Clonazepam, sold under the brand name Klonopin among others, is a benzodiazepine medication used to prevent and treat anxiety disorders, seizures, bipolar mania, agitation associated with psychosis, obsessive–compulsive disorder (OCD), and akathisia. It is a long-acting benzodiazepine. It possesses anxiolytic, anticonvulsant, sedative, hypnotic, and skeletal muscle relaxant properties. It is typically taken orally (swallowed by mouth) but is also used intravenously. Effects begin within one hour and last between eight and twelve hours in adults.
Common side effects may include sleepiness, weakness, poor coordination, difficulty concentrating, and agitation. Clonazepam may also decrease memory formation. Long-term use may result in tolerance, dependence, and life-threatening withdrawal symptoms if stopped abruptly. Dependence occurs in one-third of people who take benzodiazepines for longer than four weeks. The risk of suicide increases, particularly in people who are already depressed. Use during pregnancy may result in harm to the fetus. Clonazepam binds to GABAA receptors, thus increasing the effect of the chief inhibitory neurotransmitter γ-aminobutyric acid (GABA).
Clonazepam was patented in 1960, marketed in 1964, and went on sale in 1975 in the United States from Roche. It is available as a generic medication. In 2023, it was the 62nd most commonly prescribed medication in the United States, with more than 10million prescriptions. In many areas of the world, it is commonly used as a recreational drug.
Safety at a Glance
High Risk- It is strongly recommended that one use harm reduction practices when using this drug.
- Tolerance and addiction potential:extremely physically and psychologically addictive.
- Toxicity: Radar plot showing relative physical harm, social harm, and dependence of benzodiazepines in comparison to other drug...
- Dangerous with: Atropa belladonna, Cake, Datura, Deschloroetizolam (+23 more)
- Overdose risk: overdose is a medical emergency that may lead to a coma, permanent brain injury or death if not t...
If someone is in crisis, call 911 or Poison Control: 1-800-222-1222
Dosage
oral
Duration
oral
Total: 8 hrs – 12 hrsHow It Feels
Clonazepam is a slow, patient substance. Its onset can take thirty minutes to an hour, and it announces itself not with a rush but with a quiet subtraction. The first thing to go is the anxiety -- not suppressed or pushed aside but simply dissolved, as though the low hum of worry that had been running in the background of consciousness were attached to a dimmer switch that someone has been slowly turning down. You may not notice the change until you realize that the knot in your stomach has untied itself, that your hands have unclenched, that your breathing has deepened without any conscious effort.
As the medication reaches its full effect, a warm, heavy calm settles over the body and mind. Muscles relax from the jaw downward, and there is a sensation of the body becoming denser, more gravitationally committed to whatever surface it rests upon. The mind enters a state of serene detachment: thoughts still arise, but they carry no emotional charge. Problems that had seemed urgent and consuming now appear manageable, even trivial, like watching storm clouds pass on a television screen rather than standing beneath them. There is a mild euphoria in some -- a gentle sense of well-being that accompanies the relief from chronic anxiety -- but it is understated, more relief than pleasure.
The peak of clonazepam is a plateau rather than a summit. The effects do not intensify dramatically but rather establish themselves and persist with remarkable steadiness for hours. This is the substance's defining characteristic: its long, even keel. The sedation is present but not overwhelming at therapeutic doses; you can function, but there is a softness to the world, a sense that sharp edges have been filed down. Coordination may be slightly impaired, and there is often a gentle forgetfulness -- not amnesia exactly, but a tendency for recent events to leave lighter impressions than usual, as though written in pencil rather than ink.
The offset is so gradual as to be nearly imperceptible. The calm recedes over many hours, and the return of baseline anxiety, when it comes, arrives so slowly that it can be difficult to pinpoint when the medication stopped working. Sleep during the active period is deep and dreamless, and the following day often retains a residual calm, a faint echo of the previous day's peace that makes clonazepam feel less like a drug and more like a temporary change in the weather.
Subjective Effects
The effects listed below are based on the Subjective Effect Index (SEI), an open research literature based on anecdotal reports and personal analyses. They should be viewed with a healthy degree of skepticism. These effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects.
Physical Effects
Physical(11)
- Dehydration— A state of insufficient bodily hydration manifesting as persistent thirst, dry mouth, and physical d...
- Dizziness— A sensation of spinning, swaying, or lightheadedness that impairs balance and spatial orientation, o...
- Motor control loss— A distinct decrease in the ability to control one's physical body with precision, balance, and coord...
- Muscle relaxation— The experience of muscles throughout the body losing their rigidity and tension, becoming noticeably...
- Nausea— An uncomfortable sensation of queasiness and stomach discomfort that may or may not lead to vomiting...
- Physical euphoria— An intensely pleasurable bodily sensation that can manifest as waves of warmth, tingling electricity...
- Respiratory depression— A dangerous slowing and shallowing of breathing that can progress from barely noticeable reductions ...
- Sedation— A state of deep physical and mental calming that manifests as a progressive desire to remain still, ...
- Seizure— Uncontrolled brain electrical activity causing convulsions and loss of consciousness -- a life-threa...
- Seizure suppression— Seizure suppression is the pharmacological reduction or prevention of seizures through substances th...
- Stimulation— A state of heightened physical and mental energy characterized by increased wakefulness, elevated mo...
Cognitive & Perceptual Effects
Visual(1)
- Visual acuity suppression— Vision becomes blurred, indistinct, and out of focus, as though looking through a smudged lens. Fine...
Cognitive(16)
- Amnesia— A complete or partial inability to form new memories or recall existing ones during and after substa...
- Analysis suppression— Analysis suppression is a cognitive impairment in which the capacity for logical reasoning, critical...
- Anxiety— Intense feelings of apprehension, worry, and dread that can range from a subtle background unease to...
- Anxiety suppression— A partial to complete suppression of anxiety and general unease, producing a calm, relaxed mental st...
- Compulsive redosing— An overwhelming, difficult-to-resist urge to continuously take more of a substance in order to maint...
- Confusion— An impairment of abstract thinking marked by a persistent inability to grasp or comprehend concepts ...
- Delusion— A delusion is a fixed, false belief that is held with unshakeable certainty and is impervious to con...
- Depression— A persistent state of low mood, emotional numbness, hopelessness, and diminished interest or pleasur...
- Disinhibition— A marked reduction in social inhibitions, self-consciousness, and behavioral restraint that manifest...
- Dream potentiation— Enhanced dream vividness, complexity, and recall, often occurring as REM rebound after discontinuing...
- Dream suppression— Dream suppression is a decrease in the intensity, frequency, and recollection of dreams — ranging fr...
- Emotion suppression— A blunting or flattening of emotional experience in which feelings become muted, distant, or seeming...
- Irritability— Irritability is a sustained state of emotional reactivity in which the threshold for annoyance, frus...
- Sleepiness— A progressive onset of drowsiness, heaviness, and the desire to sleep that pulls the individual towa...
- Thought deceleration— The experience of thoughts occurring at a markedly reduced pace, as if the mind has been placed into...
- Thought disorganization— Thought disorganization is a cognitive impairment in which the normal capacity for structured, seque...
Pharmacology
Mechanism of action Clonazepam enhances the activity of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in the central nervous system to give its anticonvulsant, skeletal muscle relaxant, and anxiolytic effects. It acts by binding to the benzodiazepine site of the GABA receptors, which enhances the electric effect of GABA binding on neurons, resulting in an increased influx of chloride ions into the neurons. This further results in an inhibition of synaptic transmission across the central nervous system.
Benzodiazepines do not have any effect on the levels of GABA in the brain. Clonazepam has no effect on GABA levels and has no effect on gamma-aminobutyric acid transaminase. Clonazepam does, however, affect glutamate decarboxylase activity. It differs from other anticonvulsant drugs it was compared to in a study.
Clonazepam's primary mechanism of action is the modulation of GABA function in the brain, by the benzodiazepine receptor, located on GABAA receptors, which, in turn, leads to enhanced GABAergic inhibition of neuronal firing. Benzodiazepines do not replace GABA, but instead enhance the effect of GABA at the GABAA receptor by increasing the opening frequency of chloride ion channels, which leads to an increase in GABA's inhibitory effects and resultant central nervous system depression. In addition, clonazepam decreases the utilization of 5-HT (serotonin) by neurons and has been shown to bind tightly to central-type benzodiazepine receptors. Because clonazepam is effective in low milligram doses (0.5mg clonazepam = 10mg diazepam), it is said to be among the class of "highly potent" benzodiazepines. The anticonvulsant properties of benzodiazepines are due to the enhancement of synaptic GABA responses, and the inhibition of sustained, high-frequency repetitive firing.
Benzodiazepines, including clonazepam, bind to mouse glial cell membranes with high affinity. Clonazepam decreases release of acetylcholine in the feline brain and decreases prolactin release in rats. Benzodiazepines inhibit cold-induced thyroid-stimulating hormone (also known as TSH or thyrotropin) release. Benzodiazepines act via micromolar benzodiazepine binding sites as Ca channel blockers and significantly inhibit depolarization-sensitive calcium uptake in experimentation on rat brain cell components. This has been conjectured as a mechanism for high-dose effects on seizures in the study.
Clonazepam is a 2'-chlorinated derivative of nitrazepam, which increases its potency due to electron-attracting effect of the halogen in the ortho-position.
Pharmacokinetics Clonazepam is lipid-soluble, rapidly crosses the blood–brain barrier, and penetrates the placenta. It is extensively metabolised into pharmacologically inactive metabolites, with only 2% of the unchanged drug excreted in the urine. Clonazepam is metabolized extensively via nitroreduction by cytochrome P450 enzymes, including CYP3A4. Erythromycin, clarithromycin, ritonavir, itraconazole, ketoconazole, nefazodone, cimetidine, and grapefruit juice are inhibitors of CYP3A4 and can affect the metabolism of benzodiazepines. It has an elimination half-life of 19–60 hours. Peak blood concentrations of 6.5–13.5ng/mL were usually reached within 1–2 hours following a single 2mg oral dose of micronized clonazepam in healthy adults. In some individuals, however, peak blood concentrations were reached at 4–8 hours.
Clonazepam passes rapidly into the central nervous system, with levels in the brain corresponding with levels of unbound clonazepam in the blood serum. Clonazepam plasma levels are very unreliable amongst patients. Plasma levels of clonazepam can vary as much as tenfold between different patients.
Clonazepam has plasma protein binding of 85%. Clonazepam passes through the blood–brain barrier easily, with blood and brain levels corresponding equally with each other. The metabolites of clonazepam include 7-aminoclonazepam, 7-acetaminoclonazepam and 3-hydroxy clonazepam. These metabolites are excreted by the kidney.
It is effective for 6–8 hours in children, and 8–12 hours in adults.
Detection Methods
Standard Drug Panel Inclusion
Clonazepam is detected on standard 10-panel and extended drug screening panels. The immunoassay screens used in workplace and clinical testing target benzodiazepine metabolites broadly, and clonazepam's primary metabolite, 7-aminoclonazepam, is reliably picked up by most commercial assays. However, some older immunoassay platforms have reduced sensitivity to clonazepam compared to other benzodiazepines like diazepam or oxazepam, because 7-aminoclonazepam has a slightly different structural profile. Laboratories aware of this limitation often calibrate their cutoffs accordingly.
Urine Detection
Clonazepam and its metabolite 7-aminoclonazepam are detectable in urine for approximately 5 to 7 days after a single dose, though chronic users may test positive for up to 30 days. The standard immunoassay cutoff for benzodiazepines in urine is 300 ng/mL. Because clonazepam is metabolized primarily via nitroreduction rather than glucuronidation, some assays require hydrolysis of urine samples to improve sensitivity. The metabolite 7-aminoclonazepam is the primary analyte targeted by confirmatory methods.
Blood and Serum Detection
In blood, clonazepam is detectable for 1 to 3 days after use. Therapeutic plasma concentrations range from 20 to 70 ng/mL, and concentrations above 100 ng/mL may indicate supratherapeutic dosing. Blood testing is primarily used in clinical toxicology and forensic contexts rather than routine screening.
Hair Follicle Detection
Hair follicle testing can detect clonazepam use for up to 90 days. The parent compound and 7-aminoclonazepam are both targeted in hair analysis, though concentrations tend to be low and require sensitive analytical methods. Hair testing for benzodiazepines is less standardized than for amphetamines or opioids.
Confirmatory Methods
Gas chromatography-mass spectrometry (GC-MS) and liquid chromatography-tandem mass spectrometry (LC-MS/MS) are used for confirmation. LC-MS/MS is the preferred method due to its superior sensitivity for the 7-aminoclonazepam metabolite, with limits of detection typically below 5 ng/mL.
Reagent Testing
Reagent testing has limited utility for pharmaceutical benzodiazepines obtained from verified sources. The Zimmermann reagent produces a yellow-green color with clonazepam. The Mandelin reagent yields an orange-brown response. These tests can help distinguish benzodiazepines from non-benzodiazepine compounds but cannot differentiate between individual benzodiazepines. Fentanyl test strips should be used on any benzodiazepine obtained from unregulated sources, as counterfeit pills frequently contain fentanyl or its analogues.
Interactions
| Substance | Status | Note |
|---|---|---|
| Atropa belladonna | Dangerous | Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure |
| Cake | Dangerous | Combined CNS depression; risk of respiratory failure |
| Datura | Dangerous | Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure |
| Deschloroetizolam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Desomorphine | Dangerous | Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths |
| Diclazepam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Diphenhydramine | Dangerous | Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure |
| Dissociatives | Dangerous | — |
| Eszopiclone | Dangerous | Combined CNS depression; risk of respiratory failure |
| Etizolam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Flubromazepam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Flubromazolam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Flunitrazepam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Flunitrazolam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Gaboxadol | Dangerous | Combined CNS depression; risk of respiratory failure |
| Harmala alkaloid | Dangerous | Unpredictable potentiation of CNS depression; risk of respiratory failure |
| Lorazepam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Mephenaqualone | Dangerous | Combined CNS depression; risk of respiratory failure |
| Metizolam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Midazolam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Naloxone | Dangerous | Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths |
| Nicotine | Dangerous | Combined CNS depression; risk of respiratory failure |
| Nifoxipam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Peganum harmala | Dangerous | Unpredictable potentiation of CNS depression; risk of respiratory failure |
| Pentobarbital | Dangerous | Combined CNS depression; risk of respiratory failure |
| Phenobarbital | Dangerous | Combined CNS depression; risk of respiratory failure |
| SAMe | Dangerous | Combined CNS depression; risk of respiratory failure |
| 3-Cl-PCP | Caution | Both cause CNS depression; increased risk of vomiting, unconsciousness, and respiratory depression |
| 3-FMA | Caution | Masks the effects of each drug; risk of overdosing when one wears off before the other |
| 3-HO-PCE | Caution | Both cause CNS depression; increased risk of vomiting, unconsciousness, and respiratory depression |
| 3-HO-PCP | Caution | Both cause CNS depression; increased risk of vomiting, unconsciousness, and respiratory depression |
| 3-MeO-PCE | Caution | Both cause CNS depression; increased risk of vomiting, unconsciousness, and respiratory depression |
| 1,3-Butanediol | Low Risk & Decrease | Depressants dull psychedelic effects; benzodiazepines are commonly used as trip-killers |
| 25E-NBOH | Low Risk & Decrease | Depressants dull psychedelic effects; benzodiazepines are commonly used as trip-killers |
| 2C-T | Low Risk & Decrease | Depressants dull psychedelic effects; benzodiazepines are commonly used as trip-killers |
| 2C-T-2 | Low Risk & Decrease | Depressants dull psychedelic effects; benzodiazepines are commonly used as trip-killers |
| 2C-T-21 | Low Risk & Decrease | Depressants dull psychedelic effects; benzodiazepines are commonly used as trip-killers |
History
Clonazepam belongs to the depressant class of psychoactive substances, which encompasses a diverse range of compounds that reduce central nervous system activity.
The history of CNS depressants in medicine stretches back millennia, from the ancient use of alcohol and opium to the development of barbiturates in the early 1900s and benzodiazepines in the 1960s. Each generation of depressant drugs was initially heralded as safer than its predecessors, only for patterns of dependence and misuse to emerge with wider use.
The development of benzodiazepines represented a significant improvement in the therapeutic index over barbiturates, though concerns about dependence and long-term cognitive effects have moderated initial enthusiasm. Newer GABAergic compounds, including the Z-drugs and various research chemicals, continue this pattern of iterative development.
Clonazepam is situated within this evolving pharmacological landscape, with its own specific history of development, clinical application, and patterns of use.
Harm Reduction
It is strongly recommended that one use harm reduction practices when using this drug.
Tolerance and addiction potential:extremely physically and psychologically addictive.
Tolerance will develop to the sedative-within a couple of days of continuous use. After cessation,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.
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.
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.. Benzodiazepine overdose is a medical emergency that may lead to a coma, permanent brain injury or death if not treated promptly and properly.
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.
Toxicity & Safety
Radar plot showing relative physical harm, social harm, and dependence of benzodiazepines in comparison to other drugs. Clonazepam has a low toxicity relative to dose. However, it is potentially lethal when mixed with depressants like alcohol or opioids.
It is strongly recommended that one use harm reduction practices when using this drug.
Tolerance and addiction potential
Clonazepam is extremely physically and psychologically addictive.
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.
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.
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.
Clonazepam presents cross-tolerance with all benzodiazepines, meaning that after its consumption all benzodiazepines will have a reduced effect.
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.
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.
Dangerous interactions
Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).
Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.
Depressants (1,4-Butanediol, 2M2B, alcohol, benzodiazepines, barbiturates, GHB/GBL, methaqualone, opioids) - This combination potentiates the muscle relaxation, amnesia, sedation, and respiratory depression caused by one another. At higher doses, it can lead to a sudden, unexpected loss of consciousness along with a dangerous amount of depressed respiration. There is also an increased risk of suffocating on one's vomit while unconscious. If nausea or vomiting occurs before a loss of consciousness, users should attempt to fall asleep in the recovery position or have a friend move them into it.
Dissociatives - This combination can unpredictably potentiate the amnesia, sedation, motor control loss and delusions that can be caused by each other. It may also result in a sudden loss of consciousness accompanied by a dangerous degree of respiratory depression. If nausea or vomiting occurs before consciousness is lost, users should attempt to fall asleep in the recovery position or have a friend move them into it.
Stimulants - Stimulants mask the sedative effect of depressants, which is the main factor most people use to gauge their level of intoxication. Once the stimulant effects wear off, the effects of the depressant will significantly increase, leading to intensified disinhibition, motor control loss, and dangerous black-out states. This combination can also potentially result in severe dehydration if one's fluid intake is not closely monitored. If choosing to combine these substances, one should strictly limit themselves to a pre-set schedule of dosing only a certain amount per hour until a maximum threshold has been reached.
Addiction Potential
extremely physically and psychologically addictive
Overdose Information
overdose is a medical emergency that may lead to a coma, permanent brain injury or death if not treated promptly and properly.
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.
Dangerous Interactions
The combinations listed below may be life-threatening. Independent research should always be conducted to ensure safety when combining substances.
Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure
Combined CNS depression; risk of respiratory failure
Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure
Combined CNS depression; risk of respiratory failure
Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Combined CNS depression; risk of respiratory failure
Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Unpredictable potentiation of CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Unpredictable potentiation of CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Tolerance
| Full | within a couple of days of continuous use |
| Half | Unknown |
| Zero | 7 - 14 days |
Cross-tolerances
Legal Status
Internationally, clonazepam is included under the United Nations Convention on Psychotropic Substances in Schedule IV.
Australia: Clonazepam is available by prescription only.
Brazil: Clonazepam is a "black stripe" drug, which are available by prescription only.
Canada: Clonazepam is a Schedule IV drug.
Czech Republic: Clonazepam is a Schedule IV (List 7) substance. Sold exclusively by prescription "without a blue stripe" (§ 1, g), 2. of Nařízení vlády č. 463/2013 Sb.).
Germany: Clonazepam is controlled under Anlage III BtMG (Narcotics Act, Schedule III) as of August 1, 1986. It can only be prescribed on a narcotic prescription form, except preparations which contain up to 2 mg clonazepam in each dosage form and solutions that contain up to 0.25% and under 250 mg clonazepam in total per packaging unit.
India: Clonazepam is Schedule H in India.
Israel: Clonazepam is available by prescription only.
New Zeland: Clonazepam is a Schedule 3 controlled drug.
Norway: Clonazepam is available by prescription only.
Russia: Clonazepam is a Schedule III controlled substance as of April 2013.
Switzerland: Clonazepam is a controlled substance specifically named under Verzeichnis B. Medicinal use is permitted.
Turkey: Clonazepam is a 'green prescription' only substance and illegal when sold or possessed without a prescription.
United Kingdom: Clonazepam is a Class C drug.
United States: Clonazepam is a Schedule IV substance.
Responsible use
Psychoactive substance index
Depressants
Clonazepam (Wikipedia)
Clonazepam (Erowid Vault)
Clonazepam (Isomer Design)
Clonazepam (DrugBank)
Clonazepam (Drugs.com)
Experience Reports (2)
Tips (9)
Clonazepam withdrawal can produce severe symptoms including seizures, psychosis, and depersonalization even at therapeutic doses after prolonged use. A 10% reduction every 2-4 weeks is the recommended tapering pace. Faster tapers risk medical emergencies.
Keep a written log of your Clonazepam use including time and dose. Benzodiazepines impair memory formation, making it easy to forget you already dosed and accidentally take more. This is how many accidental overdoses happen.
Clonazepam has a long half-life (18-50 hours) which makes it better suited for tapering than short-acting benzos like Xanax. However, this also means it accumulates in your system with daily dosing. What feels like tolerance may partly be steady-state buildup. Do not keep increasing your dose.
If prescribed Clonazepam, use it as directed and have honest conversations with your doctor about any recreational use. Benzodiazepines are among the most difficult drugs to quit once dependent. Short-term use only.
Long-term clonazepam use (2+ years daily) causes measurable memory impairment. The good news from community reports is that cognitive function does recover after discontinuation, but it can take 6-12 months for memory to fully normalize. This is not permanent brain damage.
Research chemical benzodiazepines (clonazolam, flualprazolam, etc.) are significantly more potent than pharmaceutical Clonazepam. Doses measured in micrograms can cause multi-day blackouts. Use volumetric dosing.
Community Discussions (12)
See Also
References (3)
- PubChem: Clonazepam
PubChem compound page for Clonazepam (CID: 2802)
pubchem - Clonazepam - TripSit Factsheet
TripSit factsheet for Clonazepam
tripsit - Clonazepam - Wikipedia
Wikipedia article on Clonazepam
wikipedia