Validity testing is performed for the integrity of urine samples.

Validity Test Menu: Creatinine • Nitrite • pH  • Specific Gravity • Glutaraldehyde  • Oxidants • Pyridium Chlorochromate


6-Monoacetylmorphine (6-MAM)

6-Monoacetylmorphine (6-MAM) or 6-acetylmorphine (6-AM) is one of three active metabolites of heroin (diacetylmorphine), the others being morphine and the much less active 3-monoacetylmorphine (3-MAM).

6-MAM is rapidly created from heroin in the body, and then is either metabolized into morphine or excreted in the urine. Since 6-MAM is a unique metabolite to heroin, its presence in the urine confirms that heroin was the opioid used. This is significant because on a urine immunoassay drug screen, the test typically tests for morphine, which is a metabolite of a number of legal and illegal opiates/opioids such as codeine, morphine sulfate, and heroin. Trace amounts of 6-MAM, a specific metabolite of heroin, are also excreted for approximately 6-8 hours following heroin use.[1] so a urine specimen must be collected soon after the last heroin use, however, the presence of 6-MAM suggests that heroin was used as recently as within the last day. 6-MAM is naturally found in the brain of certain mammals.[2]Heroin is rapidly metabolized by esterase enzymes in the brain and has an extremely short half-life. It has also relatively weak affinity to μ-opioid receptors because the 3-hydroxy group which is essential for effective binding to the receptor is masked by the acetyl group. Therefore, heroin acts as a pro-drug, serving as a lipophilic transporter of sorts for the systemic delivery of morphine, which actively binds with μ-opioid receptors.[3][4]


Alprazolam (trade name Xanax)

Alprazolam /ælˈpræzəlæm/ or /ælˈpreɪzəlæm/ (trade name Xanax /ˈzænæks/), available under other generic names, is a short-actinganxiolytic of the benzodiazepine class of psychoactive drugs. Alprazolam, like other benzodiazepines, binds to specific sites on theGABAAreceptor. Alprazolam is commonly used and FDA approved for the medical treatment of panic disorder, and anxiety disorders, such asgeneralized anxiety disorder (GAD) or social anxiety disorder (SAD).[3][4] Alprazolam is available for oral administration in compressed tablet (CT) and extended-release capsule (XR) formulations. Alprazolam possesses anxiolytic, sedative, hypnotic, skeletal muscle relaxant, anticonvulsant, and amnestic properties.[5]

lprazolam has a fast onset of action and symptomatic relief. Ninety percent of peak effects are achieved within the first hour of using either the CT formulation or the XR formulation in preparation for panic disorder, and full peak effects are achieved in 1.5 and 1.6 hours respectively.[6][7]Peak benefits achieved for generalized anxiety disorder (GAD) may take up to a week.[8][9] Tolerance to the anxiolytic/antipanic effects is controversial with some authoritative sources reporting the development of tolerance,[10] and others reporting no development of tolerance;[3][11]tolerance will however, develop to the sedative-hypnotic effects within a couple of days.[11] Withdrawal symptoms or rebound symptoms may occur after ceasing treatment abruptly following a few weeks or longer of steady dosing, and may necessitate a gradual dose reduction.[8][12] 7-Aminoclonazepam is the metabolite of clonazepam.



Amphetamine[note 1] (pronunciation: i/æmˈfɛtəmiːn/; contracted from alpha methylphenethylamine) is a potent central nervous system (CNS)stimulant of the phenethylamine class that is used in the treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy. Amphetamine was discovered in 1887 and exists as two enantiomers: levoamphetamine and dextroamphetamine.[note 2] 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. However, 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, depression, and obesity. Amphetamine is also used as a performance and cognitive enhancer, and recreationally as an aphrodisiac and euphoriant. It is a prescription medication in many countries, and unauthorized possession and distribution of amphetamine is often tightly controlled due to the significant health risks associated with uncontrolled or heavy use.[sources 1]

The first pharmaceutical amphetamine was Benzedrine, a brand of inhalers used to treat a variety of conditions. Currently, pharmaceutical amphetamine is typically prescribed as Adderall,[note 3] dextroamphetamine, or the inactive prodrug lisdexamfetamine. Amphetamine, through activation of a trace amine receptor, increases biogenic amine and excitatory neurotransmitter activity in the brain, with its most pronounced effects targeting the catecholamine neurotransmitters norepinephrine and dopamine. At therapeutic doses, this causes emotional and cognitive effects such as euphoria, change in libido, increased wakefulness, and improved cognitive control. It induces physical effects such as decreased reaction time, fatigue resistance, and increased muscle strength.[sources 2]

Much larger doses of amphetamine are likely to impair cognitive function and induce rapid muscle breakdown. Drug addiction is a serious risk with large recreational doses, but rarely arises from medical use. 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 is also the parent compound of its own structural class, the substituted amphetamines,[note 4] which includes prominent substances such as bupropion, cathinone, MDMA (ecstasy), and methamphetamine. As a member of the phenethylamine class, amphetamine is also chemically related to the naturally occurring trace amine neuromodulators, specifically phenethylamine[note 5] and N-methylphenethylamine, both of which are produced within the human body. Phenethylamine is the parent compound of amphetamine, while N-methylphenethylamine is aconstitutional isomer that differs only in the placement of the methyl group.[sources 4]



Benzoylecgonine is a topical analgesic and the main metabolite of cocaine. Benzoylecgonine is used as the main pharmaceutical ingredient in the prescription drug Esterom, a topical solution used for the relief of muscle pain. Chemically, benzoylecgonine is ecgonine benzoate. It is a primary metabolite of cocaine.[1] Benzoylecgonine is the compound tested for in most substantive cocaine urinalyses. It is the corresponding carboxylic acid of cocaine, its methyl ester. It is formed in the liver by the metabolism of cocaine, catalysed by carboxylesterases, and subsequently excreted in the urine. It can be found in the urine for considerably longer than the cocaine itself which is generally cleared out within 5 days. Small amounts may be traced back to certain OTC (over the counter) medications, after having been metabolized in the liver.]



Buprenorphine is a semisynthetic opioid derivative of thebaine. It is a mixed agonist–antagonist opioid receptor modulator that is used to treatopioid addiction in higher dosages, to control moderate acute pain in non-opioid-tolerant individuals in lower dosages and to control moderatechronic pain in even smaller doses.[3] It is available in a variety of formulations: subutex, Suboxone, Zubsolv, Bunavail (available as buprenorphine HCl alone or buprenorphine and naloxone HCl; typically used for opioid addiction), Temgesic (sublingual tablets for moderate to severe pain), Buprenex (solutions for injection often used for acute pain in primary-care settings), Norspan and Butrans (transdermal preparations used for chronic pain).[4]



Carisoprodol is a centrally acting skeletal muscle relaxant. It is slightly soluble in water and freely soluble in alcohol, chloroform and acetone. The drug’s solubility is practically independent of pH. Carisoprodol is manufactured and marketed in the United States by Meda Pharmaceuticals[1] under the brand name Soma, and in the United Kingdom and other countries under the brand names Sanoma and Carisoma. The drug is available by itself or mixed with aspirin, and in one preparation with codeine and caffeine, as well. Although carisoprodol has significant pharmacological activity, its benefit in therapy is likely due mostly to the meprobamate metabolite as meprobamate remains in the system significantly longer and reaches a higher peak plasma concentration than the parent drug a few hours following administration. This is further evidenced by carisoprodol’s ability to maintain relevant benefits when administered 3-4 times a day despite its short half-life of only two hours.



Clonazepam[2] is a benzodiazepine drug having anxiolytic, anticonvulsant,[3] muscle relaxant, amnestic, sedative, and hypnotic properties.[4] It is marketed under the trade name Rivotril by Roche in Argentina, Australia, Belgium, Brazil, Bulgaria, Canada, Colombia, Costa Rica, Croatia, the Czech Republic, Denmark, Germany, Hungary, Ireland, Italy, Mexico, Norway, Portugal, Peru, South Africa, the United States, and Spain; Linotriland Clonotril in India, South Korea, and other parts of Europe; and under the trade name Klonopin by Roche in the United States. Other names, such as Ravotril, Rivatril, Iktorivil, Clonex, Paxam, Petril, Naze and Kriadex, are known throughout the world.[citation needed] Clonazepam has an elimination half-life of 18–50 hours to 19–60 hours,[5] and is generally considered to be an intermediate-acting benzodiazepine. Clonazepam has no active metabolites.[5] Clonazepam is a chlorinated derivative of nitrazepam[6] and therefore a chloro-nitrobenzodiazepine.[7]

Clonazepam has an intermediate onset of action, with a peak blood level occurring one to four hours after oral administration. Long-term effects of benzodiazepines include tolerance, benzodiazepine dependence, and benzodiazepine withdrawal syndrome, which occurs in one third of patients treated with clonazepam for longer than four weeks.[8]

Benzodiazepines such as clonazepam have a fast onset of action, high effectivity rate, and low toxicity in overdose; however, as with most medications, it may have drawbacks due to adverse or paradoxical effects. The benzodiazepine clorazepate may be an alternative to clonazepam due to a slow onset of tolerance and its availability in a slow-release formula to counter fluctuations in blood levels. The pharmacological property of clonazepam, as with other benzodiazepines, is the enhancement of the neurotransmitter GABA via modulation of the GABAA receptor.[8]   Alpha-Hydroxyalprazolam is a metabolite of Alprazolam


Codeine or 3-methylmorphine

Codeine or 3-methylmorphine (a naturally occurring methylated morphine) is an opiate used for its stimulant, analgesic, antitussive,antidiarrheal, antihypertensive, anxiolytic,[citation needed] antidepressant,[citation needed] sedative and hypnotic properties. It is also used to suppress premature labor contractions, myocardial infarction, and has many other potential and indicated uses. It is often sold as a salt in the form of eithercodeine sulfate or codeine phosphate in the United States and Australia; codeine hydrochloride is more common worldwide and the citrate, hydroiodide, hydrobromide, tartrate, and other salts are also seen.[2]

Codeine is the second-most predominant alkaloid in opium, at up to three percent. Although codeine can be extracted from natural sources, asemi-synthetic process is the primary source of codeine for pharmaceutical use. It is considered the prototype of the weak to midrange opioids(tramadol, dextropropoxyphene, dihydrocodeine, hydrocodone, oxycodone).

It is on the WHO Model List of Essential Medicines, a list of the most important medication needed in a basic health system.[3]


Desipramine (also known as desmethylimipramine)

Desipramine (also known as desmethylimipramine) is a tricyclic antidepressant (TCA). It inhibits the reuptake of norepinephrine and to a minor extent serotonin. It is used to treat depression, but not considered a first line treatment since the introduction of SSRI antidepressants. Desipramine is an active metabolite of imipramine. It is sold under the brand names Norpramin, and Pertofrane.[2]

Medical uses It is primarily used for the treatment of depression.[2] It may also be useful to treat symptoms of attention deficit hyperactivity disorder.[3] Evidence of benefit is only in the short term and with concerns of side effects its overall usefulness is not clear.[4]

It has also been tried, albeit with little evidence of efficacy, in the treatment of cocaine dependence.[5] Evidence for usefulness in neuropathic pain is also poor.[6]

Adverse effects[edit]

Desipramine tends to be less sedating than other TCAs and tends to produce fewer anticholinergic effects like dry mouth, urinary retention, blurred vision, memory impairment and constipation.[7]


Diazepam (first marketed as Valium)

Diazepam /daɪˈæzɨpæm/, first marketed as Valium /ˈvæliəm/ by Hoffmann-La Roche, is a benzodiazepine drug. It is commonly used to treat a wide range of conditions, including anxiety, panic attacks, insomnia, seizures (including status epilepticus), muscle spasms (such as in tetanuscases), restless legs syndrome, alcohol withdrawal syndrome, benzodiazepine withdrawal syndrome, opioid withdrawal syndrome, and Ménière’s disease. It may also be used before certain medical procedures (such as endoscopies) to reduce tension and anxiety, and in some surgical procedures to induce amnesia (it may be used to hasten the onset of intravenous (IV) anesthesia while reducing dose requirements or as the sole agent when IV anesthesia is not available or is contraindicated).[1][2]

It possesses anxiolytic, anticonvulsant, hypnotic, sedative, skeletal muscle relaxant, and amnestic properties.[3] The pharmacological action of diazepam enhances the effect of the neurotransmitter gamma-Aminobutyric acid (GABA) by binding to the benzodiazepine site on the GABAAreceptor (via the constituent chlorine atom) leading to central nervous system depression.[4]

Adverse effects of diazepam include anterograde amnesia (especially at higher doses) and sedation, as well as paradoxical effects such as excitement, rage, or worsening of seizures in epileptics. Benzodiazepines also can cause or worsen depression, particularly after extended periods of use[citation needed]. Long-term effects of benzodiazepines such as diazepam include tolerance, benzodiazepine dependence, andbenzodiazepine withdrawal syndrome upon dose reduction. After cessation of benzodiazepines, cognitive deficits may persist for at least six months and longer than six months may be needed for recovery from some deficits.[4] Diazepam also has physical dependence potential and can cause serious problems of physical dependence with long-term use. Compared to other benzodiazepines, though, physical withdrawal from diazepam following long-term use is usually far more mild due to its long elimination half-life. Diazepam is the drug of choice for treating benzodiazepine dependence, with its low potency, long duration of action, and availability of low-dose tablets, making it ideal for gradual dose reduction and the circumvention of withdrawal symptoms.[5] Diazepam can also be used to treat depression,[citation needed] but newer drugs are generally favored as more effective.

Advantages of diazepam are a rapid onset of action[6] and high efficacy rates, which are important for managing acute seizures, anxiety attacks, and panic attacks; benzodiazepines also have a relatively low toxicity in overdose.[4] Diazepam is a core medicine in the World Health Organization’s Essential Drugs List, the minimum medical needs for a basic health-care system.[7] Diazepam, first synthesized by Leo Sternbach,[8] has been one of the most frequently prescribed medications in the world since its launch in 1963.



EDDP is the most important metabolite of methadone. It is excreted in the bile and urine together with the other metabolite EMPD. EDDP is formed by N-demthylation and cyclisation of methadone in the liver. The part of the unchanged excreted methadone is variable and depends on the urine’s pH value, dose, and the patient’s metabolism. Therefore, detection of the metabolite EDDP instead of methadone itself is useful because interferences of the patient’s metabolism are avoided. EDDP can be detected within 4 to 6 hours after use. It can be cleared by the body within 2 to 3 days after use.


Fentanyl (also known as fentanil)

Fentanyl (also known as fentanil, brand names Sublimaze,[3] Actiq, Durogesic, Duragesic, Fentora, Matrifen, Haldid, Onsolis,[4] Instanyl,[5]Abstral,[6] Lazanda[7] and others[8]) is a potent, synthetic opioid analgesic with a rapid onset and short duration of action.[9] It is a strong agonist at the μ-opioid receptors. Historically, it has been used to treat breakthrough pain and is commonly used in pre-procedures as a pain reliever as well as an anesthetic in combination with a benzodiazepine.

Fentanyl is approximately 80 to 100 times more potent than morphine and roughly 15 to 20 times more potent than heroin.[10][11]

Fentanyl was first synthesized by Paul Janssen in 1960[12] following the medical inception of pethidine several years earlier. Janssen developed fentanyl by assaying analogues of the structurally related drug pethidine for opioid activity.[13] The widespread use of fentanyl triggered the production of fentanyl citrate (the salt formed by combining fentanyl and citric acid in a 1:1 stoichiometry),[14] which entered the clinical practiceas a general anaesthetic under the trade name Sublimaze in the 1960s. Following this, many other fentanyl analogues were developed and introduced into medical practice, including sufentanil, alfentanil, remifentanil, and lofentanil.

In the mid-1990s, fentanyl was first introduced for widespread palliative use with the clinical introduction of the Duragesic patch, followed in the next decade by the introduction of the first quick-acting prescription formulations of fentanyl for personal use, the Actiq lollipop and Fentorabuccal tablets. Through the delivery method of transdermal patches, as of 2012 fentanyl was the most widely used synthetic opioid in clinical practice,[citation needed] with several new delivery methods now available, including a sublingual spray for cancer patients.[15][16]

Fentanyl and its derivatives are used recreationally. Deaths have resulted from both recreational and improper medical use.[17]



Hydrocodone is a semi-synthetic opioid synthesized from codeine, one of the opioid alkaloids found in the opium poppy. It is a narcoticanalgesic used orally as an antitussive/cough suppressant, but also commonly taken orally for relief of moderate to severe pain.[1]

Hydrocodone is prescribed predominantly within the United States, with the International Narcotics Control Board reporting that 99% of the worldwide supply in 2007 was consumed in the United States.[2] The Administrative Controlled Substances Code Number (ACSCN) for hydrocodone is 9193 and the aggregate production quota for 2014 is 99,625 kilograms in the U.S.[3][4] Hydrocodone is used to treat moderate to severe pain and as an antitussive to treat cough.[1] In one study comparing the potency of hydrocodone to that of oxycodone, it was found that it took 50% more hydrocodone to achieve the same degree of miosis (pupillary contraction).[5] The investigators interpreted this to mean that oxycodone is about 50% more potent than hydrocodone. However, in a study of emergency room patients with fractures, it was found that an equal amount of either drug provided about the same degree of pain relief, indicating that there is little practical difference between them when used for that purpose.[6] Some references state that the analgesic action of hydrocodone begins in 20–30 minutes and lasts about 4–8 hours.[7] The manufacturer’s information says onset of action is about 10–30 minutes and duration is about 4–6 hours.[8] Recommended dosing interval is 4–6 hours.



Hydromorphone, a more common synonym for dihydromorphinone (not to be confused with dihydromorphine, which is a different derivative of the morphine family), commonly a hydrochloride (brand names Palladone, Dilaudid, and numerous others) is a very potent centrally actinganalgesic drug of the opioid class. It is a derivative of morphine; to be specific, a hydrogenated ketone thereof, and comparatively, hydromorphone is to morphine as hydrocodone is to codeine and, therefore, a semi-synthetic drug. It is in medical terms an opioid analgesic and in legal terms a narcotic. Hydromorphone is commonly used in the hospital setting, mostly intravenously (IV) because its bioavailability orally, rectally, and intranasally is very low. Sublingual administration(under the tongue) is usually superior to swallowing for bioavailability and effects, however Hydromorphone, like most opiates, is bitter and hydrophilic, not lipophilic, so is absorbed poorly/slowly through mouth membranes.[4]

Hydromorphone is much more soluble in water than morphine and therefore hydromorphone solutions can be produced to deliver the drug in a smaller volume of water. The hydrochloride salt is soluble in three parts of water whereas a gram of morphine hydrochloride dissolves in 16 ml of water; for all common purposes the pure powder for hospital use can be used to produce solutions of virtually arbitrary concentration. When the powder has appeared on the street, this very small volume of powder needed for a dose means that overdoses are likely for those who mistake it for heroin or other powdered narcotics, especially those that have been cut or ‘stepped on’ already.

Very small quantities of hydromorphone are detected in assays of opium on rare occasions; it appears to be produced by the plant under circumstances and by processes which are not understood at this time and may include the action of bacteria. A similar process and/or other metabolic processes in the plant may very well be responsible for the very low quantities of hydrocodone also found on rare occasions in opium and alkaloid mixtures derived therefrom; dihydrocodeine, oxymorphol, oxycodone, oxymorphone, metopon and possibly other derivatives of morphine and/or hydromorphone also are found in trace amounts in opium.



JWH 018 is a mildly selective agonist of the peripheral cannabinoid (CB2) receptor, derived from the aminoalkylindole WIN 55,212-2. The Ki values for binding central cannabinoid (CB1) and CB2 receptors are 9.0 and 2.94 nM, respectively, for a CB1:CB2 ratio of 3.06.1 JWH 018 is one of several synthetic CBs which have been included in smoking mixtures. JWH 018 N-(5-hydroxypentyl) metabolite is a major urinary metabolite of JWH 018, characterized by monohydroxylation of the N-alkyl chain.2 In urine samples, this metabolite is almost completely glucuronidated.



JWH 073 is a potent cannabimimetic that has been identified as an adulterant in smoking mixtures. JWH 073 N-(3-hydroxybutyl) metabolite is expected to be produced during the metabolism of JWH 073 by human liver microsomes in vitro, generated by the oxidation of the aminoalkyl chain.1,2 The biological actions of this metabolite are unknown.



Ketamine (INN) is a medication used mainly for starting and maintaining anesthesia. Other uses include sedation in intensive care, as a pain killer, as treatment of bronchospasm, as a treatment for complex regional pain syndrome and as an antidepressant. It induces a trance like state while providing pain relief, sedation, and memory loss.[2] Heart function, breathing and airway reflexes generally remain functional.[2]

Common side effects include a number of psychological reactions as the medication wears.[3] This may include agitation, confusion andpsychosis among others.[3][4] Elevated blood pressure and muscle tremors are relatively common, while low blood pressure and a decrease in breathing is less so.[3][4] Spasms of the larynx may rarely occur.[3]

Pharmacologically, ketamine is classified as an NMDA receptor antagonist, but it also acts at numerous other sites (including opioid receptorsand monoamine transporters).[5] Like other drugs in its class, such as phencyclidine (PCP), it is classified as a dissociative agent.[6]

Ketamine was first developed in 1962.[7] It is on the WHO Model List of Essential Medicines, a list of essential medicines that should be available in a health system.[8] Its hydrochloride salt is sold as Ketanest, Ketaset, and Ketalar. Its use as a recreational drug has been associated with several high-profile deaths.[9]



Lorazepam (trademarked as Ativan or Orfidal) is a high-potency, intermediate-duration, 3-hydroxy benzodiazepine drug, often used to treat anxiety disorders.[4] Lorazepam has all six intrinsic benzodiazepine effects including the ability to: reduce anxiety, interfere with new memory formation, reduce agitation/induce sleep, treat seizures, treat nausea and vomiting, and relax muscles.[5][6] Lorazepam is used for the short-term treatment of anxiety, insomnia, acute seizures including status epilepticus, and sedation of hospitalized patients, as well as sedation of aggressive patients.[6][7][8][9] Lorazepam is also the most common benzodiazepine used to decrease the likelihood of agitation and seizures in patients who have overdosed on stimulant drugs.[10]

After its introduction in 1977, lorazepam’s main use was to treat anxiety. Among benzodiazepines, lorazepam has a relatively high physical addiction potential.[5][11] Lorazepam also has misuse potential; the main types of misuse are for recreational purposes or continued use against medical advice.[12] Lorazepam’s ability to reduce agitation, induce sleep, and interfere with the formation of new memories are sometimes used to aid in date rape in a manner similar to GHB.[13][14]

Long-term effects of benzodiazepines include tolerance, dependence, a benzodiazepine withdrawal syndrome, and cognitive impairments which may not completely reverse after stopping treatment; however, for most patients, cognitive impairment is not severe. Withdrawal symptoms can range from anxiety and insomnia to seizures and psychosis. Due to tolerance and dependence, lorazepam is recommended for short-term use, up to two to four weeks only. Adverse effects, including inability to form new memories, depression, and paradoxical effects such as excitement or worsening of seizures, may occur. Children and the elderly are more sensitive to the adverse effects of benzodiazepines.[5][15][16] Lorazepam impairs body balance and standing steadiness and is associated with falls and hip fractures in the elderly.[1



MDMA (contracted from 3,4-methylenedioxy-methamphetamine) is a psychoactive drug of the substituted methylenedioxyphenethylamineand substituted amphetamine classes of drugs that is consumed primarily for its euphoric and empathogenic effects. Pharmacologically, MDMA acts as a serotonin-norepinephrine-dopamine releasing agent and reuptake inhibitor. MDMA has become widely known as “ecstasy” (shortened to “E”, “X”, or “XTC”), usually referring to its tablet street form, although this term may also include the presence of possible adulterants. The UK term “Mandy” and the US term “Molly” colloquially refer to MDMA in a crystalline powder form that is relatively free of adulterants.[5][6] “Molly” can sometimes also refer to the related drugs methylone, MDPV, mephedrone or any other of the pharmacological group of compounds commonly known as bath salts.[12]

Possession of MDMA is illegal in most countries. Some limited exceptions exist for scientific and medical research. For 2012, the UNODCestimated between 9.4 and 28.24 million people globally used MDMA at least once in the past year. This was broadly similar to the number ofcocaine, amphetamine, and opioid users, but far fewer than the global number of cannabis users.[13] It is taken in a variety of contexts far removed from its roots in psychotherapeutic settings, and is commonly associated with dance parties (or “raves”) and electronic dance music.[14]Medical reviews have noted that MDMA has some limited therapeutic benefits in certain mental health disorders, but has potential adverse effects, such as neurotoxicity and addiction, associated with its use.[15][16] More research is needed in order to determine if its potential usefulness in posttraumatic stress disorder (PTSD) treatment outweighs the risk of persistent neuropsychological harm to a patient.



Meperidine is used to relieve moderate to severe pain. Meperidine is in a class of medications called narcotic analgesics, a group of pain medications similar to morphine. It works by changing the way the body senses pain. Meperidine comes as a tablet and a syrup (liquid) to take by mouth. It is usually taken with or without food every 3 to 4 hours as needed for pain. Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand.

Swallow the tablets whole: do not chew or crush them.

If you are taking meperidine syrup, use a dose-measuring spoon or cup to measure the correct amount of liquid for each dose, not a regular household spoon. Mix your dose with half a glass of water and swallow the mixture. Swallowing undiluted meperidine syrup may numb the mouth.

Your doctor will probably adjust your dose of meperidine during your treatment. Be sure to tell your doctor about any pain and side effects you experience while taking this medication. This will help your doctor find the dose that is best for you.

Meperidine can be habit-forming. Take meperidine exactly as directed. Do not take a larger dose, or take it more often or for a longer period of time than you were told by your doctor. Do not snort or try to inject the tablets. Meperidine may cause serious side effects or death if it is taken or used in these ways.

If you have taken meperidine for longer than a few weeks, do not stop taking the medication without talking to your doctor. Your doctor will probably decrease your dose gradually. If you suddenly stop taking meperidine, you may experience withdrawal symptoms. Withdrawal symptoms may include: restlessness, watery eyes, stuffy nose, yawning, sweating, chills, muscle pain, irritability, nervousness, stomach pain, upset stomach, vomiting, loss of appetite, diarrhea, fast breathing, fast heartbeat, and back pain.



Meprobamate (marketed under the brand names Miltown by Wallace Laboratories, Equanil by Wyeth, and Meprospan) is acarbamate derivative which is used as an anxiolytic drug. It was the best-selling minor tranquilizer for a time, but has largely been replaced by the benzodiazepines due to their wider therapeutic index (lower toxicity) and lower incidence of serious side effects.



Methadone (also known as Symoron, Dolophine, Amidone, Methadose, Physeptone, Heptadon and many other names) is a syntheticopioid. It is used medically as an analgesic and a maintenance anti-addictive and reductive preparation for use by patients with opioid dependence. It was developed in Germany in 1937, mainly because Germany required a reliable internal source of opioids. It is an acyclic analog of morphine and heroin. Methadone acts on the same opioid receptors as these drugs, and has many of the same effects. Methadone is also used in managing severe chronic pain, owing to its long duration of action, strong analgesic effect, and very low cost. Methadone was introduced into the United States in 1947 by Eli Lilly and Company. The number of drug-poisoning deaths involving methadone increased from 784 deaths in 1999 to 5,518 deaths in 2007; then it declined to 4,418 deaths in 2011.[3]

Methadone is listed under Schedule I of the Single Convention On Narcotic Drugs 1961 and is regulated similarly to morphine in most countries. In the United States, it is a Schedule II Narcotic controlled substance with an ACSCN of 9250 and a 2013 annual aggregate manufacturing quota of 25 metric tons, down from just under 30 in 2012. One intermediate in the manufacturing process, 4-cyano-2-dimethylamino-4,4-diphenyl butane, is also listed as a Schedule II Narcotic Intermediate controlled substance with ACSCN 9254 and a quota of 32.5 metric tons.Levomethadone is presumably under Schedule II as an isomer of methadone. The salts of methadone in common medical use are the hydrochloride (free base conversion ratio 0.89) and hydrobromide (0.79); the tartrate was used in the past.[4]

Methadone is mainly used in the treatment of opioid dependence. It has cross-tolerance (tolerance to similar drugs) with other opioids includingheroin and morphine, and offers very similar effects but a longer duration of effect. Oral doses of methadone can stabilise patients by mitigatingopioid withdrawal syndrome or making it more tolerable. Higher doses of methadone can block the euphoric effects of heroin, morphine, and similar drugs. As a result, properly dosed methadone patients can reduce or stop altogether their use of these substances.



Methamphetamine[note 1] (pronunciation: /ˌmɛθæmˈfɛtəmiːn/; contracted from N-methyl-alpha-methylphenethylamine) is a potent central nervous system (CNS) stimulant of the phenethylamine and amphetamine classes that is used as a recreational drug and, rarely, to treatattention deficit hyperactivity disorder (ADHD) and obesity. Methamphetamine exists as two enantiomers, dextrorotary and levorotary.[note 2]Dextromethamphetamine is a stronger CNS stimulant than levomethamphetamine; however, both are neurotoxic, addictive and produce the same toxicity symptoms at high doses. Although rarely prescribed due to the potential risks, methamphetamine hydrochloride is approved by the United States Food and Drug Administration (USFDA) under the trade name Desoxyn. Recreationally, methamphetamine is used to increase sexual desire, lift the mood, and increase energy, allowing some users to engage in sexual activity continuously for several days straight.

Methamphetamine may be sold illegally, either as pure dextromethamphetamine or in an equal parts mixture of the right and left-handed molecules (i.e., 50% levomethamphetamine and 50% dextromethamphetamine). Both dextromethamphetamine and racemic methamphetamine are schedule II controlled substances in the United States. Similarly, the production, distribution, sale, and possession of methamphetamine is restricted or illegal in many other countries due to its placement in schedule II of the United Nations Convention on Psychotropic Substancestreaty. In contrast, levomethamphetamine is an over-the-counter drug in the United States.[note 3]

In low doses, methamphetamine can cause an elevated mood and increase alertness, concentration, and energy in fatigued individuals. At higher doses, it can induce psychosis, rhabdomyolysis and cerebral hemorrhage. Methamphetamine is known to have a high potential for abuse andaddiction. Heavy recreational use of methamphetamine may result in psychosis or lead to post-acute-withdrawal syndrome, a withdrawal syndrome that can persist for months beyond the typical withdrawal period.[i] Unlike amphetamine, methamphetamine is neurotoxic to humans, damaging both dopamine and serotonin neurons in the CNS.[i] Contrary to the long-term use of amphetamine,[iii] there is evidence that methamphetamine causes brain damage from long-term use in humans;[ii] this damage includes adverse changes in brain structure and function, such as reductions in gray matter volume in several brain regions and adverse changes in markers of metabolic integrity



Morphine (INN) (/ˈmɔrfiːn/) (sold under nearly a hundred trade names) is an opioid analgesic drug. It is the main psychoactive chemical inopium. In medicine, morphine is regarded as the gold standard in management of severe pain. Like other opioids, such as oxycodone,hydromorphone, and heroin, morphine acts directly on the central nervous system (CNS) to relieve pain.

Morphine has a high potential for addiction; tolerance and psychological dependence develop rapidly, although physiological dependence may take several months to develop. Tolerance to respiratory depression and euphoria develops more rapidly than tolerance to analgesia, and many chronic pain patients are therefore maintained on a stable dose for years. However, its effects can also reverse fairly rapidly, worsening pain through hyperalgesia.

Morphine is the most abundant opiate found in opium, the dried latex from unripe seedpods of Papaver somniferum (the opium poppy). Morphine was the first active ingredient purified from a plant source. It is one of at least 50 alkaloids of several different types present in opium, poppy straw concentrate, and other poppy derivatives. The primary source of morphine is chemical extraction from opium. It is a Schedule II drug in theUnited States, Class A in the United Kingdom, and Schedule I in Canada.

Morphine was first isolated in 1804 by Friedrich Sertürner, which is generally believed to be the first ever isolation of a natural plant alkaloid in history. Sertürner began distributing it in 1817, and Merck began marketing it commercially in 1827. At the time, Merck was a single small chemists’ shop. Morphine was more widely used after the invention of the hypodermic syringe in 1857. Sertürner originally named the substancemorphium after the Greek god of dreams, Morpheus (Greek: Μορφεύς), for its tendency to cause sleep.[2] It is on the WHO Model List of Essential Medicines, a list of the most important medications needed in a basic health system.



Norbuprenorphine is a major active metabolite of the opioid modulator buprenorphine. It is a μ-opioid, δ-opioid, and nociceptin receptor full agonist,[1][2] and a κ-opioid receptor partial agonist.[2] In rats, unlike buprenorphine, norbuprenorphine produces marked respiratory depressionbut with very little antinociceptive effect.[3] In explanation of these properties, norbuprenorphine has been found to be a high affinity P-glycoprotein substrate, and in accordance, shows very limited blood-brain-barrier penetration.



Nordazepam (marketed under brand names Nordaz, Stilny, Madar, Vegesan, and Calmday), also known as desoxydemoxepam,, anddesmethyldiazepam, is a 1,4-benzodiazepine derivative. Like other benzodiazepine derivatives, it has amnesic, anticonvulsant,anxiolytic, muscle relaxant, and sedative properties. However, it is used primarily in the treatment of anxiety. It is an activemetabolite of diazepam, chlordiazepoxide, clorazepate, prazepam, pinazepam, and medazepam.



Norfentanyl is a major urinary metabolite of fentanyl, a potent synthetic analgesic sold under various trade names including Sublimaze, Duragesic, Actiq, and Fentora. This Certified Spiking Solution® is suitable for numerous GC/MS or LC/MS testing applications from clinical toxicology and forensic analysis to urine drug testing and pain prescription monitoring.



This Certified Spiking Solution® is applicable for use as starting material in calibrators or controls for a variety of LC/MS or GC/MS applications including pain prescription monitoring, urine drug testing, forensic analysis, clinical toxicology, and pharmaceutical research. Norhydrocodone is an inactive primary urinary metabolite of the analgesic hydrocodone. Hydrocodone, a semi-synthetic opioid derived from codeine and thebaine, is used as a painkiller and as an antitussive


Norpethidine (Normeperidine, Pethidine Intermediate B)

Norpethidine (Normeperidine, Pethidine Intermediate B) is a 4-phenylpiperidine derivative that is both a metabolite of and a precursor topethidine (meperidine). It is scheduled by UN Single Convention on Narcotic Drugs.

Norpethidine is a controlled drug because of its potential uses in manufacturing both pethidine itself and a range of N-substituted derivatives, but it has little opioid activity in its own right. Instead, norpethidine acts as a stimulant and causes convulsions.[1][2]

Build up of norpethidine is a major complication when pethidine is used in medicine as an analgesic, as when pethidine is used in high doses[3] or administered by intravenous infusion,[4] norpethidine can accumulate in the body at a faster rate than it is being excreted, particularly in elderly patients[5] or those with compromised liver or kidney function,[6] resulting in a range of toxic effects, mainly convulsions, but also myoclonus[7] andhyponatremia.[8] These complications can be serious and have sometimes resulted in death.[9]

Metabolism of pethidine to norpethidine is carried out mainly by the CYP enzymes, CYP2B6, CYP2C19 and CYP3A4, in the liver, and since the activity of these enzymes can vary between individuals and can be influenced by concurrent use of other drugs, the rate and extent of norpethidine production can be difficult to predict.


Noroxycodone (marketed under the trade name OxyContin)

Noroxycodone is a major urinary metabolite of oxycodone, an opiate drug marketed under the trade name OxyContin for treatment of moderate to severe pain. This certified solution standard is suitable for use as starting material in calibrators and controls for a variety of LC/MS or GC/MS applications from clinical toxicology and forensic analysis to pain prescription monitoring, urine drug testing and pharmaceutical research. Since opiate drugs are classified as controlled substances, Cerilliant offers most opiate reference standards as DEA-exempt solutions for added convenience



Nortriptyline is a tricyclic antidepressant. It affects chemicals in the brain that may become unbalanced.

Nortriptyline is used to treat symptoms ofdepression.

Nortriptyline may also be used for purposes not listed in this medication guide.



Oxazepam[1] (marketed in English-speaking countries under the brand names Alepam, Bonare, Medopam, Murelax, Noripam, Opamox, Ox-Pam, Purata, Serax and Serepax, as Vaben in Israel, as Sobril and Oxascand in Sweden, as Oxapax in Denmark, as Sobril and Alopam in Norway, as Sobril or Oxascand in Iceland and Sweden, Zaxpam in India, and Praxiten in Croatia), (marketed in French-speaking countries asSeresta) is a short-to-intermediate-acting 3-hydroxy benzodiazepine derivative.[2][3] Oxazepam is used extensively since the 1960s for the treatment of anxiety and insomnia and in the control of symptoms of alcohol withdrawal. It is a metabolite of diazepam, prazepam, andtemazepam,[4] and has moderate amnesic, anxiolytic, anticonvulsant, hypnotic, sedative, and skeletal muscle relaxant properties compared to other benzodiazepines.



Oxycodone is a semisynthetic opioid synthesized from thebaine, an opioid alkaloid found in the Persian poppy and one of the many opioid alkaloids found in the opium poppy. It is an analgesic generally indicated for relief of moderate to severe pain. It was developed in 1917 in Germany[4][5] as one of several new semi-synthetic opioids in an attempt to improve on the existing opioids.[1]

Oxycodone is available as single-ingredient medication in immediate release and controlled release. Parenteral formulations of 10 mg/mL and 50mg/mL are available in the U.K. for IV/IM administration.[6] Combination products formulated with non-narcotic ingredients such as nonsteroidal anti-inflammatory drugs (NSAID) and paracetamol (acetaminophen) are also available as immediate release formulations; a combination with naloxone is available in managed-release tablets, naloxone which precipitates opioid withdrawal if the tablet is tampered with.


Oxymorphone (Opana, Numorphan, Numorphone) or 14-Hydroxydihydromorphinone

Oxymorphone (Opana, Numorphan, Numorphone) or 14-Hydroxydihydromorphinone is a powerful semi-synthetic opioid analgesic (painkiller) first developed in Germany in 1914,[2] patented in the USA by Endo Pharmaceuticals in 1955[3] and introduced to the United States market in January 1959 and other countries around the same time.[1]

The brand name Numorphan is derived by analogy to the Nucodan name for an oxycodone product (or vice versa) as well as Paramorphan/Paramorfan for dihydromorphine and Paracodin (dihydrocodeine). The only commercially available salt of oxymorphone in most of the world at this time is the hydrochloride, which has a free base conversion ratio of 0.891, and oxymorphone hydrochloride monohydrate has a factor of 0.85.[4] It is a Schedule II controlled substance in the United States with an ACSCN of 9652. The 2013 DEA annual manufacturing quotas were 18 375 kilos for conversion (a number of drugs can be made from oxymorphone, both painkillers and opioid antagonists like naloxone) and 6875 kilos for direct manufacture of end-products.[5]

The onset of analgesia after parenteral administration is about 5–10 minutes and after rectal administration, 15–30 minutes.[1] The duration of analgesia is 3–4 hours for immediate-release tablets and 12 hours for extended-release tablets.[1] It is also a minor metabolite of oxycodone, which is formed by CYP2D6-mediated O-demethylation.



Phencyclidine (a complex clip of the chemical name 1-(1-phenylcyclohexyl)piperidine), commonly initialized as PCP and known colloquially as Angel Dust and by many other names,[1] is a dissociative drug. PCP was brought to market in the 1950s as an anesthetic pharmaceutical drug but was soon taken off the market in 1965 due to the high prevalence of dissociative hallucinogenic side effects. Likewise ketamine was discovered by Parke Davis researchers as a better tolerated derivative for use as an anesthetic pharmaceutical drug. Since this time a number of synthetic derivatives of PCP have been sold as dissociative drugs for recreational and non-medical use.[2]

In chemical structure, PCP is a member of the arylcyclohexylamine class, and, in pharmacology, it is a member of the family of dissociative anesthetics. PCP works primarily as an NMDA receptor antagonist, where it blocks the activity of the NMDA receptor. Like most hallucinogenic drugs, there is risk of abuse with PCP.[3][4] In the 1970s the US media demonized PCP and PCP users giving many outlandish claims including that PCP gave users superhuman strength. As a recreational drug, PCP may be ingested orally, smoked, insufflated or injected.


Propoxyphene BRAND NAME: Darvon, Darvon-N, Dolene

DRUG CLASS AND MECHANISM: Propoxyphene is a narcotic pain-reliever and cough suppressant but is weaker than morphine, codeine, and hydrocodone. The precise mechanism of action is not known but may involve stimulation of opioid (narcotic) receptors in the brain. Propoxyphene increases pain tolerance and decreases discomfort but the presence of pain still is apparent. In addition to pain reduction, propoxyphene also causes sedation and respiratory depression. The FDA approved propoxyphene in August 1957.



Tapentadol (brand names: Nucynta, Palexia, in India available as TAPAL by MSN Labs) is a centrally acting opioid analgesic of the benzenoid class with a dual mode of action as an agonist of the μ-opioid receptor and as a norepinephrine reuptake inhibitor.[2] Its analgesic properties come into effect within thirty-two minutes of oral administration, and last for 4–6 hours.[3]

It is similar to tramadol in its dual mechanism of action; namely, its ability to activate the mu opioid receptor and inhibit the reuptake of norepinephrine.[3] Unlike tramadol, it has only weak effects on the reuptake of serotonin, is a significantly more potent opioid and has no known active metabolites.[3][4] Its general potency is somewhere between that of tramadol and morphine,[5] with an analgesic efficacy comparable to that of oxycodone despite a far lower incidence of side effects.[6]

It was approved by the US FDA on the 26th of August 2011,[7] by the MHRA of the UK on the 4th of February 2011[8] and by the TGA of Australia on the 24th of December 2010.



Temazepam (brand names Restoril – 15 mg/30 mg and Normison, among others) is an intermediate-acting 3-hydroxy hypnotic of thebenzodiazepine class of psychoactive drugs. It is the 3-hydroxy analogue of diazepam, and one of diazepam’s primary active metabolites. Temazepam is approved for the short-term treatment of insomnia. In addition, temazepam has anxiolytic (antianxiety), anticonvulsant, and skeletal muscle relaxant properties.

(-)-11-nor-9-carboxy-delta9-thc (THCA)


11-nor-9-Carboxy-THC, also known as 11-nor-9-carboxy-delta-9-tetrahydrocannabinol, 11-nor-9-carboxy-delta-9-THC, 11-COOH-THC,THC-COOH, and THC-11-oic acid, is the main secondary metabolite of tetrahydrocannabinol (THC) which is formed in the body after cannabis is consumed.

11-COOH-THC is formed in the body by oxidation of the active metabolite 11-Hydroxy-THC (also known as 11-OH-THC) by liver enzymes. It is then metabolized further by conjugation with glucuronide,[2] forming a water-soluble congener which can be more easily excreted by the body.[3]

11-COOH-THC is not psychoactive itself, but has a long half-life in the body of up to several days (or even weeks in very heavy users[citation needed]),[4][5][6] making it the main metabolite tested for when blood or urine testing for cannabis use. More selective tests are able to distinguish between 11-OH-THC and 11-COOH-THC, which can help determine how recently cannabis was consumed;[7][8] if only 11-COOH-THC is present then the cannabis was used some time ago and any impairment in cognitive ability or motor function will have dissipated, whereas if both 11-OH-THC and 11-COOH-THC are present then the cannabis was consumed more recently and motor impairment may still be present.

Some jurisdictions where cannabis use is decriminalized or permitted under some circumstances use such tests when determining whether drivers were legally intoxicated and therefore unfit to drive, with the comparative levels of THC, 11-OH-THC and 11-COOH-THC being used to derive a “blood cannabis level” analogous to the blood alcohol level used in prosecuting impaired drivers.[9] On the other hand in jurisdictions where cannabis is completely illegal, any detectable levels of 11-COOH-THC may be deemed to constitute driving while intoxicated, even though this approach has been criticized as tantamount to prohibition of “driving whilst being a recent user of cannabis” regardless of the presence or absence of any actual impairment that might impact on driving performance.

While 11-COOH-THC does not have any psychoactive effects in its own right, it may still have a role in the analgesic and antiinflammatory effects of cannabis,[10][11][12] and has also been shown to moderate the effects of THC itself which may help explain the difference in subjective effects seen between occasional and regular users of cannabis



Tramadol (marketed as Ultram, and as generics) is an opioid pain medication which is used to treat moderate to moderately severepain.[4] When taken as an immediate-release oral formulation, the onset of pain relief usually occurs within about an hour.[5] It has two different mechanisms. First, it binds to the μ-opioid receptor. Second, it inhibits the reuptake of serotonin and norepinephrine.[6][7]

Serious side effects may include: seizures, increased risk of serotonin syndrome, decreased alertness, and drug addiction. Common side effects include: constipation, itchiness and nausea, among others. A change in dosage may be recommended in those with kidney or liver problems. Its use is not recommended in women who are breast feeding or those who are at risk of suicide.[4]

It is marketed as a racemic mixture of both R- and S-stereoisomers.[1] This is because the two isomers complement each other’s analgesic activity.[1] It is often combined with paracetamol as this is known to improve the efficacy of tramadol in relieving pain.[1]Tramadol is metabolised to O-desmethyltramadol, which is a more potent opioid.[8] It is of the benzenoid class.

It was launched and marketed as Tramal by the German pharmaceutical company Grünenthal GmbH in 1977 in West Germany, even though it would take another 20 years for it to be launched in English-speaking countries such as the UK, U.S., and Australia.

References : Wikipedia and Cirilliant