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DMAA / DMHA

1,3-Dimethylamylamine · Octodrine

DMAA (1,3-dimethylamylamine) and its close analog DMHA (octodrine / 2-amino-6-methylheptane) are synthetic aliphatic-amine stimulants sold, illegally, in pre-workout and weight-loss "supplements." Both are potent sympathomimetic pressor agents. The main danger is cardiovascular: DMAA has been directly linked in published case reports to cerebral (hemorrhagic and subarachnoid) hemorrhage in young adults, and its supplement use was associated by the U.S. FDA with over 100 adverse-event reports and 6 deaths, prompting a 2013 ban. Marketed claims that DMAA/octodrine are "natural" geranium/Aconitum/Kigelia constituents are not supported by analytical chemistry; they are synthetic. DMHA is even less studied than DMAA, with essentially no modern human safety data at the supra-pharmacologic doses found in supplements (often >2-3x the old European pharmaceutical octodrine dose). Products are frequently adulterated with multiple undeclared stimulants in untested cocktails. This is a risk-forward monograph: lead with the danger of stroke, hypertensive emergency, and sudden cardiac events, and do not treat any dose as "safe."

Clinical readoutPED-adjacent · stimulant
Hepatic strainModerate
CardiovascularHigh
HPTA suppressionNone
Half-life
DMAA: terminal ha…
Route
Oral is the studied rou…
Evidence
C
Active
DMAA: peak plasma conce…
1·t½2·t½3·t½4·t½5·t½
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ DMAA: terminal half-life ~8.4 h (mean 8.45 ± 1.9 h) after a single 25 mg oral dose in 7 men (Schilling/Bloomer 2013). DMHA/octodrine: not characterized in modern human PK studies.
Pharmacology

Mechanism of action

Both are indirect/direct-acting sympathomimetic amines structurally related to amphetamine and to other aliphatic-amine stimulants (e.g., tuaminoheptane). DMAA acts as a competitive substrate-like ligand at the human dopamine transporter (DAT): in vitro it competitively inhibits dopamine uptake, binds the S1 substrate site, drives an outward-facing-to-closed conformational change, and stimulates DAT endocytosis via cocaine- and PKA-sensitive mechanisms, mirroring amphetamine — though this is preclinical (HEK-cell/computational) data only. Functionally, DMAA raises blood pressure as a pressor/vasoconstrictor; in a human crossover study it increased systolic and diastolic BP dose-dependently without raising heart rate, and the increase was not explained by rises in circulating norepinephrine or epinephrine, suggesting direct vascular alpha-adrenergic-type action. DMHA/octodrine is a historically pharmaceutical sympathomimetic with a very similar structure; its supplement-relevant mechanism is presumed analogous but is not characterized in modern controlled human studies.
Kinetics

Pharmacokinetics

Half-life

DMAA: terminal half-life ~8.4 h (mean 8.45 ± 1.9 h) after a single 25 mg oral dose in 7 men (Schilling/Bloomer 2013). DMHA/octodrine: not characterized in modern human PK studies.

Active duration

DMAA: peak plasma concentration reached ~3-5 h post-ingestion (mean ~70 ng/mL at 25 mg); acute hemodynamic (BP) effects in dosing studies peaked around 60 min. With an ~8.5 h half-life, ~5 half-lives (~2 days) are needed for near-complete elimination — relevant for washout/monitoring, not for evading drug testing. DMHA duration: unknown.

Route

Oral is the studied route in supplements/'party pills.' Recreational insufflation/other routes are described anecdotally but not pharmacokinetically characterized.

Metabolism & clearance

DMAA oral clearance ~20 L/h and oral volume of distribution ~236 L in the single human PK study; full metabolic pathway and route of excretion are not well characterized in humans. DMHA/octodrine metabolism and clearance are essentially uncharacterized in modern literature. No adequate human data on clearance in renal or hepatic impairment for either compound.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • Acute pressor effect: dose-dependent rise in systolic and diastolic blood pressure (DMAA alone and combined with caffeine) in a small human crossover study
  • Stimulant/sympathomimetic subjective effects: alertness, appetite suppression, perceived exercise-performance enhancement (marketed uses; efficacy not established in controlled trials)
  • Self-reported tachycardia, tremor, dizziness, and numbness/tingling among regular users in a military survey population
  • DMHA/octodrine: presumed stimulant and pressor effects by analogy to DMAA and to its historical pharmaceutical use, but not demonstrated in modern controlled human studies at supplement doses
Safety

Adverse effects by system

Cardiovascular

Most serious system. DMAA raises blood pressure (pressor effect) and is linked in case reports to cerebral hemorrhage, subarachnoid hemorrhage, and hemorrhagic stroke in young adults, plus self-reported tachycardia; FDA associated DMAA supplements with adverse events up to heart attack and with deaths. Risk is amplified by caffeine co-ingestion, exertion, and higher-than-labeled doses. DMHA cardiovascular risk is presumed similar but not directly documented.

Hepatic

Acute liver injury and acute liver failure (including cases requiring transplantation and a death) have been reported in users of DMAA-labeled products such as OxyELITE Pro; however, causal attribution to DMAA specifically is confounded — implicated products were multi-ingredient, some reformulated versions did not contain DMAA, and at least one detailed reanalysis disputed supplement causality for the Hawaii cluster. Treat hepatotoxicity as a real product-level signal with uncertain attribution to DMAA itself. DMHA-specific hepatic data: none.

Endocrine / HPTA

No adequate human data. DMAA/DMHA are stimulants, not hormonal agents, and there is no evidence of direct hypothalamic-pituitary-gonadal-axis suppression. Any endocrine effects would be indirect (e.g., stress/catecholaminergic). Not characterized.

Reproductive

No adequate human data on fertility, pregnancy, or reproductive outcomes for DMAA or DMHA. Use in pregnancy is not studied and should be avoided.

Neuropsychiatric

Stimulant-class effects (agitation, anxiety, insomnia) are expected by drug class and mechanism (DAT interaction); self-reported neurologic symptoms (dizziness, tremor, numbness/tingling) were more common in regular DMAA users. No adequate controlled human psychiatric-outcome data; dependence/abuse potential is plausible given amphetamine-like DAT activity but not quantified.

Renal

No adequate human data specifically evaluating renal toxicity. Theoretical concern from severe hypertension, potential exertional/heat stress, and rhabdomyolysis exists but is not established in primary literature for these compounds.

Hematologic

No adequate human data on direct hematologic toxicity. (Bleeding events reported are intracranial hemorrhages driven by the hypertensive/vascular mechanism, not a documented primary coagulopathy.)

Dermatologic

No known specific dermatologic effects and no adequate human data.

Recovery

HPTA suppression & recovery

Suppression: No known direct HPTA suppression; not characterized in humans

DMAA/DMHA are stimulants, not anabolic or hormonal agents, and there is no primary human evidence that they directly suppress the hypothalamic-pituitary-gonadal axis, so no SERM-based recovery protocol is indicated or supported for these compounds. Do not use a SERM to 'recover' from a stimulant. If HPTA or hormonal concerns exist (including from concurrent use of other agents), evaluation and any intervention should be directed by a qualified endocrinologist rather than self-managed; this monograph does not endorse any multi-drug recovery regimen.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Blood pressure and heart rate (baseline and monitored)Liver function tests (ALT, AST, bilirubin, ALP) given the product-level hepatotoxic signalBasic metabolic panel / renal functionECG if palpitations, chest pain, or known cardiac riskNeuroimaging (CT/MRI) urgently if any neurologic symptoms suggest hemorrhage

Cadence: There is no established safe-monitoring schedule because these substances are not approved for human use; the risk-forward recommendation is to not use them. If exposure has occurred, baseline evaluation and prompt clinician assessment are warranted, and any new symptom should trigger immediate medical attention rather than scheduled self-monitoring.

Warning signs — seek care
  • Sudden severe ('thunderclap') headache, worst-of-life headache, or neck stiffness — possible intracranial/subarachnoid hemorrhage: call emergency services
  • Chest pain, severe palpitations, fainting, or shortness of breath
  • Very high blood pressure readings, confusion, focal weakness, vision changes, or slurred speech
  • Dark urine, jaundice, right-upper-quadrant pain, nausea, or unexplained fatigue (possible liver injury)
  • Severe agitation, hyperthermia, or muscle pain (possible sympathomimetic toxicity/rhabdomyolysis)
Do not use if

Contraindications

  • Any cardiovascular disease, hypertension, or history of stroke/cerebral aneurysm/vascular malformation
  • Concurrent caffeine or other stimulants (additive pressor effect demonstrated for DMAA + caffeine)
  • Strenuous exertion or heat exposure while dosed (compounds cardiovascular and heat-injury risk)
  • Concurrent MAO inhibitors or other sympathomimetics/serotonergic-adrenergic drugs
  • Pregnancy and breastfeeding (no safety data)
  • Known or suspected liver disease, given the product-level hepatotoxicity signal and unknown metabolism
  • Use of undeclared multi-stimulant products (adulteration with untested stimulant cocktails is common)
  • Psychiatric conditions liable to worsen with stimulants (anxiety, psychosis, substance use disorder)
Combinations

Interaction profile

  • MajorWith an anabolic steroid: Additive cardiovascular strain
  • MajorWith a stimulant: Additive cardiovascular strain
  • ModerateWith a SARM: Additive cardiovascular strain
  • MajorWith thyroid hormone: Additive cardiovascular strain
  • ModerateWith a GLP-1 / incretin agonist: Additive cardiovascular strain
  • ModerateWith a melanocortin agonist: Additive hypertension
  • MajorWith a QT-prolonging drug: QT prolongation
  • ContraindicatedWith DNP: Additive cardiovascular strain

Check a specific combination in the interaction checker.

Harm reduction

Reducing harm & when to stop

  • The lowest-risk choice is not to use DMAA or DMHA; neither is approved for human consumption and both are banned from supplements and in sport (WADA).
  • Never combine with caffeine or other stimulants — additive blood-pressure elevation is documented for DMAA + caffeine.
  • Do not use before or during intense exercise or in heat; exertion plus a pressor stimulant raises the risk of cardiovascular and heat-related emergencies.
  • Assume label doses are unreliable: products are frequently adulterated with multiple undeclared stimulants at variable, sometimes supra-pharmacologic amounts.
  • Seek emergency care immediately for sudden severe headache, chest pain, fainting, focal weakness, vision/speech changes, or very high blood pressure — these can signal stroke or a cardiac event.
  • Stop use and get liver testing / medical review for jaundice, dark urine, right-upper-quadrant pain, or unexplained fatigue.
  • People with any cardiovascular, cerebrovascular, hepatic, or psychiatric condition, and anyone pregnant or breastfeeding, should not use these compounds.
  • Discuss any use, symptoms, or hormonal/health concerns with a physician; for endocrine questions defer to an endocrinologist. This monograph is informational and not an endorsement of use.
Evidence

Citations (14)

Every clinical claim above is tied to a primary source. Overall evidence grade C — graded to the best available evidence for its core claims.

  1. 01

    DMAA is a synthetic sympathomimetic pressor agent linked to cerebral hemorrhage in adults after use; originally patented as a nasal decongestant.

    Case seriesPMID 22575212 ↗

  2. 02

    A 21-year-old man suffered a cerebral hemorrhage shortly after ingesting DMAA-containing 'party pills.'

    Case reportPMID 21358791 ↗

  3. 03

    Single 25 mg oral DMAA dose in men: terminal half-life ~8.45 h, peak plasma ~70 ng/mL at 3-5 h, oral clearance ~20 L/h, Vd ~236 L; resting HR/BP/temperature largely unaffected at this single low dose, with peak levels ~15-30x lower than in adverse-event case reports.

    RCTPMID 24090077 ↗

  4. 04

    DMAA alone and with caffeine dose-dependently increased systolic and diastolic blood pressure and rate-pressure product without increasing heart rate, not explained by circulating norepinephrine/epinephrine.

    RCTPMID 22030947 ↗

  5. 05

    After >100 illness reports including 6 deaths, the FDA warned to cease DMAA sales; in a 4374-person military survey, regular DMAA users were 2-3x more likely to report tachycardia, tremors, dizziness, and numbness/tingling.

    CohortPMID 29151367 ↗

  6. 06

    DMAA competitively inhibits the human dopamine transporter, binds the S1 substrate site, and stimulates transporter endocytosis, mechanistically resembling amphetamine (preclinical/in-vitro and computational).

    PreclinicalPMID 37348963 ↗

  7. 07

    Seven service members using OxyELITE Pro (a DMAA-labeled supplement) developed acute liver injury, two requiring liver transplantation.

    Case seriesPMID 24916713 ↗

  8. 08

    A Hawaii outbreak of acute hepatitis/hepatic failure was associated with OxyELITE Pro (44 cases; 2 transplants, 1 death); the hepatotoxic mechanism was not identified and product matched labeled ingredients.

    Case seriesPMID 26538199 ↗

  9. 09

    An independent CIOMS-based reanalysis disputed causality, attributing most Hawaii cluster liver-disease cases to other causes rather than the supplement — confounding attribution of hepatotoxicity to DMAA.

    Case seriesPMID 26626645 ↗

  10. 10

    DMAA is listed among dietary-supplement ingredients associated with hepatotoxicity/liver injury in a tabular clinical review.

    ReviewPMID 27070596 ↗

  11. 11

    DMAA is not a genuine natural constituent of rose geranium; analytical evidence supports a synthetic origin.

    ReviewPMID 23322353 ↗

  12. 12

    Octodrine (DMHA / 2-amino-6-methylheptane) and 1,4-DMAA were found as undeclared stimulants in US supplements; octodrine at ~72 mg per serving, more than twice the highest historical European pharmaceutical dose (8-33 mg); DMAA has been investigated as potentially contributing to hemorrhagic strokes and sudden death.

    Case seriesPMID 29115866 ↗

  13. 13

    1,5-DMHA/octodrine in supplements (up to 112 mg/serving, >3x highest pharmaceutical dose) is of synthetic, not natural, origin based on enantiomeric ratios and synthesis byproducts.

    Case seriesPMID 29454882 ↗

  14. 14

    Supplements labeled with one stimulant frequently contain multiple prohibited/experimental stimulants (including DMAA, octodrine) in cocktails never tested in humans, with unknown safety.

    Case seriesPMID 33755516 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice