 4]
https://en.wikipedia.org/wiki/Amphetamine
d-Deprenyl, also known as or dextro-N-propargyl-N-methylamphetamine, is an MAO-B inhibitor that metabolizes into d-amphetamine and d-methamphetamine and is therefore also a norepinephrine-dopamine releasing agent.[1][2][3][4][5] It is the opposite enantiomer of l-deprenyl (selegiline).
l-Deprenyl, also an MAO-B inhibitor, metabolizes to l-amphetamine and l-methamphetamine, which are both norepinephrine releasing agents. In contrast, d-deprenyl additionally has dopaminergic effects and has been found to be reinforcingin scientific research, whereas l-deprenyl is not known to have any appreciable psychological reinforcement.[6][7]
In addition to its actions as an MAO-B inhibitor and NDRA, d-deprenyl has been found to bind with high affinity to the σ1 receptor (Ki = 79 nM) similarly to various other amphetamine derivatives.[8][9] Its l-isomer, selegiline, binds with 3.5-fold lower affinity in comparison.[8][9]
https://en.wikipedia.org/wiki/D-Deprenyl
Ethylone, also known as 3,4-methylenedioxy-N-ethylcathinone (MDEC, βk-MDEA), is a recreational designer drug classified as an entactogen, stimulant, and psychedelic of the phenethylamine, amphetamine, and cathinone chemical classes. It is the β-keto analogue of MDEA ("Eve"). Ethylone has only a short history of human use and is reported to be less potent than its relative methylone.[citation needed]In the United States, it began to be found in cathinone products in late 2011.[1]
Very little data exists about the pharmacological properties, metabolism, and toxicity of ethylone, and although several ethylone-related deaths have been reported, the cause of death was not due to ingestion of ethylone.[1]
https://en.wikipedia.org/wiki/Ethylone
β-Keto-1,3-benzodioxolyl-N-ethylbutanamine (Eutylone, bk-EBDB, N-Ethylbutylone) is a stimulant and empathogenic compound developed in the 1960s,[1] which has been reported as a novel designer drug,[2] first being reported to the EMCDDA in 2014 but becoming widespread internationally in 2019-2020 following bans on the related compound ephylone.[3][4][5]
Legal status[edit]
Sweden's public health agency suggested classifying Eutylone as a hazardous substance, on September 25, 2019.[6]
https://en.wikipedia.org/wiki/Eutylone
Bupropion, sold under the brand names Wellbutrin and Zyban among others, is an atypical antidepressant primarily used to treat major depressive disorder and to support smoking cessation.[6][7] Bupropion is an effective antidepressant on its own, but it is also popular as an add-on medication in the cases of incomplete response to the first-line selective serotonin reuptake inhibitor (SSRI) antidepressant.[7][8]Bupropion has several features that distinguish it from other antidepressants: it does not usually cause sexual dysfunction;[7] it is not associated with weight gain[7] and sleepiness,[9] and it is more effective than SSRIs at improving symptoms of hypersomnia and fatigue.[10]
Common adverse effects of bupropion with the greatest difference from placebo are dry mouth, nausea, constipation, insomnia, anxiety, tremor, and excessive sweating.[11] Raised blood pressure is notable.[12] Rare but serious side effects include seizure,[11] liver toxicity,[13] psychosis,[14] and risk of overdose.[15] Bupropion use during pregnancy may be associated with increased odds of congenital heart defects.[16]
Bupropion acts as a norepinephrine–dopamine reuptake inhibitor and a nicotinic receptor antagonist.[5] Chemically, it is an aminoketone that belongs to the class of substituted cathinones and more generally that of substituted amphetamines and substituted phenethylamines.[1][17]
Bupropion was invented by Nariman Mehta, who worked at Burroughs Wellcome, in 1969.[18] It was first approved for medical use in the United States in 1985.[19]Bupropion was originally called by the generic name amfebutamone, before being renamed in 2000.[20] In 2018, it was the 27th most commonly prescribed medication in the United States, with more than 24 million prescriptions.[21][22]
https://en.wikipedia.org/wiki/Bupropion
Ethylbenzodioxolylbutanamine (EBDB; Ethyl-J) is a lesser-known entactogen, stimulant, and psychedelic. It is the N-ethyl analogue of benzodioxylbutanamine(BDB; "J"), and also the α-ethyl analogue of methylenedioxyethylamphetamine(MDEA; "Eve").
EBDB was first synthesized by Alexander Shulgin. In his book PiHKAL, the minimum dosage consumed was 90 mg, and the duration is unknown.[1] EBDB produced few to no effects at the dosage range tested in PiHKAL, but at higher doses of several hundred milligrams it produces euphoric effects similar to those of methylbenzodioxylbutanamine (MBDB; "Eden", "Methyl-J"), although milder and shorter lasting.[citation needed]
Very little data exists about the pharmacological properties, metabolism, and toxicity of EBDB.
https://en.wikipedia.org/wiki/1,3-Benzodioxolyl-N-ethylbutanamine
Pyrovalerone (Centroton, 4-Methyl-β-keto-prolintane, Thymergix, O-2371)[1] is a psychoactive drug with stimulant effects via acting as a norepinephrine-dopamine reuptake inhibitor (NDRI), and is used for the clinical treatment of chronic fatigue or lethargy[2] and as an anorectic or appetite suppressant for weight loss purposes. It was developed in the late 1960s and has since been used in France and several other European countries, and although pyrovalerone is still occasionally prescribed, it is used infrequently due to problems with abuse and dependence.[3] It is closely related on a structural level to a number of other stimulants, such as MDPV and prolintane (Promotil, Katovit).
Side effects of pyrovalerone include anorexia or loss of appetite, anxiety, fragmented sleep or insomnia, and trembling, shaking, or muscle tremors. Withdrawal following abuse upon discontinuation often results in depression.
The R-enantiomer of pyrovalerone is devoid of activity.[4]
https://en.wikipedia.org/wiki/Pyrovalerone
Metirosine (INN and BAN; α-Methyltyrosine, Metyrosine USAN, AMPT) is an antihypertensive drug. It inhibits the enzyme tyrosine hydroxylase and, therefore, catecholamine synthesis, which, as a consequence, depletes the levels of the catecholamines dopamine, adrenaline and noradrenaline in the body.
It is available as a generic medication.[1]
https://en.wikipedia.org/wiki/Metirosine
Synephrine, or, more specifically, p-synephrine, is an alkaloid, occurring naturally in some plants and animals, and also in approved drugs products as its m-substituted analog known as neo-synephrine.[1] p-Synephrine (or formerly Sympatoland oxedrine [BAN]) and m-synephrine are known for their longer acting adrenergiceffects compared to epinephrine and norepinephrine. This substance is present at very low concentrations in common foodstuffs such as orange juice and other orange (Citrus species) products, both of the "sweet" and "bitter" variety. The preparations used in traditional Chinese medicine (TCM), also known as Zhi Shi, are the immature and dried whole oranges from Citrus aurantium (Fructus Aurantii Immaturus). Extracts of the same material or purified synephrine are also marketed in the US, sometimes in combination with caffeine, as a weight-loss-promoting dietary supplement for oral consumption. While the traditional preparations have been in use for millennia as a component of TCM-formulas, synephrine itself is not an approved OTC drug. As a pharmaceutical, m-synephrine (phenylephrine) is still used as a sympathomimetic (i.e. for its hypertensive and vasoconstrictor properties), mostly by injection for the treatment of emergencies such as shock, and rarely orally for the treatment of bronchial problems associated with asthma and hay-fever.[a]
It is important to distinguish between studies concerning synephrine as a single chemical entity (synephrine can exist in the form of either of two stereoisomers, d- and l-synephrine, which are chemically and pharmacologically distinct), and synephrine which is mixed with other drugs and/or botanical extracts in a "Supplement", as well as synephrine which is present as only one chemical component in a naturally-occurring mixture of phytochemicals such as the rind or fruit of a bitter orange. Mixtures containing synephrine as only one of their chemical components (regardless of whether these are of synthetic or natural origin) should not be assumed to produce exactly the same biological effects as synephrine alone.[2]
In physical appearance, synephrine is a colorless, crystalline solid and is water-soluble. Its molecular structure is based on a phenethylamine skeleton and is related to those of many other drugs and to the major neurotransmitters epinephrine and norepinephrine.
https://en.wikipedia.org/wiki/Synephrine
Orciprenaline, also known as metaproterenol, is a bronchodilator used in the treatment of asthma.[1][2] Orciprenaline is a moderately selective β2 adrenergic receptor agonist that stimulates receptors of the smooth muscle in the lungs, uterus, and vasculature supplying skeletal muscle, with minimal or no effect on α adrenergic receptors. The pharmacologic effects of β adrenergic agonist drugs, such as orciprenaline, are at least in part attributable to stimulation through β adrenergic receptors of intracellular adenylyl cyclase, the enzyme which catalyzes the conversion of ATP to cAMP. Increased cAMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from many cells, especially from mast cells.
https://en.wikipedia.org/wiki/Orciprenaline
Dopexamine is a synthetic analogue of dopamine that is administered intravenously in hospitals to reduce exacerbations of heart failure and to treat heart failure following cardiac surgery. It is not used often, as more established drugs like epinephrine, dopamine, dobutamine, norepinephrine, and levosimendan work as well. It works by stimulating beta-2 adrenergic receptors and peripheral dopamine receptor D1 and dopamine receptor D2. It also inhibits the neuronal re-uptake of norepinephrine.
The most common adverse effects include fast heart beats and nausea.
It was discovered by scientists at Fisons, which licensed it to Ipsen in 1993, and Ipsen in turn licensed it to Élan in 1999. Ipsen licensed rights in North America and Japan to Circassia in 2008; the drug had never been approved in those countries. Dopexamine went off-patent in 2010.
https://en.wikipedia.org/wiki/Dopexamine
Diphenidine (1,2-DEP, DPD, DND) is a dissociative anesthetic that has been sold as a designer drug.[1][2][3] The synthesis of diphenidine was first reported in 1924, and employed a Bruylants reaction analogous to the one that would later be used to discover phencyclidine in 1956.[1] Shortly after the 2013 UK ban on arylcyclohexylamines, diphenidine and the related compound methoxphenidinebecame available on the grey market.[1] Anecdotal reports describe high doses of diphenidine producing "bizarre somatosensory phenomena and transient anterograde amnesia."[1] Diphenidine and related diarylethylamines have been studied in vitro as treatments for neurotoxic injury and are antagonists of the NMDA receptor.[4][5][6][7][8] In dogs diphenidine exhibits greater antitussive potency than codeine phosphate.[9][10]
Electrophysiological analysis demonstrates that the amplitude of NMDA-mediated fEPSPs are reduced by diphenidine and ketamine to a similar extent, with diphenidine displaying a slower onset of antagonism.[6] The two enantiomers of diphenidine differ greatly in their ability to block the NMDA receptor, with the more potent (S)-enantiomer possessing affinity forty times higher than the (R)-enantiomer.[5] Since diphenidine's introduction in 2013 vendors have stated the drug "acts on dopamine transport" yet no data concerning the action of diphenidine on the dopamine transporter was published until 2016.[1] Diphenidine's highest affinity is for the NMDA receptor, but it does display submicromolar affinity for the σ1 receptor, σ2receptor and dopamine transporter.[11][12]
Since 2014 there have been several published reports of diphenidine being sold in combination with other research chemicals, particularly synthetic cannabinoids and stimulants in Japanese herbal incense blends.[13][14][15] The first reported seizure concerned a Japanese product called "fragrance powder" containing diphenidine and benzylpiperazine.[16] A herbal incense sold in the Shizuoka Prefecture under the name "Aladdin Spacial [sic] Edition" was found to contain diphenidine and 5F-AB-PINACA at concentrations of 289 mg/g and 55.5 mg/g, respectively.[13] A product called ‘‘Herbal Incense. The Super Lemon’’ containing AB-CHMINACA, 5F-AMB, and diphenidine was implicated in a fatal poisoning.[14] Most recently diphenidine consumed in conjunction with three substituted cathinones, three benzodiazepines, and alcohol was implicated in a fatal ingestion of "bath salt" and "liquid aroma" products in Japan.[17]
In Canada, MT-45 and its analogues were made Schedule I controlled substances.[18] Possession without legal authority can result in maximum seven years imprisonment. Further, Health Canada amended the Food and Drug Regulations in May, 2016 to classify DND as a restricted drug. Only those with a law enforcement agency, person with an exemption permit or institutions with Minister's authorization may possess the drug.
https://en.wikipedia.org/wiki/Diphenidine
Dizocilpine (INN), also known as MK-801, is a noncompetitive antagonist of the N-Methyl-D-aspartate (NMDA) receptor, a glutamate receptor, discovered by a team at Merck in 1982.[1] Glutamate is the brain's primary excitatory neurotransmitter. The channel is normally blocked with a magnesium ion and requires depolarization of the neuron to remove the magnesium and allow the glutamate to open the channel, causing an influx of calcium, which then leads to subsequent depolarization.[2]Dizocilpine binds inside the ion channel of the receptor at several of PCP's binding sites thus preventing the flow of ions, including calcium (Ca2+), through the channel. Dizocilpine blocks NMDA receptors in a use- and voltage-dependent manner, since the channel must open for the drug to bind inside it.[3] The drug acts as a potent anti-convulsant and probably has dissociative anesthetic properties, but it is not used clinically for this purpose because of the discovery of brain lesions, called Olney's lesions (see below), in laboratory rats. Dizocilpine is also associated with a number of negative side effects, including cognitive disruption and psychotic-spectrum reactions. It inhibits the induction of long term potentiation[4] and has been found to impair the acquisition of difficult, but not easy, learning tasks in rats[5][6] and primates.[7] Because of these effects of dizocilpine, the NMDA receptor pore-blocker ketamine is used instead as a dissociative anesthetic in human medical procedures. While ketamine may also trigger temporary psychosis in certain individuals, its short half-life and lower potency make it a much safer clinical option. However, dizocilpine is the most frequently used non-competitive NMDA receptor antagonist in animal models to mimic psychosis for experimental purposes.
Dizocilpine has also been found to act as a nicotinic acetylcholine receptorantagonist.[8][9][10] It has been shown to bind to and inhibit the serotonin and dopamine transporters as well.[11][12]
https://en.wikipedia.org/wiki/Dizocilpine
Dobutamine is a medication used in the treatment of cardiogenic shock and severe heart failure.[2][3] It may also be used in certain types of cardiac stress tests.[2] It is given by injection into a vein or intraosseous as a continuous infusion.[2] The amount of medication needs to be adjusted to the desired effect.[2] Onset of effects is generally seen within 2 minutes.[2]
Common side effects include a fast heart rate, an irregular heart beat, and inflammation at the site of injection.[2][4] Use is not recommended in those with idiopathic hypertrophic subaortic stenosis.[2] It primarily works by direct stimulation of β1 receptors, which increases the strength of the heart's contractions.[2] Generally it has little effect on a person's heart rate.[2]
Dobutamine was approved for medical use in the United States in 1978.[2] It is available as a generic medication.[4] It was initially made from isoproterenol.[3]
https://en.wikipedia.org/wiki/Dobutamine
Etafedrine (INN) or ethylephedrine is a long-acting bronchodilator and has the brand name Nethaprin. It was previously commercially available as both the free base and as the hydrochloride salt from Sanofi-Aventis (now Sanofi) but is now no longer marketed.
Pharmacology[edit]
Unlike ephedrine and tyramine, etafedrine does not induce the release of epinephrine or norepinephrine and instead acts as a selective β2 adrenoreceptor agonist, thereby mediating its bronchodilator effects.[1]
https://en.wikipedia.org/wiki/Etafedrine
Famprofazone (Gewodin, Gewolen) is a nonsteroidal anti-inflammatory agent(NSAID) of the pyrazolone series which is available over-the-counter in some countries such as Taiwan.[1][2][3] It has analgesic, anti-inflammatory, and antipyreticeffects.[1][2] Famprofazone has been known to produce methamphetamine as an active metabolite, with 15-20% of an oral dose being converted to it.[4][5] As a result, famprofazone has occasionally been implicated in causing positives on drug tests for amphetamines.[3]
https://en.wikipedia.org/wiki/Famprofazone
Hexapradol (INN) is a psychostimulant drug which was never marketed.[1]
It also had cytoprotective/antiulcer properties.[2]
https://en.wikipedia.org/wiki/Hexapradol
Theodrenaline (INN), also known as noradrenalinoethyltheophylline, is a chemical linkage of norepinephrine (noradrenaline) and theophylline used as a cardiac stimulant.[1]
It is sometimes combined with cafedrine.[1]
https://en.wikipedia.org/wiki/Theodrenaline
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