intoxicant.wiki2catechol4school
Layout
Depressant

Diazepam

Also called Valium, Diastat, Mother's Little Helper, Apaurin

Original Wikipedia articleen.wikipedia.org/wiki/Diazepam revision used (24 October 2026)

Why a "revision used" link? Anyone can edit Wikipedia at any time, so the article you open today may not say what it said when we read it. This link opens the exact version we read on 24 October 2026, frozen as it was. It is the only way to check that every quote on this page matches its source word for word. Newer versions may correct or change things. When we re-check this page against a newer version, the edit log records it. How we cite

Common dose · Oral5–15 mg PW
Onset20–40 minutes PW
Total4–8 hours PW
After-effects12–36 hours PW

Dosage

When sources disagree, both rows are shown as published. Nothing is averaged or merged.

Oral

SourceThresholdLightCommonStrongHeavy
PsychonautWiki1 mg PW2.5–5 mg PW5–15 mg PW15–30 mg PW30 mg+ PW
TripSit–2.5–5 mg TS5–15 mg TS–15–30 mg. TS

TripSit dose text

TripSit's factsheet also states its doses as text.

Light: 2.5-5mg Common: 5-15mg Heavy: 15-30mg. TS

What dose are you on? (self-reported, unverified)
Read this first. These numbers come from anonymous visitors typing in a box. Nobody checks them. People misjudge, mistype, troll, or take untested products of unknown strength. They are not a dose guide and never override the sourced table above. They exist only so the sourced ranges can be compared with what people say they take. If you are deciding what to take, use the sourced table, start low, and read the risks section.
Running self-reports

No reports yet.

Reports are anonymous, one per browser per day per route. Counts under 20 are shown but marked as too few to mean anything. Until accounts launch, reports stay in this browser only.

Duration

Route · sourceOnsetCome-upPeakOffsetTotalAfter-effects
Oral · PsychonautWiki20–40 minutes PW–60–90 minutes PW–4–8 hours PW12–36 hours PW

TripSit factsheet

Onset
30-90 minutes TS
Duration
10-24 hours TS
Aftereffects
1-120 hours TS

Mixing

Acute combinations: what happens when these are taken close together. Entries backed by a medical journal or agency are listed first.

Backed by medical journals

Awaiting sourcePeer-reviewed reports on acute combinations, from PubMed and the journals the harm reduction sites cite.

Other documented combinations

  • Dangerous Depressants (1,4-Butanediol, 2-methyl-2-butanol, alcohol, barbiturates, GHB/GBL, methaqualone, opioids) - This combination can result in dangerous or even fatal levels of respiratory depression. These substances potentiate the muscle relaxation, sedation and amnesia caused by one another and can lead to unexpected loss of consciousness at high doses. There is also an increased risk of vomiting during unconsciousness and death from the resulting suffocation. If this occurs, users should attempt to fall asleep in the recovery position or have a friend move them into it. PW
  • Dangerous Dissociatives - This combination can result in an increased risk of vomiting during unconsciousness and death from the resulting suffocation. If this occurs, users should attempt to fall asleep in the recovery position or have a friend move them into it. PW
  • Dangerous Stimulants - It is dangerous to combine benzodiazepines with stimulants due to the risk of excessive intoxication. Stimulants decrease the sedative effect of benzodiazepines, which is the main factor most people consider when determining their level of intoxication. Once the stimulant wears off, the effects of benzodiazepines will be significantly increased, leading to intensified disinhibition as well as other effects. If combined, one should strictly limit themselves to only dosing a certain amount of benzodiazepines per hour. This combination can also potentially result in severe dehydration if hydration is not monitored. PW

TripSit combination chart

TripSit rates each pairing. Only pairings with a number carry a citation from TripSit. See the whole chart, with TripSit's note for every pairing.

Dangerous

alcohol TStramadol TS

Unsafe

pcp TS

Caution

dextromethorphan TSketamine TSmxe TS

Low Risk & Decrease

amt TScaffeine TScannabis TScocaine TSdmt TSlsd TSmdma TSmescaline TSmushrooms TSnitrous TS

Risks and toxicity

Diazepam has a low toxicity relative to dose. However, it is potentially lethal when mixed with depressants like alcohol or opioids.[22] PW

It is strongly recommended that one use harm reduction practices, such as volumetric dosing, when using this substance to ensure the administration of the intended dose. PW

Lethal dosage

The oral LD₅₀ (lethal dose in 50% of the population) of diazepam is 720 mg/kg in mice and 1240 mg/kg in rats. D. J. Greenblatt and colleagues reported in 1978 on two patients who had taken 500 and 2000 mg of diazepam, went into moderately deep comas, and were discharged within 48 hours without having experienced any important complications in spite of having high concentrations of diazepam and its metabolites esmethyldiazepam, oxazepam, and temazepam (according to samples taken in the hospital and as follow-up).[23][24] PW

Although not usually fatal when taken alone, a diazepam overdose is considered a medical emergency and generally requires the immediate attention of medical personnel. The antidote for an overdose of diazepam (or any other benzodiazepine) is flumazenil (Anexate). This drug is only used in cases with severe respiratory depression or cardiovascular complications. Because flumazenil is a short-acting drug and the effects of diazepam can last for days, several doses of flumazenil may be necessary. Artificial respiration and stabilization of cardiovascular functions may also be necessary.[23][25][26][27] PW

Tolerance and addiction potential

Diazepam is extremely physically and psychologically addictive. PW

Tolerance will develop to the sedative-hypnotic effects within a couple of days of continuous use. After cessation, the tolerance returns to baseline in 7-14 days. However, in certain cases this may take significantly longer in a manner which is proportional to the duration and intensity of one's long-term usage.[28] PW

Withdrawal symptoms or rebound symptoms may occur after ceasing usage abruptly following a few weeks or longer of steady dosing, and may necessitate a gradual dose reduction. For more information on tapering from benzodiazepines in a controlled manner, please see this guide.[29][30] PW

Benzodiazepine discontinuation is notoriously difficult; it is potentially life-threatening for individuals using regularly to discontinue use without tapering their dose over a period of weeks. There is an increased risk of hypertension, seizures, and death. Drugs which lower the seizure threshold such as tramadol should be avoided during withdrawal.[31] PW

Diazepam presents cross-tolerance with all benzodiazepines, meaning that after its consumption all benzodiazepines will have a reduced effect. PW

Overdose

Benzodiazepine overdose may occur when a benzodiazepine is taken in extremely heavy quantities or concurrently with other depressants. This is particularly dangerous with other GABAergic depressants such as barbiturates and alcohol since they work in a similar fashion, but bind to distinct allosteric sites on the GABAA receptor, thus their effects potentiate one another. Benzodiazepines increase the frequency in which the chlorine ion pore opens on the GABAA receptor while barbiturates increase the duration in which they are open, meaning when both are consumed, the ion pore will open more frequently and stay open longer. Benzodiazepine overdose is a medical emergency that may lead to a coma, permanent brain injury or death if not treated promptly and properly.[32] PW

Symptoms of a benzodiazepine overdose may include severe thought deceleration, slurred speech, confusion, delusions, respiratory depression, coma or death. Benzodiazepine overdoses may be treated effectively in a hospital environment, with generally favorable outcomes. Benzodiazepine overdoses are sometimes treated with flumazenil, a GABAA antagonist, however care is primarily supportive in nature.[33] PW

Dangerous interactions

Although many drugs are safe on their own, they can become dangerous and even life-threatening when combined with other substances. The list below contains some common potentially dangerous combinations, but may not include all of them. Certain combinations may be safe in low doses of each but still increase the potential risk of death. Independent research should always be done to ensure that a combination of two or more substances is safe before consumption. PW

TripSit factsheet

Avoid
All other CNS depressants[2–7] TS

Testing

Awaiting sourceReagent reactions and test kit guidance from a harm reduction testing service.

Effects

Memory loss, Blackout potential, Motor skill impairment, Dizziness, Depression, Irritability, Aggression, Rage, Personality changes, Drowsiness, Appetite fluctuation, Euphoria, Relaxation, Anxiety suppression, Muscle relaxation, Emotional and social dissociation or de-realization (normally seen with long term use). TS

Overview

(also known as Valium) is a depressant substance of the benzodiazepine class. Its mechanism of action is to increase the effects of the inhibitory neurotransmitter GABA.[1] PW⚠ The source page had been vandalised when it was read: the substance's name at the start was replaced by a link, so the sentence has no subject.

A very common and widely prescribed benzodiazepine with hypnotic and sedative qualities. The metre by which other benzodiazepines are compared. May cause amnesia and lowered inhibitions in excess. Has a relatively long half-life in comparison with other benzodiazepines.[2–7] TS

Diazepam, sold under the brand name Valium among others, is a medication of the benzodiazepine family that acts as an anxiolytic. It is used to treat a range of conditions, including anxiety, seizures, alcohol withdrawal syndrome, muscle spasms, insomnia, and restless legs syndrome. It may also be used to cause memory loss during certain medical procedures. It can be taken orally (by mouth), as a suppository (inserted into the rectum), intramuscularly (injected into muscle), intravenously (injection into a vein) or used as a nasal spray. When injected intravenously, effects begin in one to five minutes and last up to an hour. When taken by mouth, effects begin after 15 to 60 minutes.[8–12] WP

Common side effects include sleepiness and trouble with coordination. Serious side effects are rare. They include increased risk of suicide, decreased breathing, and a paradoxical increased risk of seizures if used too frequently in those with epilepsy. Occasionally, excitement or agitation may occur. Long-term use can result in tolerance, dependence, and withdrawal symptoms on dose reduction. Abrupt stopping after long-term use can be potentially dangerous. After stopping, cognitive problems may persist for six months or longer. It is not recommended during pregnancy or breastfeeding. Its mechanism of action works by increasing the effect of the neurotransmitter gamma-aminobutyric acid (GABA).[8][10][13–16] WP

Diazepam was patented in 1959 by Hoffmann-La Roche. It has been one of the most frequently prescribed medications in the world since its launch in 1963. In the United States it was the best-selling medication between 1968 and 1982, selling more than 2 billion tablets in 1978 alone. In 2023, it was the 183rd most commonly prescribed medication in the United States, with more than 2 million prescriptions. In 1985 the patent expired, and there are more than 500 brands available on the market. It is on the World Health Organization's List of Essential Medicines.[8][17–21] WP

History

History

Diazepam was the second benzodiazepine invented by Leo Sternbach of Hoffmann-La Roche at the company's Nutley, New Jersey, facility following chlordiazepoxide (Librium), which was approved for use in 1960. Released in 1963 as an improved version of Librium, diazepam became incredibly popular, helping Roche to become a pharmaceutical industry giant. It is 2.5 times more potent than its predecessor, which it quickly surpassed in terms of sales. After this initial success, other pharmaceutical companies began to introduce other benzodiazepine derivatives.[34][35] WP

Medical professionals adopted the benzodiazepines as an improvement over barbiturates, which have a comparatively narrow therapeutic index, and are far more sedative at therapeutic doses. The benzodiazepines are also far less dangerous; death rarely results from diazepam overdose, except in cases where it is consumed with large amounts of other depressants (such as alcohol or opioids). Benzodiazepine drugs such as diazepam initially had widespread public support, but with time the view changed to one of growing criticism and calls for restrictions on their prescription.[36][37] WP

Marketed by Roche using an advertising campaign conceived by the William Douglas McAdams Agency under the leadership of Arthur Sackler, diazepam was the top-selling pharmaceutical in the United States from 1969 to 1982, with peak annual sales in 1978 of 2.3 billion tablets. Diazepam, along with oxazepam, nitrazepam and temazepam, represents 82% of the benzodiazepine market in Australia. While psychiatrists continue to prescribe diazepam for the short-term relief of anxiety, neurology has taken the lead in prescribing diazepam for the palliative treatment of certain types of epilepsy and spastic activity, for example, forms of paresis. It is also the first line of defense for a rare disorder called stiff-person syndrome.[35][38][39][40] WP⚠ Wikipedia itself has flagged this text: citation needed.

Pharmacology

Pharmacology

Diazepam is a long-acting "classical" benzodiazepine. Other classical benzodiazepines include chlordiazepoxide, clonazepam, lorazepam, oxazepam, nitrazepam, temazepam, flurazepam, bromazepam, and clorazepate. Diazepam has anticonvulsant properties. Benzodiazepines act via micromolar benzodiazepine binding sites as calcium channel blockers and significantly inhibit depolarization-sensitive calcium uptake in rat nerve cell preparations.[57][58][59] WP

Diazepam inhibits acetylcholine release in mouse hippocampal synaptosomes. This has been found by measuring sodium-dependent high-affinity choline uptake in mouse brain cells in vitro, after pretreatment of the mice with diazepam in vivo. This may play a role in explaining diazepam's anticonvulsant properties.[60] WP

Diazepam binds with high affinity to glial cells in animal cell cultures. Diazepam at high doses has been found to decrease histamine turnover in mouse brain via diazepam's action at the benzodiazepine-GABA receptor complex. Diazepam also decreases prolactin release in rats.[61][62][63] WP

Mechanism of action

Benzodiazepines are positive allosteric modulators of the GABA type A receptors (GABAA). The GABAA receptors are ligand-gated chloride-selective ion channels that are activated by GABA, the major inhibitory neurotransmitter in the brain. The binding of benzodiazepines to this receptor complex promotes the binding of GABA, which in turn increases the total conduction of chloride ions across the neuronal cell membrane. This increased chloride ion influx hyperpolarizes the neuron's membrane potential. As a result, the difference between resting potential and threshold potential is increased, and firing is less likely. As a result, the arousal of the cortical and limbic systems in the central nervous system is reduced.[64] WP

The GABAA receptor is a heteromer composed of five subunits, the most common ones being two αs, two βs, and one γ (α2β2γ). For each subunit, many subtypes exist (α1–6, β1–3, and γ1–3). GABAA receptors containing the α1 subunit mediate the sedative, anterograde amnesic, and partly the anticonvulsive effects of diazepam. GABAA receptors containing α2 mediate the anxiolytic actions and, to a large degree, the myorelaxant effects. GABAA receptors containing α3 and α5 also contribute to benzodiazepines myorelaxant actions, whereas GABAA receptors comprising the α5 subunit were shown to modulate the temporal and spatial memory effects of benzodiazepines. Diazepam is not the only drug to target these GABAA receptors. Drugs such as flumazenil also bind to GABAA to induce their effects.[65][66] WP

Diazepam appears to act on areas of the limbic system, thalamus, and hypothalamus, inducing anxiolytic effects. Benzodiazepine drugs, including diazepam, increase the inhibitory processes in the cerebral cortex.[67] WP

The anticonvulsant properties of diazepam and other benzodiazepines may be in part or entirely due to binding to voltage-dependent sodium channels rather than GABAA receptors. Sustained repetitive firing seems limited by benzodiazepines' effect of slowing recovery of sodium channels from inactivation.[68] WP

The muscle relaxant properties of diazepam are produced via inhibition of polysynaptic pathways in the spinal cord.[69] WP

Pharmacokinetics

Diazepam can be administered orally, intravenously (it is always diluted, as it is painful and damaging to veins), intramuscularly (IM), or as a suppository.[70] WP

The onset of action is one to five minutes for IV administration and 15–30 minutes for IM administration. The duration of diazepam's peak pharmacological effects is 15 minutes to one hour for both routes of administration. The half-life of diazepam, in general, is 30–56 hours. Peak plasma levels occur between 30 and 90 minutes after oral administration and between 30 and 60 minutes after intramuscular administration; after rectal administration, peak plasma levels occur after 10 to 45 minutes. Diazepam is highly plasma protein-bound, with 96–99% of the absorbed drug being protein-bound. The distribution half-life of diazepam is two to 13 minutes.[15][64][71] WP

Diazepam is highly lipid-soluble and is widely distributed throughout the body after administration. It easily crosses both the blood–brain barrier and the placenta, and is excreted into breast milk. After absorption, diazepam is redistributed into muscle and adipose tissue. Continual daily doses of diazepam quickly build to a high concentration in the body (mainly in adipose tissue), far above the actual dose for any given day.[15][70] WP

Diazepam is stored preferentially in some organs, including the heart. Absorption by any administered route and the risk of accumulation is significantly increased in the neonate, and withdrawal of diazepam during pregnancy and breastfeeding is clinically justified.[72] WP

Diazepam undergoes oxidative metabolism by demethylation (CYP2C9, 2C19, 2B6, 3A4, and 3A5), hydroxylation (CYP3A4 and 2C19) and glucuronidation in the liver as part of the cytochrome P450 enzyme system. It has several pharmacologically active metabolites. The main active metabolite of diazepam is desmethyldiazepam (also known as nordazepam or nordiazepam). Its other active metabolites include the minor active metabolites temazepam and oxazepam. These metabolites are conjugated with glucuronide and are excreted primarily in the urine. Because of these active metabolites, the serum values of diazepam alone are not useful in predicting the effects of the drug. Diazepam has a biphasic half-life of about one to three days and two to seven days for the active metabolite desmethyldiazepam. Most of the drug is metabolized; little diazepam is excreted unchanged. The elimination half-life of diazepam and also the active metabolite desmethyldiazepam increases significantly in the elderly, which may result in prolonged action, as well as accumulation of the drug during repeated administration.[15][70][73] WP

Synthesis

The synthesis of diazepam was first achieved through a reaction pathway developed by Leo Sternbach and his team at Hoffmann-La Roche in the late 1950s. WP

Sternbach's method commenced with 2-amino-5-chlorobenzophenone, which undergoes cyclocondensation with glycine ethyl ester hydrochloride to construct the benzodiazepine core. This core is subsequently alkylated at the nitrogen in the 1-position using dimethyl sulfate in the presence of sodium methoxide and methanol under reflux conditions. Although the direct transformation from 2-amino-5-chlorobenzophenone to Nordazepam is conceptually straightforward, an alternative approach involving the treatment of 2-amino-5-chlorobenzophenone with chloroacetyl chloride, succeeded by ammoniation and heating, culminates in Nordazepam with enhanced yield and facilitates easier purification processes.[74] WP

Detection in body fluids

Diazepam may be quantified in blood or plasma to confirm a diagnosis of poisoning in hospitalized patients, provide evidence in an impaired driving arrest, or assist in a medicolegal death investigation. Blood or plasma diazepam concentrations are usually in a range of 0.1–1.0 mg/L in persons receiving the drug therapeutically. Most commercial immunoassays for the benzodiazepine class of drugs cross-react with diazepam, but confirmation and quantitation are usually performed using chromatographic techniques.[75][76][77] WP

Environmental

Diazepam is a common environmental contamination finding near human settlements.[78] WP

Chemistry

Formula
C16H13ClN2O PC
CAS number
439-14-5 PC
Molar mass (g/mol)
284.74 PC
IUPAC name (computed by PubChem)
7-chloro-1-methyl-5-phenyl-3H-1,4-benzodiazepin-2-one PC
SMILES
CN1C(=O)CN=C(C2=C1C=CC(=C2)Cl)C3=CC=CC=C3 PC
InChIKey
AAOVKJBEBIDNHE-UHFFFAOYSA-N PC
PubChem CID
3016

User reports

Erowid erowid.org

Listings
Awaiting sourceExperience Vault listing and report categories.
Top stories
Awaiting sourceShort summaries of the most-read reports, each linked, saying only what the report says.

Bluelight bluelight.org

Listings
Awaiting sourceTrip report threads and this substance's discussion forum.
Top stories
Awaiting sourceShort summaries of the most-read reports, each linked, saying only what the report says.

Reddit reddit.com

Listings
Awaiting sourceTrip report posts and the relevant subreddits.
Top stories
Awaiting sourceShort summaries of the most-read reports, each linked, saying only what the report says.

Pop culture

No references added yet.

Add a reference

Registered users can add songs, films, books, shows, games and art about this substance. Link a source that names the substance, such as the work's Wikipedia article, a review or an interview, not only the work itself. Entries are voted on and moderated like every other value on this page.

Opens when accounts launch.

References

  1. Other https://www.google.com/search?q=A+mild+but+pleasant+feeling+Total+dose%3A+45%2C4+mg+of+diazepam+Background%3A+I%27ve+been+using+diazepam+for+restless+leg+syndrome+for+the+last+15+days%2C+with+doses+ranging+between+1%2C4+and+50+mg+a+day.+Here%27s+the+report+from+today%27s+experience+with+this+substance%3A+T%3A+0%3A00+7.30+P.M.+%3A+I+ingested+15+mg+of+diazepam+(75+drops+of+oral+solution)+with+30+ml+of+water+(empty+stomach).+T%3A+0%3A15+7%3A45+P.M.+I+ingest+another+5+mg+of+diazepam+with+oral+drops+T%3A+0%3A30+8%3A00+P.M.+%3A+i+take+5+mg+of+diazepam+keeping+the+drops+under+the+toungue+T%3A+1%3A30%3A+9%3A00+P.M.%3A+I+smoke+a+small+joint+of+hashish+(0.2+g)+T%3A2%3A10+9%3A40+P.M.+%3A+I+assumed+12%2C2+mg+of+diazepam+orally+(61+gocce)+T%3A+2%3A20+9.50+P.M.+%3A+Wow%2C+onlu+10+minutes+have+passed+but+I%27m+feeling+a+relaxed+sensation+of+euphoria+washing+over+me%2C+concentrated+in+the+stomach+zone.+I+wasn%27t+expenting+a+so+fast+onset+from+this+compound%2C+interesting.+I%27ll+keep+you+updated+on+the+effects.+T%3A+2%3A30+10.00+P.M.+%3A+Effects+are+slightly+rising%2C+with+sedation+becoming+more+appaerent+T%3A+2%3A45+10.15+P.M.+%3A+Effects+seem+to+not+increase+more%2C+they%27re+kinda+platoing.+I%27m+going+to+take+5+more+mg+in+10+minutes+if+effects+don%27t+increase+further.+T%3A+2%3A55+10.25+P.M.+%3A+I+ingested+the+8.2+mg+(41+drops)+with+a+little+bit+of+water%2C+as+always.+Now+we+wait+for+Effects+to+show+T%3A+3%3A00+22.30+P.M.+%3A+Effects+of+the+second+booster+dose+are+coming+up+faster+than+the+ones+of+the+prior+dose+taken%2C+I%27m+feeling+warm%2C+fuzzy+and+my+muscles+are+relaxed.+T%3A+3%3A30+23%3A00%3A+The+intensity+of+the+feeling+has+not+increased%2C+It+seems+like+it%27s+platouing.+I%27ll+keep+you+updated%2C+but+I+don%27t+expect+anyting+interesting+from+this+experience+anymore.+The+effects+of+this+substance+last+30+minutes+to+an+hour+and+then+fades+away%2C+I+think+this+has+to+do+with+my+benzo+tollerance.+T%3A+4%3A10+11.40%3A+Effects+are+gradually+declining%2C+I%27m+feeling+more+sober+after+having+eaten+a+full+pita+with+chease+and+ham.+T%3A+4%3A50+00.20%3A+I%27m+coming+down%2C+the+sensation+is+decreasing+in+its+intensity+and+I%27m+slowly+but+steadily+going+back+to+baseline.+T%3A+5%3A10+00.40%3A+effects+have+vanished+complitely%2C+now+I+Just+feel+normal+tiredness+(it%27s+00.40%2C+so+It%27s+pretty+late)+I+conclude+this+experience+report+by+saying+that+I+enjoyed+the+effects%2C+but+they+were+way+more+single+than+i+would+have+expected.&client=ms-android-xiaomi-terr2-rso2&sourceid=chrome-mobile&ie=UTF-8&chrome_dse_attribution=1
  2. Journal / agency Alcohol and benzodiazepines in fatal poisonings
  3. Journal / agency NMDA receptor antagonists potently suppress the spontaneous withdrawal signs induced by discontinuation of long-term diazepam treatment in Fischer
  4. Journal / agency Dual intoxication with diazepam and amphetamine: this drug interaction probably potentiates myocardial ischemia
  5. Journal / agency Effect of omeprazole and cimetidine on plasma diazepam levels
  6. Journal / agency Bioavailability of intranasal vs. rectal diazepam
  7. Journal / agency Dosing feasibility and tolerability of intranasal diazepam in adults with epilepsy
  8. Journal / agency Calcaterra NE, Barrow JC. Classics in chemical neuroscience: diazepam (valium). ACS Chemical Neuroscience. April 2014. doi:10.1021/cn5000056 · PMID 24552479 · PMC3990949
  9. Journal / agency Diazepam
  10. Other Diazepam
  11. Journal / agency Valtoco – diazepam spray. 13 January 2020
  12. Journal / agency Dhaliwal JS, Saadabadi A. StatPearls [Internet]. September 2022. PMID 30725707
  13. Journal / agency Valium – diazepam tablet. 8 November 2019
  14. Journal / agency Dodds TJ. Prescribed Benzodiazepines and Suicide Risk: A Review of the Literature. The Primary Care Companion for CNS Disorders. March 2017. doi:10.4088/PCC.16r02037 · PMID 28257172
  15. Journal / agency Riss J, Cloyd J, Gates J, Collins S. Benzodiazepines in epilepsy: pharmacology and pharmacokinetics. Acta Neurologica Scandinavica. August 2008. doi:10.1111/j.1600-0404.2008.01004.x · PMID 18384456
  16. Other Perkin RM. Pediatric hospital medicine: textbook of inpatient management. 2008
  17. Other Fischer J, Ganellin CR. Analogue-based Drug Discovery. 2006
  18. Other 5-ARYL-3H-1,4-BENZODIAZEPIN-2(1H)-ONES
  19. Other Top 300 of 2023
  20. Other Diazepam Drug Usage Statistics, United States, 2014 - 2023
  21. Other World Health Organization. The selection and use of essential medicines 2023: web annex A: World Health Organization model list of essential medicines: 23rd list (2023). 2023
  22. Journal / agency Mandrioli, R., Mercolini, L., Raggi, M. A. Benzodiazepine metabolism: an analytical perspective. Current Drug Metabolism. October 2008. doi:10.2174/138920008786049258
  23. Other http://www.drugs.com/diazepam.html
  24. Journal / agency Greenblatt, D. J., Woo, E., Allen, M. D., Orsulak, P. J., Shader, R. I. Rapid recovery from massive diazepam overdose. JAMA. 20 October 1978
  25. Other Diazepam (PIM 181)
  26. Other Diazepam (Diazepam Injection): Uses, Dosage, Side Effects, Interactions, Warning
  27. Other Barondes, S. H. Better than Prozac: creating the next generation of psychiatric drugs. 2003
  28. Other Janicak, P. G., Marder, S. R., Pavuluri, M. N. Principles and Practice of Psychopharmacotherapy. 25 October 2010
  29. Journal / agency Verster, J. C., Volkerts, E. R. Clinical Pharmacology, Clinical Efficacy, and Behavioral Toxicity of Alprazolam: A Review of the Literature. CNS Drug Reviews. 7 June 2006. doi:10.1111/j.1527-3458.2004.tb00003.x
  30. Other Galanter, M., Kleber, H. D. The American Psychiatric Publishing Textbook of Substance Abuse Treatment. 2008
  31. Journal / agency Lann, M. A., Molina, D. K. A fatal case of benzodiazepine withdrawal. The American Journal of Forensic Medicine and Pathology. June 2009. doi:10.1097/PAF.0b013e3181875aa0
  32. Journal / agency Twyman, R. E., Rogers, C. J., Macdonald, R. L. Differential regulation of gamma-aminobutyric acid receptor channels by diazepam and phenobarbital. Annals of Neurology. March 1989. doi:10.1002/ana.410250302
  33. Journal / agency Hoffman, E. J., Warren, E. W. Flumazenil: a benzodiazepine antagonist. Clinical Pharmacy. September 1993
  34. Other Pollack A. Roche to Shut Former U.S. Headquarters. 26 June 2012
  35. Other Sample I. Leo Sternbach's Obituary. 3 October 2005
  36. Other Barondes SH. Better Than Prozac. 2003
  37. Journal / agency Marshall KP, Georgievskava Z, Georgievsky I. Social reactions to Valium and Prozac: a cultural lag perspective of drug diffusion and adoption. Research in Social & Administrative Pharmacy. June 2009. doi:10.1016/j.sapharm.2008.06.005 · PMID 19524858
  38. Other How the American opiate epidemic was started by one pharmaceutical company. 4 March 2015
  39. Journal / agency Mant A, Whicker SD, McManus P, Birkett DJ, Edmonds D, Dumbrell D. Benzodiazepine utilisation in Australia: report from a new pharmacoepidemiological database. Australian Journal of Public Health. December 1993. doi:10.1111/j.1753-6405.1993.tb00167.x · PMID 7911332
  40. Other Diazepam: indications. 24 January 2005
  41. Other International Narcotics Control Board (2003)
  42. Other Poisons Standard December 2019. November 14, 2019
  43. Other https://laws-lois.justice.gc.ca/eng/acts/C-38.8/page-12.html#h-95661
  44. Other https://eur-lex.europa.eu/resource.html?uri=cellar:6b5e9beb-1d9b-11ea-95ab-01aa75ed71a1.0001.02/DOC_1&format=PDF
  45. Other https://www.zakonyprolidi.cz/cs/2013-463
  46. Other Zweite Verordnung zur Änderung betäubungsmittelrechtlicher Vorschriften
  47. Other Anlage III BtMG
  48. Other Постановление Правительства РФ от 04.02.2013 N 78 “О внесении изменений в некоторые акты Правительства Российской Федерации” - КонсультантПлюс
  49. Other Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien
  50. Other Drugs licensing
  51. Other List of controlled Drugs
  52. Other Anlage III (zu § 1 Abs. 1) verkehrsfähige und verschreibungsfähige Betäubungsmittel. 2001
  53. Other Poisons Standard June 2018
  54. Other San Quentin State Prison Operational Procedure 0–770, Execution By Lethal Injection (pp. 44 & 92
  55. Other Execution by lethal injection procedures. 9 September 2013
  56. Other Nebraska executes Carey Dean Moore for murders of Omaha cab drivers Maynard Helgeland, Reuel Van Ness Jr. 14 August 2018
  57. Journal / agency Braestrup C, Squires RF. Pharmacological characterization of benzodiazepine receptors in the brain. European Journal of Pharmacology. April 1978. doi:10.1016/0014-2999(78)90085-7 · PMID 639854
  58. Journal / agency Chweh AY, Swinyard EA, Wolf HH, Kupferberg HJ. Effect of GABA agonists on the neurotoxicity and anticonvulsant activity of benzodiazepines. Life Sciences. February 1985. doi:10.1016/0024-3205(85)90193-6 · PMID 2983169
  59. Journal / agency Taft WC, DeLorenzo RJ. Micromolar-affinity benzodiazepine receptors regulate voltage-sensitive calcium channels in nerve terminal preparations. Proceedings of the National Academy of Sciences of the United States of America. May 1984. doi:10.1073/pnas.81.10.3118 · PMID 6328498 · PMC345232
  60. Journal / agency Miller JA, Richter JA. Effects of anticonvulsants in vivo on high affinity choline uptake in vitro in mouse hippocampal synaptosomes. British Journal of Pharmacology. January 1985. doi:10.1111/j.1476-5381.1985.tb17368.x · PMID 3978310 · PMC1987204
  61. Journal / agency Gallager DW, Mallorga P, Oertel W, Henneberry R, Tallman J. 3HDiazepam binding in mammalian central nervous system: a pharmacological characterization. The Journal of Neuroscience. February 1981. doi:10.1523/JNEUROSCI.01-02-00218.1981 · PMID 6267221 · PMC6564145
  62. Journal / agency Oishi R, Nishibori M, Itoh Y, Saeki K. Diazepam-induced decrease in histamine turnover in mouse brain. European Journal of Pharmacology. May 1986. doi:10.1016/0014-2999(86)90236-0 · PMID 3089825
  63. Journal / agency Grandison L. Suppression of prolactin secretion by benzodiazepines in vivo. Neuroendocrinology. 1982. doi:10.1159/000123330 · PMID 6979001
  64. Other National Highway Traffic Safety Administration Drugs and Human Performance Fact Sheet- Diazepam
  65. Other Tan KR, Rudolph U, Lüscher C. Hooked on benzodiazepines: GABAA receptor subtypes and addiction. 2011
  66. Journal / agency Whirl-Carrillo M, McDonagh EM, Hebert JM, Gong L, Sangkuhl K, Thorn CF, Altman RB, Klein TE. Pharmacogenomics knowledge for personalized medicine. Clinical Pharmacology and Therapeutics. October 2012. doi:10.1038/clpt.2012.96 · PMID 22992668 · PMC3660037
  67. Journal / agency Zakusov VV, Ostrovskaya RU, Kozhechkin SN, Markovich VV, Molodavkin GM, Voronina TA. Further evidence for GABA-ergic mechanisms in the action of benzodiazepines. Archives Internationales de Pharmacodynamie et de Thérapie. October 1977. PMID 23084
  68. Journal / agency McLean MJ, Macdonald RL. Benzodiazepines, but not beta-carbolines, limit high-frequency repetitive firing of action potentials of spinal cord neurons in cell culture. The Journal of Pharmacology and Experimental Therapeutics. February 1988. doi:10.1016/S0022-3565(25)24414-7 · PMID 2450203
  69. Journal / agency Date SK, Hemavathi KG, Gulati OD. Investigation of the muscle relaxant activity of nitrazepam. Archives Internationales de Pharmacodynamie et de Thérapie. November 1984. PMID 6517646
  70. Other Munne P. Diazepam. 1998
  71. Other Langsam Y. Diazepam (Valium and Others)
  72. Journal / agency Olive G, Dreux C. Pharmacologic bases of use of benzodiazepines in peréinatal medicine. Archives Françaises de Pédiatrie. January 1977. PMID 851373
  73. Journal / agency Vozeh S. Pharmacokinetic of benzodiazepines in old age. Schweizerische Medizinische Wochenschrift. November 1981. PMID 6118950
  74. Journal / agency Stempel A, Reeder E, Sternbach LH. Quinazolines and 1,4-benzodiazepines. XXVII. Mechanism of ring enlargement of quinazoline 3-oxides with alkali to 1,4-benzodiazepin-2-one 4-oxides. The Journal of Organic Chemistry. December 1965. doi:10.1021/jo01023a063 · PMID 4158669
  75. Journal / agency Jones AW, Holmgren A, Kugelberg FC. Concentrations of scheduled prescription drugs in blood of impaired drivers: considerations for interpreting the results. Therapeutic Drug Monitoring. April 2007. doi:10.1097/FTD.0b013e31803d3c04 · PMID 17417081
  76. Journal / agency Fraser AD, Bryan W. Evaluation of the Abbott ADx and TDx serum benzodiazepine immunoassays for analysis of alprazolam. Journal of Analytical Toxicology. 1991. doi:10.1093/jat/15.2.63 · PMID 1675703
  77. Other Baselt R. Disposition of Toxic Drugs and Chemicals in Man. 2011
  78. Journal / agency Chia MA, Lorenzi AS, Ameh I, Dauda S, Cordeiro-Araújo MK, Agee JT, Okpanachi IY, Adesalu AT. Susceptibility of phytoplankton to the increasing presence of active pharmaceutical ingredients (APIs) in the aquatic environment: A review. Aquatic Toxicology. May 2021. doi:10.1016/j.aquatox.2021.105809 · PMID 33780670

Text and values on this page are quoted from PsychonautWiki (CC BY-SA 4.0), Wikipedia (CC BY-SA 4.0), TripSit factsheets, PubChem (public domain). Each value links to the exact revision it came from.