Also known as

sparkle, woof woof




This is a relatively new synthetic (man-made) drug. It is said to have similar effects to MDMA (ecstasy) but there is very little information on dose and adverse effects available. It was produced in the 1990's with the aim of creating a drug that was less toxic than other types in the same group (e.g. MDMA) to be used as an anti-depressant or appetite suppressant [1].

What does it look like?

It is most commonly found as a powder [1].




  • threshold - 20 - 40 mg,
  • light - 40 - 100 mg,
  • common - 100 - 175 mg,
  • strong - 175 - 300 mg,
  • heavy - 300 mg + [2].

How long do its effects last?

Onset of effects

  • oral - 20 - 40 minutes [2].
  • all ROA's - 30 - 60 minutes [3].

Come up

  • oral - 30 - 60 minutes [2].


  • oral - 2 - 2.5 hours [2].


  • oral - 1 - 2 hours [2].

Duration of effects

  • oral - 4 - 6 hours [2], all ROA's - 4 - 6 hours [3].



Methylenedioxy-2-aminoindane (MDAI) is a drug originally synthesised by the American pharmacologist and medicinal chemist, David E. Nichols during the 1990's at Purdue University. Ordinarily, it appears as a tan-coloured, crystalline powder.

MDAI is derived from the drug -3, 4-methylenedioxyamphetamine (MDA) - a single structural alteration is the only difference between the two drugs. However, due to this structural change occurring in the region responsible for typical amphetamine-like responses, significant pharmacological differences are seen when comparing MDAI with MDA.

MDAI has been shown to strongly stimulate the release of the neurotransmitter serotonin in research models and can therefore be described as being a 'selective serotonin releasing agent' (SSRA). Serotonin (or 5-HT), is mainly found in the intestines and central nervous system where it is involved in the regulation of processes such as: intestinal movement, sleep, mood, appetite, memory and learning.

The extent to which MDAI stimulates serotonin release is comparable to that seen with MDA but less than is seen with 3, 4-methylenedioxy-N-methylamphetamine (MDMA).

In humans, MDAI has been shown to produce heightened feelings of empathy, love and emotional closeness with others. Drugs producing these effects are known as entactogens (or empathogens) and in addition to MDAI, include MDMA and related 'MDxx' drugs.

In contrast to many similar drugs, MDAI has been found to be largely non-stimulating and has so far proven to cause neurotoxicity when taken by without any other drugs. Reliable data concerning toxic effects on the heart (a known problem with many amphetamine and amphetamine-like drugs) has yet to be gathered for MDAI.

MDAI has also been found to inhibit the reuptake (movement back into cells) of serotonin as well as (to a lesser degree) the neurotransmitters dopamine (involved in regulating reward-seeking behaviour) and norepinephrine (or noradrenaline - a primary stress hormone).

Subjective user reports have indicated that mild pharmacological effects are seen at doses between 150mg - 250mg, with significant effects above this. However, factors such as a user's weight, previous usage and metabolism are just some variables that would determine an individual's response to MDAI.

Adulteration with other drugs (including the now illegal drug mephedrone), has been found in samples being sold as MDAI and this could also significantly alter the pharmacological and toxic effects produced [1].

MDAI has been shown to inhibit the reuptake of serotonin and has a selective affinity for the serotonin receptor. Studies show that the brains of animals treated with MDAI have greater extracellular concentrations of monoamine neural transmitters, most significantly serotonin. For comparison, MDAI is similar in potency with releasing serotonin to MDA, but significantly less potent than MDMA [4]. This is done by inhibiting the reuptake and reabsorption of the neurotransmitters after they have performed their function of transmitting a neural impulse, essentially allowing them to accumulate, be reused and cause entactogenic effects [2].

Mode of use

  • Snorted - usually divided into lines and snorted (insufflated) via rolled up paper or 'bumped'/'keyed' i.e. small amount sniffed.
  • Swallowed - swallowed (ingested) by 'bombing'. A 'bomb' is prepared by wrapping individual doses in cigarette paper [1].


Physical effects

  • physical euphoria,
  • spontaneous physical sensations,
  • tactile enhancement,
  • sedation,
  • dehydration,
  • difficulty urinating,
  • increased perspiration,
  • temperature regulation suppression,
  • temporary erectile dysfunction [2].

Cognitive effects

  • anxiety,
  • cognitive euphoria,
  • depression,
  • irritability,
  • mindfulness,
  • time distortion,
  • empathy, affection and sociability enhancement,
  • immersion enhancement,
  • increased music appreciation,
  • wakefulness,
  • anxiety suppression,
  • cognitive fatigue,
  • motivation suppression,
  • thought deceleration [2].

Visual effects

  • acuity enhancement,
  • colour enhancement,
  • tracers,
  • vibrating vision [2].

Auditory effects

  • auditory enhancement [2].

After effects

  • anxiety,
  • cognitive fatigue,
  • depression,
  • irritability,
  • motivation suppression,
  • thought deceleration,
  • wakefulness [2].

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 [2].

  • 25x-NBOMe - Both the NBOMe series and this compound induce powerful stimulation and their interaction may cause severe side-effects. These can include thought loops, seizures, increased blood pressure, vasoconstriction, increased heart rate, and heart failure (in extreme cases).
  • alcohol - It is dangerous to combine alcohol, a depressant, with stimulants due to the risk of excessive intoxication. Stimulants decrease the sedative effect of alcohol which is the main factor most people consider when determining their level of intoxication. Once the stimulant wears off, the effects of alcohol will be significantly increased, leading to intensified disinhibition as well as respiratory depression. If combined, one should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • DXM - This combination may cause increased heart rate and panic attacks.
  • MXE - Increased heart rate and blood pressure may occur.
  • Tramadol - This combination can increase the risk of seizures.
  • MDMA - The neurotoxic effects of MDMA may be increased when combined with other stimulants.
  • Cocaine - This combination may increase strain on the heart [2].


  • αMT,
  • Tramadol - Tramadol and stimulants both increase the risk of seizures.
  • MAOIs - MAO-B inhibitors can increase the potency and duration of phenethylamines unpredictably. MAO-A inhibitors with amphetamine can lead to hypertensive crises [3].


  • DOx - The combined stimulating effects of the two can lead to an uncomfortable body-load, while the focusing effects of amphetamine can easily lead to thought loops. Coming down from amphetamines while the DOx is still active can be quite anxiogenic.
  • NBOMes - Amphetamines and NBOMes both provide considerable stimulation. When combined they can result in tachycardia, hypertension, vasoconstriction and in extreme cases heart failure. The anxiogenic and focusing effects of stimulants are also not good in combination with psychedelics as they can lead to unpleasant thought loops. NBOMes are known to cause seizures and stimulants can increase this risk.
  • 2C-T-x - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences. In extreme cases, they can result in severe vasoconstriction, tachycardia, hypertension, and in extreme cases heart failure.
  • 5-MeO-xxT - The anxiogenic and focusing effects of stimulants increase the chance of unpleasant thought loops. The combination is generally unnecessary because of the stimulating effects of psychedelics.
  • DXM - Both substances raise heart rate, in extreme cases, panic attacks caused by these drugs have led to more serious heart issues.
  • PCP - This combination can easily lead to hypermanic states [3].


MDAI is covered by The Psychoactive Substances Act. It was introduced in the UK on the 26th May 2016 and it makes it an offence to manufacture, export/import (i.e. buying from a non-UK website), supply or offer to supply any psychoactive substance, if likely to be used for its psychoactive effects. Despite being psychoactive, alcohol, nicotine, tobacco and caffeine are exempt from the act.

Under the new regulations, possession with intent to supply is an offence. Possession is not an offence, except in a 'custodial institution' (e.g. prison, young offenders centre).

Penalties range from civil sanctions to a 7 year prison sentence but some offences will be considered to be aggravated, including selling to under 18s or around schools and children's homes etc [5].

Harm reduction

MDAI can be fast acting and powerful, so it's important to know your own limits; if you're new to it, start with small doses until you find your tolerance. If you don't feel the effects immediately, don't redose, wait at least an hour before taking any more [1].

  • it can interact with other substances (particularly alcohol) so try not to use anything else at the same time,
  • if snorting, clean out your nose after use and do not share snorting equipment,
  • try to use with friends (but remember that sharing can be considered supply) or at the very least make sure someone you trust knows where you are and can get help if necessarye [1].


MDAI was first investigated in the 1990's at Purdue University by David E. Nicholas, as a selective serotonin releasing agent. Until 2009, when it first became available to the public in headshops and via online legal high sellers, there was very little history with the drug [1].


  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 MDAI, 2017,
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 MDAI, 2017,
  3. 3.0 3.1 3.2 3.3 3.4 MDAI, 2017,
  4. Johnson, M. P. and Conarty, P. F. and Nichols D. E., [3H]monoamine releasing and uptake inhibition properties of 3,4-methylenedioxymethamphetamine and p-chloroamphetamine analogs, European Journal of Pharmacology, 1991, 200, 1, 9-16,
  5. MDAI, 2017,