How long does Codeine last?

The total duration of Codeine via oral is 3 hours to 6 hours. Onset typically occurs within 30 minutes to 45 minutes. Peak effects last 3 hours to 5 hours.

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Codeine — SubstanceWiki

Codeine

Substituted morphinans · Opioids

47 dangerous interactions — combining Codeine with certain substances may be life-threatening.

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Opioids(Substituted morphinans)

Quick Dosage

oral100–150 mg (common)

Total duration (oral)3hr–6hr

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Codeine is an opiate and prodrug of morphine mainly used to treat pain, coughing, and diarrhea. It is commonly used as a recreational drug. It is found naturally in the sap of the opium poppy, Papaver somniferum. It is typically used to treat mild to moderate degrees of pain. Greater benefit may occur when combined with paracetamol (acetaminophen) as codeine/paracetamol or a nonsteroidal anti-inflammatory drug (NSAID) such as aspirin or ibuprofen. Evidence does not support its use for acute cough suppression in children. In Europe, it is not recommended as a cough medicine for those under 12 years of age. It is generally taken orally. It usually starts working after half an hour, with maximum effect at two hours. Its effects last for about four to six hours. Codeine exhibits abuse potential similar to other opioid medications, including a risk of addiction and overdose. Common side effects include nausea, vomiting, constipation, itchiness, lightheadedness, and drowsiness. Serious side effects may include breathing difficulties and addiction. Whether it can be used safely during pregnancy is unclear. Care should be used during breastfeeding, as it may result in opiate toxicity in the baby. Its use as of 2016 is not recommended for children. Codeine works by being broken down by the liver into morphine; how quickly this occurs depends on a person's genetics. Codeine was discovered in 1832 by Pierre Jean Robiquet. In 2013, about 361,000 kg (795,000 lb) of codeine were produced

How It Feels

Codeine is the gentlest introduction to the opioid landscape. It arrives not as a wave but as a whisper -- a soft, diffuse warmth that begins in the stomach and migrates outward over the course of thirty to forty-five minutes. The onset is so gradual that you may not notice the transition from sober to altered; instead, you simply realize at some point that the world has become slightly softer, slightly kinder, as though someone has turned down the contrast on reality by a few degrees.

The warmth is modest but genuine. It settles into the muscles like a mild sunburn in reverse -- instead of heat radiating outward from irritated skin, comfort radiates inward, loosening knots of tension you had forgotten you were carrying. The body becomes pleasantly heavy without becoming immobile. You can still move, still function, but there is a gentle gravitational pull toward stillness, toward sitting down, toward letting the couch absorb your weight. A mild drowsiness accompanies this heaviness, softening the edges of wakefulness without pulling you fully into sleep.

Emotionally, codeine produces a quiet optimism. Worries that loomed large an hour ago now seem manageable, even trivial. There is no dramatic euphoria, no sense of chemical bliss -- rather, an absence of anxiety, a filling-in of the low places in your emotional terrain. Conversations become slightly easier. Music sounds a touch richer. The itching that accompanies stronger opioids may appear here in its mildest form, a faint tickle on the bridge of the nose or the surface of the arms, barely noticeable.

The peak, such as it is, lasts two to three hours and has a plateau-like quality. There is no dramatic crest, no moment where the experience suddenly intensifies. Instead, the warmth simply holds steady, a reliable companion rather than a spectacular event. Nausea may surface, particularly on an empty stomach, accompanied by mild constipation that serves as a reminder of the compound's pharmacological lineage. The visual field remains largely unchanged, though there may be a subtle softening of focus, a slight dreaminess to the way light plays across surfaces.

The comedown is gentle and forgiving. The warmth thins out gradually, like fog burning off in morning sun. There is no rebound anxiety, no harsh return to baseline. Instead, a mild lethargy persists for an hour or two after the primary effects fade, accompanied by a vague contentment that makes the transition back to ordinary consciousness almost imperceptible. Sleep comes easily if desired, and it is deep and restorative, sometimes accompanied by vivid but pleasant dreams that evaporate on waking.

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(14)

Appetite suppression— A distinct decrease in hunger and desire to eat, ranging from reduced interest in food to complete d...
Constipation— A slowing or cessation of bowel movements resulting in difficulty passing stool, commonly caused by ...
Cough suppression— A decreased desire and need to cough, medically known as antitussive action, which can also allow in...
Headache— A painful sensation of pressure, throbbing, or aching in the head that can range from a dull backgro...
Increased heart rate— A noticeable acceleration of heartbeat that can range from a subtle awareness of one's pulse to a fo...
Itchiness— A persistent, diffuse urge to scratch the skin that arises without any external irritant, most commo...
Motor control loss— A distinct decrease in the ability to control one's physical body with precision, balance, and coord...
Nausea— An uncomfortable sensation of queasiness and stomach discomfort that may or may not lead to vomiting...
Pain relief— A suppression of negative physical sensations such as aches and pains, ranging from dulled awareness...
Physical euphoria— An intensely pleasurable bodily sensation that can manifest as waves of warmth, tingling electricity...
Pupil constriction— A visible narrowing of the pupil diameter (miosis) that reduces the size of the dark center of the e...
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...

Cognitive & Perceptual Effects

Visual(3)

Double vision— The visual experience of seeing a single object as two separate, overlapping images, similar to cros...
Geometry— The experience of perceiving complex, ever-shifting geometric patterns superimposed over the visual ...
Internal hallucination— Vivid, detailed visual experiences perceived within an imagined mental landscape that can only be se...

Cognitive(10)

Amnesia

Pharmacology

Codeine is not itself centrally active, and must first be converted via first-pass metabolism into morphine by the cytochrome P450 enzyme CYP2D6 (as such, it is a prodrug for morphine). Codeine is also metabolized into the inactive norcodeine via the CYP3A4 enzyme system. Both resultant forms are conjugated by UGT2B7 into their corresponding 3-glucuronide.

Some percentage of the population produces less CYP2D6 enzymes and so experience a significant reduction of effects from codeine in comparison to that of the average person. However, others produce CYP2D6 enzymes in higher quantities which can result in hypersensitivity to the drug. Some methods of potentiating opioids, such as using grapefruit juice throughout the day before consumption, inhibits the CYP3A4 enzyme. This results in less codeine being converted into norcodeine which leaves more to be metabolized into morphine. This also indicates a lacking capability in the metabolism of codeine into morphine when a user consumes antihistamines such as diphenhydramine prior to the ingestion of codeine.

There is an upper limit to the amount of codeine which can be converted by enzymatic metabolism into morphine throughout an individual session. This limit is commonly referred to as the "ceiling dose", which is commonly believed to be around 400mg. Consuming higher doses will lead to greater side effects such as itchiness and nausea, but will not increase euphoria.

The active metabolites of codeine, notably morphine, exert their effects by binding to and activating opioid receptors, mainly the μ-opioid receptor. This occurs because opioids structurally mimic endogenous endorphins which are naturally found within the body and also work upon the μ-opioid receptor set. The way in which opioids structurally mimic these natural endorphins results in their euphoria, pain relief, muscle relaxing and anxiolytic effects. This is because endorphins are responsible for reducing pain, causing sleepiness, and feelings of pleasure. They can be released in response to pain, strenuous exercise, orgasm, or general excitement.

Codeine itself is a weak ligand for the opioid receptors. However, its main active metabolite, morphine, shows much stronger agonistic effects.

Binding affinities (Ki)

Mu opioid agonist - 589 nM
Kappa opioid agonist - 18061 nM
Delta opioid agonist - 11442 nM

Detection Methods

Standard Drug Panel Inclusion

Codeine is a natural or semi-synthetic opiate that is detected on standard 5-panel drug screens under the opiates channel. The standard opiate immunoassay targets morphine and codeine as primary analytes, and Codeine or its metabolites will trigger a positive result due to structural similarity to the morphine backbone. Most workplace, clinical, and probation drug tests include opiate detection at a 2000 ng/mL or 300 ng/mL cutoff.

Urine Detection

Codeine can be detected in urine for approximately 2 to 3 days after the last dose. The primary metabolic pathways involve glucuronidation, O-demethylation, and N-demethylation. Key urinary metabolites include glucuronide conjugates and, depending on the specific compound, morphine or hydromorphone as downstream metabolites. Hydration status, urinary pH, body mass, and metabolic rate all influence the exact detection window.

Blood and Saliva Detection

Codeine is detectable in blood for approximately 6 to 24 hours after administration. Oral fluid (saliva) testing can detect Codeine for approximately 24 to 48 hours post-dose. Blood and oral fluid testing are most commonly used in emergency medicine, pain management compliance monitoring, and roadside testing programs.

Hair Follicle Detection

Hair follicle testing can detect Codeine for up to 90 days (approximately 1.5 inches of hair growth). Opiate incorporation into hair is well-characterized, and most commercial hair testing panels include the opiates category. A standard hair test screens for codeine, morphine, and 6-monoacetylmorphine; Codeine or its metabolites will typically be captured under this panel.

Confirmatory Testing

Immunoassay screening results for opiates are confirmed using gas chromatography-mass spectrometry (GC-MS) or liquid chromatography-tandem mass spectrometry (LC-MS/MS). These methods can distinguish between specific opiates, identifying Codeine and its metabolites with high specificity. Confirmation testing eliminates false positives from poppy seed consumption or structural analogues.

Reagent Testing

Marquis reagent produces a purple to violet color with Codeine, consistent with the morphine-class opiate reaction. Mecke reagent yields a deep blue-green to blue color. Mandelin reagent produces a grey-brown reaction. These reagent responses are characteristic of the opiate class and can help differentiate opiates from synthetic opioids, which may show different or no reactions.

Interactions

Substance	Status	Note
3-Cl-PCP	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
3-HO-PCE	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
3-HO-PCP	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
3-MeO-PCE	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
3-MeO-PCMo	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
3-MeO-PCP	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
4-MeO-PCP	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Alcohol	Dangerous	—
Atropa belladonna	Dangerous	Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure
Benzodiazepines	Dangerous	—
Cake	Dangerous	Severe respiratory depression risk; leading cause of polydrug overdose
Datura	Dangerous	Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure
Deschloroetizolam	Dangerous	Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Deschloroketamine	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Desomorphine	Dangerous	Compounding respiratory depression and overdose risk
Diclazepam	Dangerous	Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Diphenhydramine	Dangerous	Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure
Diphenidine	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Ephenidine	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Eszopiclone	Dangerous	Severe respiratory depression risk; leading cause of polydrug overdose
Etizolam	Dangerous	Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Flubromazepam	Dangerous	Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Flubromazolam	Dangerous	Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Flunitrazepam	Dangerous	Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Flunitrazolam	Dangerous	Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Gaboxadol	Dangerous	Severe respiratory depression risk; leading cause of polydrug overdose
GBL	Dangerous	—
GHB	Dangerous	—
Harmala alkaloid	Dangerous	Risk of serotonin syndrome and severe respiratory depression; potentially fatal
HXE	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Inhalants	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Ketamine	Dangerous	—
Lorazepam	Dangerous	Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Memantine	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Mephenaqualone	Dangerous	Severe respiratory depression risk; leading cause of polydrug overdose
Metizolam	Dangerous	Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Midazolam	Dangerous	Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
MXiPr	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Naloxone	Dangerous	Compounding respiratory depression and overdose risk
Nicotine	Dangerous	Severe respiratory depression risk; leading cause of polydrug overdose
Nifoxipam	Dangerous	Severe respiratory depression risk; leading cause of polydrug overdose
O-PCE	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
PCE	Dangerous	Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Peganum harmala	Dangerous	Risk of serotonin syndrome and severe respiratory depression; potentially fatal
Pentobarbital	Dangerous	Severe respiratory depression risk; leading cause of polydrug overdose
Phenobarbital	Dangerous	Severe respiratory depression risk; leading cause of polydrug overdose
SAMe	Dangerous	Severe respiratory depression risk; leading cause of polydrug overdose
3-FMA	Caution	Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off
4-MMC	Caution	Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off
8-Chlorotheophylline	Caution	Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off
Adrafinil	Caution	Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off
Benzydamine	Caution	Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off
Bromantane	Caution	Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off
Dichloropane	Caution	Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off
Ephedrine	Caution	Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off
Hexedrone	Caution	Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off
Methcathinone	Caution	Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off
Oxiracetam	Caution	Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off
Phenylpiracetam	Caution	Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off
Rhodiola Rosea	Caution	Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off
Nitrous	Uncertain	—
Psilocybin Mushrooms	Low Risk & No Synergy	No significant pharmacological interaction; opioids may slightly dull the psychedelic experience

Showing 62 key interactions out of 82 total.

History

Codeine, or 3-methylmorphine, is an alkaloid found in the opium poppy, Papaver somniferum var. album, a plant in the family Papaveraceae. Opium poppy has been cultivated and utilized throughout human history for a variety of medicinal (analgesic, anti-tussive and anti-diarrheal) and hypnotic properties linked to the diversity of its active components, which include morphine, codeine and papaverine.

Codeine is found in concentrations of 1% to 3% in opium prepared by the latex method from unripe pods of Papaver somniferum. The name codeine is derived from the Ancient Greek (, "poppy head"). The relative proportion of codeine to morphine, the most common opium alkaloid at 4% to 23%, tends to be somewhat higher in the poppy straw method of preparing opium alkaloids.

Until the beginning of the 19th century, raw opium was used in diverse preparations known as laudanum (see Thomas de Quincey's Confessions of an English Opium-Eater, 1821) and paregoric elixirs, several which were popular in England since the beginning of the 18th century; the original preparation seems to have been elaborated in Leiden, the Netherlands around 1715 by a chemist Jakob Le Mort; in 1721 the London Pharmacopoeia mentions an Elixir Asthmaticum, replaced by the term Elixir Paregoricum ("pain soother") in 1746.

The progressive isolation of opium's several active components opened the path to improved selectivity and safety of the opiates-based pharmacopeia.

Morphine had already been isolated in Germany by in 1804. Codeine was first isolated in 1832 in France by , already famous for the discovery of alizarin, the most widespread red dye, while working on refined morphine extraction processes. Robiquet is also credited with discovering caffeine independently of Pelletier, Caventou, and Runge. The first crystal structure would have to wait until 1954.

Codeine and morphine, as well as opium, were used in an attempt to treat diabetes in the 1880s and thereafter, as recently as the 1950s.

Numerous codeine salts have been prepared since the drug was discovered. The most commonly used are the hydrochloride (freebase conversion ratio 0.805, i.e. 10 mg of the hydrochloride salt is equivalent in effect to 8.05 mg of the freebase form), phosphate (0.736), sulphate (0.859), and citrate (0.842).

Codeine is the most widely used opiate in the world.

Names:

It is often sold as a salt in the form of either codeine sulfate or codeine phosphate in the United States, United Kingdom, and Australia. Codeine hydrochloride is more common worldwide and the citrate, hydroiodide, hydrobromide, tartrate, and other salts are also seen. The chemical name for codeine is morphinan-6-ol, 7,8-didehydro-4,5-epoxy-3-methoxy-17-methyl-, (5α,6α)-

Recreational use:

can be created with codeine syrup (pictured).]] A heroin (diamorphine) or other opiate/opioid addict may use codeine to ward off the effects of withdrawal during periods where their preferred drug is unavailable or unaffordable.

Codeine is also available in conjunction with the anti-nausea medication promethazine in the form of a syrup. Brand named as Phenergan with Codeine or in generic form as promethazine with Codeine, it began to be mixed with soft drinks in the 1990s as a recreational drug, called "syrup", "lean", or "purple drank". Rapper Pimp C, from the group UGK, died from an overdose of this combination.

Codeine is used in illegal drug laboratories to make morphine.

Toxicity & Safety

Codeine has a low toxicity relative to dose. As with all opioids, long-term effects can vary but can include diminished libido, apathy and memory loss. Some people may also have an allergic reaction to codeine, such as the swelling of skin and rashes. It is also potentially lethal when mixed with depressants like alcohol or benzodiazepines.

It is strongly recommended that one use harm reduction practices when using this drug.

Tolerance and addiction potential

As with other opioids, the chronic use of codeine can be considered moderately addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal symptoms may occur if a person suddenly stops their usage.

Tolerance to many of the effects of codeine develops with prolonged and repeated use. The rate at which this occurs develops at different rates for different effects, with tolerance to the constipation-inducing effects developing particularly slowly for instance. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). Codeine presents cross-tolerance with all other opioids, meaning that after the consumption of codeine all opioids will have a reduced effect.

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.

Alcohol - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess. Memory blackouts are likely
Stimulants - Stimulants increase respiration rate which allows for a higher dose of opiates than would otherwise be used. If the stimulant wears off first then the opiate may overcome the user and cause respiratory arrest.
Benzodiazepines - Central nervous system and/or respiratory-depressant effects may be additively or synergistically present. The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position blackouts/memory loss likely.
DXM - Generally considered to be toxic. CNS depression, difficulty breathing, heart issues, and liver toxicity have been observed. Additionally if one takes DXM, their tolerance of opiates goes down slightly, thus causing additional synergistic effects.
GHB/GBL - The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position
Ketamine - Both substances bring a risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position.
MAOIs - Coadministration of monoamine oxidase inhibitors (MAOIs) with certain opioids has been associated with rare reports of severe adverse reactions. There appear to be two types of interaction, an excitatory and a depressive one. Symptoms of the excitatory reaction may include agitation, headache, diaphoresis, hyperpyrexia, flushing, shivering, myoclonus, rigidity, tremor, diarrhea, hypertension, tachycardia, seizures, and coma. Death has occurred in some cases.
MXE - MXE can potentiate the effects of opioids but also increases the risk of respiratory depression and organ toxicity.
Nitrous - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position. Memory blackouts are common.
PCP - PCP may reduce opioid tolerance, increasing the risk of overdose.
Tramadol - Increased risk of seizures. Tramadol itself is known to induce seizures and it may have additive effects on seizure threshold with other opioids. Central nervous system- and/or respiratory-depressant effects may be additively or synergistically present.
Grapefruit - While grapefruit is not psychoactive, it may affect the metabolism of certain opioids. Tramadol, oxycodone, and fentanyl are all primarily metabolized by the enzyme CYP3A4, which is potently inhibited by grapefruit juice. This may cause the drug to take longer to clear from the body. it may increase toxicity with repeated doses. Methadone may also be affected. Codeine and hydrocodone are metabolized by CYP2D6. People who are on medicines that inhibit CYP2D6, or that lack the enzyme due to a genetic mutation will not respond to codeine as it can not be metabolized into its active product: morphine.

Addiction Potential

Moderately addictive. Lower abuse potential than stronger opioids due to lower euphoric ceiling, but dependence still develops with regular use. Codeine-containing cough syrups ("lean," "purple drank") are subject to widespread abuse. Tolerance and physical dependence develop similarly to other opioids but generally at a milder level.

Overdose Information

Opioid overdose from Codeine is a critical medical emergency that kills rapidly through respiratory depression. Every second counts.

Signs of opioid overdose (recognize any of these):

Extremely slow, shallow, or absent breathing
Blue or gray lips, fingernails, or skin
Pinpoint (very small) pupils
Gurgling or snoring sounds
Unresponsive to voice or painful stimulation
Limp body, pale face

EMERGENCY RESPONSE — ACT IMMEDIATELY:

Call emergency services (911 in US)
Administer naloxone (Narcan) if available — intranasal spray or intramuscular injection. Naloxone temporarily reverses opioid overdose. A second dose may be needed after 2-3 minutes if no response.
Begin rescue breathing if the person is not breathing — tilt head back, lift chin, give one breath every 5 seconds
Place in recovery position if breathing but unconscious
Stay with them — naloxone wears off in 30-90 minutes and overdose can recurNaloxone access: In many jurisdictions, naloxone is available without prescription at pharmacies. Carrying naloxone saves lives. Learn how to use it.

Dangerous Interactions

The combinations listed below may be life-threatening. Independent research should always be conducted to ensure safety when combining substances.

3-Cl-PCPDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

3-HO-PCEDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

3-HO-PCPDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

3-MeO-PCEDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

3-MeO-PCMoDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

3-MeO-PCPDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

4-MeO-PCPDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

AlcoholDangerous

Atropa belladonnaDangerous

Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure

BenzodiazepinesDangerous

CakeDangerous

Severe respiratory depression risk; leading cause of polydrug overdose

DaturaDangerous

Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure

DeschloroetizolamDangerous

Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths

DeschloroketamineDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

DesomorphineDangerous

Compounding respiratory depression and overdose risk

DiclazepamDangerous

Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths

DiphenhydramineDangerous

Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure

DiphenidineDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

EphenidineDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

EszopicloneDangerous

Severe respiratory depression risk; leading cause of polydrug overdose

EtizolamDangerous

Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths

FlubromazepamDangerous

Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths

FlubromazolamDangerous

Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths

FlunitrazepamDangerous

Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths

FlunitrazolamDangerous

Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths

GaboxadolDangerous

Severe respiratory depression risk; leading cause of polydrug overdose

GBLDangerous

GHBDangerous

Harmala alkaloidDangerous

Risk of serotonin syndrome and severe respiratory depression; potentially fatal

HXEDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

InhalantsDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

KetamineDangerous

LorazepamDangerous

Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths

MemantineDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

MephenaqualoneDangerous

Severe respiratory depression risk; leading cause of polydrug overdose

MetizolamDangerous

Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths

MidazolamDangerous

Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths

MXiPrDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

NaloxoneDangerous

Compounding respiratory depression and overdose risk

NicotineDangerous

Severe respiratory depression risk; leading cause of polydrug overdose

NifoxipamDangerous

Severe respiratory depression risk; leading cause of polydrug overdose

O-PCEDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

PCEDangerous

Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration

Peganum harmalaDangerous

Risk of serotonin syndrome and severe respiratory depression; potentially fatal

PentobarbitalDangerous

Severe respiratory depression risk; leading cause of polydrug overdose

PhenobarbitalDangerous

Severe respiratory depression risk; leading cause of polydrug overdose

SAMeDangerous

Severe respiratory depression risk; leading cause of polydrug overdose

Legal Status

Australia: In Australia, codeine preparations are Schedule 4 (Prescription Only) medications when combined with other substances. Preparations containing pure codeine (e.g., codeine phosphate tablets or codeine phosphate linctus) are available on prescription and are considered Schedule 8 (Controlled Drug (Possession without authority illegal)). Schedule 8 drugs are drugs that are available to be prescribed but are heavily restricted to prevent abuse and dependence. Possessing Schedule 8 drugs without authority is a criminal offense and can have varying punishments depending on the state of prosecution.
Austria: Codeine is legal for medical use under the AMG (Arzneimittelgesetz Österreich) and illegal when sold or possessed without a prescription under the SMG (Suchtmittelgesetz Österreich).
Canada: In Canada, codeine is available over the counter in combination tablets with the following restrictions: no more than 8 mg per dosage unit and it must be combined with at least two other active ingredients. It is kept behind the counter, to be sold on request-- generally to those 18 and over-- after a brief consultation and at the pharmacist's discretion. The other active ingredients most commonly consist of another non-opioid analgesic (300 mg acetaminophen, as in Tylenol No. 1; or 325 mg aspirin, as in 222s) and 15 mg caffeine. OTC tablets containing ibuprofen are generally unavailable. Preparations with a codeine content higher than 8 mg per dosage unit, or fewer than two other active ingredients, are available on prescription.
Denmark: In Denmark, codeine is sold over the counter with max 9.6 mg in the mixture. The item is given over the counter, with no prescriptions. The strongest available over the counter preparation containing codeine has 9.6 mg (with aspirin, brand name Kodimagnyl); anything stronger requires a prescription for legal possession.
Finland: In Finland, codeine cough syrups with a maximum strength of 1mg/ml is sold in pharmacies over the counter. Codeine isn't available in pill form without a prescription. Any stronger cough syrup and combination painkillers (codeine with paracetamol or ibuprofen such as Panacod, Co-codamol, and Ardinex) require a prescription.
France: In France, most preparations containing codeine do not require a doctor's prescription. Example products containing codeine include Néocodion (cough pills, and syrup), Codoliprane (codeine with paracetamol), Prontalgine and Migralgine (codeine, paracetamol, and caffeine). Codeine is regulated/controlled substance (schedule 2) since 2017 after a decision of the "Minister of Health" Agnès Buzyn, it is therefore now under prescription only and raw pure codeine is not available altogether anymore. The most common prescribed codeine brands are Klipal and Codoliprane, both mixed with paracetamol heavily. Klipal being the strongest ratio, 50mg codeine for 600mg paracetamol.
Germany: Codeine is a controlled substance under Anlage III of the BtMG. It can only be prescribed on a narcotic prescription form. There is an exception for preparations, containing up to 2,5% or 100mg codeine per unit, which can be prescribed on a regular prescription if not prescripted to an alcohol or drug dependent person.
Greece: Codeine is classed as an illegal drug in Greece, and individuals possessing it could conceivably be arrested, even if they were legitimately prescribed it in another country. It is sold only with a doctor's prescription.
Hong Kong: In Hong Kong, codeine is regulated under Laws of Hong Kong, Dangerous Drugs Ordinance, Chapter 134, Schedule 1. It can be used legally only by health professionals and for university research purposes. The substance can be given by pharmacists under a prescription. However, codeine is available without prescription from licensed pharmacists in doses up to 0.1%
Iceland: Preparations of paracetamol and codeine require a prescription in Iceland.
India: Codeine preparations require a prescription in India. Preparation of paracetamol and codeine is available in India. Codeine is also present in various cough syrups as codeine phosphate.
Iran: Preparations of codeine in Iran normally comes with paracetamol, but can be purchased over-the-counter. Iran's deputy health minister reported that codeine is Iran's best selling OTC medication. The recreational use of codeine has also become widespread throughout Iran but authorities continue to let codeine be purchased without permission from a doctor, although the pharmacist may ask for the identification of the purchaser to verify they are 18 years or older to buy.
Ireland: Codeine remains a semi non-prescriptive, over-the-counter drug up to a limit of 12.8 mg per pill, but codeine products must be out of the view of the public. Products containing more than 12.8 mg codeine are available on prescription only.
Italy: Codeine tablets or preparations require a prescription in Italy. Preparations of paracetamol and codeine are available in Italy as Co-Efferalgan and Tachidol.
Japan: Codeine and similar mid-level centrally acting agents in combination with non-opioid analgesics, antihistamines, vitamins, inert GI agents like kaolin & pectin, mild laxatives, antacids, and herbal preparations, can be purchased over the counter, with 10 mg being the ceiling for OTC dispensing.
Maldives: The Maldives takes an infamously strict line on medicines, with many common drugs, anything containing codeine is banned unless you have a notarized and authenticated doctor's prescription. Visitors breaking the rules, even inadvertently, have been deported or imprisoned.
Poland: Codeine is listed in "Wykaz środków odurzających i substancji psychotropowych" group " II-N" which means it's legal to use in scientific and medical pruposes, and is available over the counter in doses of 15mg in combination with 500mg paracetamol (Antidol) or 300mg sulfogaiacol (Thiocodin), or 10mg in combination with thyme extract (Neoazarina). However a pharmacy worker can refuse to sell it if they believe the client is a minor or wants to use it for drug abuse purposes.
Romania: Codeine is sold OTC (when combined with another active ingredient), the limit being 12.8mg of codeine per pill, which is seen in Nurofen Plus. Any amount above 12.8mg/unit requires a prescription, whether it has another ingredient or not.
Russia: According to ITAR-Tass and Austria Presse-Agentur, OTC availability of codeine products was rescinded nationwide in 2012 because of the discovery of the Krokodil method of underground desomorphine synthesis.
Spain: Codeine tablets or preparations require a prescription in Spain, although this is often not enforced and many pharmacies will sell codeine products without the requirement of a prescription.
Sri Lanka: Codeine preparations are available as over the counter pharmacy medicines in Sri Lanka. The most common preparation is Panadeine, which contains 500 mg of Paracetamol and 8 mg of Codeine.
Sweden: Codeine is Schedule III under Swedish law, which means it is heavily regulated and sold only to those who have a prescription.
Switzerland: Codeine is a controlled substance specifically named under Verzeichnis A. Medicinal use is permitted. Some preparations containing codeine are included in Verzeichnis C, while certain ones are excluded.
Turkey: Codeine is a 'red prescription' only substance and illegal when sold or possessed without a prescription.
United Arabian Emirates: The UAE takes an exceptionally strict line on medicines, with many common drugs, notably anything with containing codeine being banned unless you have a notarized and authenticated doctor's prescription. Visitors breaking the rules, even inadvertently, have been deported or imprisoned. The US Embassy to the UAE maintains an unofficial list of what may not be imported.
United Kingdom: Under the Misuse of Drugs Act 1971 codeine is a Class B controlled substance or a Class A drug when prepared for injection. The possession of controlled substances without a prescription is a criminal offense. However, certain preparations of codeine are exempt from this restriction under Schedule 5 of the Misuse of Drugs Regulations 2001. It is thus legal to possess codeine without a prescription, provided that it is compounded with at least one other active or inactive ingredient and that the dosage of each tablet, capsule, etc does not exceed 100 mg or 2.5% concentration in the case of liquid preparations.
United States: In the United States, codeine is regulated by the Controlled Substances Act. Federal law dictates that codeine be a Schedule II controlled substance when used in products for pain-relief that contain codeine alone or more than 90 mg per dosage unit. Tablets of codeine in combination with aspirin or acetaminophen (paracetamol/Tylenol) made for pain relief are listed as Schedule III; and cough syrups are Schedule III or V, depending on the formula.
Responsible use
Extraction of opioids from painkiller products
Depressants
Oxycodone
Kratom
Codeine (Wikipedia)
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Friswell J, Phillips C, Holding J, Morgan CJ, Brandner B, Curran HV. (2008). Acute effects of opioids on memory functions of healthy men and women. Psychopharmacology (Berl.). 198 (2): 243–50. https://doi.org/10.1007/s00213-008-1123-x.
Schmidt, H., Vormfelde, S. V., Klinder, K., Gundert-Remy, U., Gleiter, C. H., Skopp, G., Aderjan, R. and Fuhr, U. (2002), Affinities of Dihydrocodeine and its Metabolites to Opioid Receptors. Pharmacology & Toxicology, 91: 57–63. https://doi.org/10.1034/j.1600-0773.2002.910203.x
Koch T, Höllt V. (2008). Role of receptor internalization in opioid tolerance and dependence. Pharmacol. Ther. 117 (2): 199–206. https://doi.org/10.1016/j.pharmthera.2007.10.003
Pert, C. B., Pasternak, G., & Snyder, S. H. (1973). Opiate Agonists and Antagonists Discriminated by Receptor Binding in Brain. Science, 182 (4119), 1359-1361. https://doi.org/10.1126/science.182.4119.1359
Stefano GB, Ptáček R, Kuželová H, Kream RM. (2012). Endogenous morphine: up-to-date review (2011). Folia Biol. (Praha). 58 (2): 49–56. PMID 22578954.

=References=

Full	develops with prolonged and repeated use
Half	3 - 7 days
Zero	1 - 2 weeks

Codeine

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