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Research compound — not a dietary supplement
DNP (2,4-Dinitrophenol) is a research compound, not a regulated dietary supplement. It is sold for research or off-label use. The evidence below is largely preclinical (animal and in-vitro) or early-stage, so no evidence score is assigned. This page is provided for transparency and education — it is not a recommendation to use. Consult a qualified healthcare provider, and be aware that purity, dosing, and legal status vary by jurisdiction.
What the evidence says
Most DNP (2,4-Dinitrophenol) studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality studies published 1934–2022.
Based on 6 studies
Confidence
LowBy outcome
DNP (2,4-Dinitrophenol) has an evidence score of 3/10 — emerging evidence based on 6 indexed studies. An industrial chemical and 1930s diet drug that causes real, rapid fat loss by short-circuiting the mitochondria — and that KILLS people. It has no safe dose: the gap between an 'effective' dose and a fatal one is razor-thin, and overdose causes runaway hyperthermia, tachycardia and acidosis with NO antidote. Withdrawn for human use in the 1930s after thousands were harmed (cataracts, agranulocytosis, death); now sold illicitly online as a 'fat burner' with case-fatality around 11–17%. This entry exists to document a popular, deadly drug honestly — not to endorse it. The lethal danger IS the headline. Representative study: PMID 21739343.
The commonly studied dose of DNP (2,4-Dinitrophenol) is No legitimate or recommended dose. DNP is an illicit, unregulated industrial chemical with no antidote and a razor-thin, unpredictable margin between an 'effective' and a fatal dose; metabolism varies widely between people, so any dose can be lethal. We do NOT provide a dosing protocol. If exposure is suspected, treat it as a medical emergency and contact emergency services and poison control immediately.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
Tesofensine
Mostly mechanism / observationalAn INVESTIGATIONAL triple monoamine (noradrenaline / dopamine / serotonin) reuptake inhibitor developed for obesity. Originally trialled for Parkinson's and Alzheimer's disease, it failed there but produced unexpectedly large weight loss — and its phase-2 TIPO-1 trial (Astrup, Lancet 2008) delivered roughly twice the weight loss of the drugs approved at the time (~9-11% at 0.5-1.0 mg). Honest appraisal: it is NOT approved in any major market, the headline efficacy rests mainly on phase-2 data, the pivotal TIPO-1 paper carries a journal Expression of Concern, and the centrally-acting monoaminergic mechanism brings a real cardiovascular (heart-rate) and psychiatric (mood/anxiety, insomnia) trade-off. NOT a dietary supplement and NOT a longevity drug — listed for reference only.
Last reviewed June 2026 · evidence from 6 studies · how we score
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
DNP (2,4-Dinitrophenol) — mitochondrial uncoupler sold illicitly for fat loss
An industrial chemical and 1930s diet drug that causes real, rapid fat loss by short-circuiting the mitochondria — and that KILLS people. It has no safe dose: the gap between an 'effective' dose and a fatal one is razor-thin, and overdose causes runaway hyperthermia, tachycardia and acidosis with NO antidote. Withdrawn for human use in the 1930s after thousands were harmed (cataracts, agranulocytosis, death); now sold illicitly online as a 'fat burner' with case-fatality around 11–17%. This entry exists to document a popular, deadly drug honestly — not to endorse it. The lethal danger IS the headline.
DNP genuinely causes rapid fat loss by uncoupling oxidative phosphorylation, but it is lethal: it has a razor-thin margin between an effective and a fatal dose, no antidote, and a documented case-fatality of roughly 11–17% in poison-centre series. It was abandoned for human use in the 1930s after cataracts, agranulocytosis and deaths, and the modern internet-sold product continues to kill. The danger — not any benefit — defines the verdict, so it scores low.
2,4-Dinitrophenol (DNP) is an industrial chemical — historically a wood preservative, dye precursor, and explosives component — that is also one of the most effective and most dangerous weight-loss agents ever used in humans.
It works by uncoupling oxidative phosphorylation: DNP is a protonophore that carries protons across the inner mitochondrial membrane, dissipating the proton-motive force that ATP synthase normally harnesses.
The cell's response is to burn fuel faster and faster in a futile attempt to restore the gradient, releasing the energy as heat rather than ATP. Metabolic rate rises sharply and body fat is consumed — which is exactly why it produces dramatic weight loss, and exactly why it kills.
In the early 1930s the Stanford clinical pharmacologist Maurice Tainter (with Cutting and Stockton) popularised DNP as an obesity drug, and it was taken by an estimated 100,000+ Americans within about a year.
The harms surfaced quickly: a razor-thin therapeutic index, fatal hyperthermia, plus cataracts (some causing blindness), agranulocytosis, and deaths. Mainstream physicians abandoned it, and the 1938 US Food, Drug, and Cosmetic Act gave regulators the power to stop its sale; it has not been an approved human drug since.
DNP never went away. Since roughly 2010 it has resurged as an internet-sold 'fat burner' marketed to bodybuilders and dieters as yellow capsules or powder, and fatal poisonings have climbed across the UK, US, Australia and beyond. The toxicology is unforgiving. There is NO antidote.
In overdose the same uncoupling that drives weight loss becomes uncontrolled thermogenesis: severe hyperthermia, tachycardia, tachypnoea, profuse sweating, agitation, metabolic acidosis and rapid death, often within hours, and sometimes after a delay.
Metabolism of DNP varies widely between people, so a dose tolerated by one person can be lethal in another. Poison-centre series report case-fatality on the order of 11–17%, and the largest toxicology review counted dozens of published deaths spanning a century.
Tachycardia, hyperpyrexia, acidosis and agitation/confusion independently predict death. The honest summary: DNP unquestionably causes weight loss — by the physical mechanism of mitochondrial uncoupling — but there is no safe dose, no antidote, and a documented, ongoing toll of death.
This is not a dietary supplement, not a longevity drug, and not a research probe with a credible therapeutic future at these doses. It is documented here because it is popular and deadly, so that the danger is stated plainly rather than left to grey-market marketing.
If exposure is suspected, this is a medical emergency — call emergency services and a poison control centre immediately.
DNP is a lipophilic weak acid that shuttles protons across the inner mitochondrial membrane, collapsing the proton-motive force that ATP synthase depends on. Oxidative phosphorylation is 'uncoupled': substrate oxidation continues but yields heat instead of ATP.
To restore the lost gradient, cells oxidise fuel faster and faster, driving up basal metabolic rate, oxygen consumption and body temperature. This futile cycle is the source of both the weight loss and the lethal hyperthermia.
The same uncoupling that consumes fat at modest doses becomes uncontrolled, unstoppable thermogenesis as the dose rises — with wide person-to-person variability in metabolism, no antidote, and a narrow, unpredictable gap between an 'effective' and a fatal dose.
How DNP (2,4-Dinitrophenol) works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Tap node to isolate • Pinch to zoom • Tap edge for research
No legitimate or recommended dose. DNP is an illicit, unregulated industrial chemical with no antidote and a razor-thin, unpredictable margin between an 'effective' and a fatal dose; metabolism varies widely between people, so any dose can be lethal. We do NOT provide a dosing protocol. If exposure is suspected, treat it as a medical emergency and contact emergency services and poison control immediately.
Can be taken without food
| Form | Type |
|---|---|
| 💊None — illicit, unregulated industrial chemical with no safe human dose | Recommended |
There is no legitimate pharmaceutical form. DNP was withdrawn from human use in the 1930s and is sold today only as an illicit grey-market 'fat burner'.
Minimum: 1 weeks
Optimal: 1 weeks
Cycling: Not required
Note: No approved or safe timing — DNP is a lethal uncoupler with no antidote. This library does not endorse or schedule its use.
Dose-response data unavailable. The current published research for DNP (2,4-Dinitrophenol) does not provide sufficient dose-specific outcome data to generate reliable dose-response curves.
Refer to the Dosage & Timing section above for recommended dose ranges based on available evidence.
DNP does cause genuine, rapid weight and fat loss by raising metabolic rate — this is the physical mechanism documented since the 1930s. The effect is real; it is inseparable from the lethal risk.
Uncontrolled heat production causes severe hyperthermia, sweating and tachypnoea that can be rapidly fatal. There is no antidote; cooling and supportive care are all that is available.
Toxicity presents as tachycardia, agitation/confusion, metabolic acidosis and raised lactate — the independent predictors of death. Onset can be delayed and deterioration is sudden.
The harms that ended its medical use in the 1930s included cataracts (some causing blindness) and agranulocytosis, alongside deaths — chronic harms beyond acute poisoning.
Avoid absolutely — DNP is lethal with no antidote and no safe dose; it was abandoned for human use after deaths, cataracts and agranulocytosis.
Avoid — the modern resurgence in illicit 'fat burner' sales has driven rising fatal poisonings; perceived dosing 'experience' does not protect against the narrow, variable lethal margin.
Avoid entirely — toxic and never safely studied.
Additive hyperthermia, tachycardia and metabolic strain — a documented fatal combination (e.g. DNP plus clenbuterol). Compounds the lethal heat-generating effect.
DNP was never developed as a modern drug, so interactions are uncharacterised; any agent that adds cardiovascular, thermogenic or metabolic stress raises the danger.
Tip: There is NO antidote. Overdose causes runaway hyperthermia, tachycardia, acidosis and death, often within hours. Poison-centre case-fatality is ~11–17%. Suspected exposure is a medical emergency — call emergency services and poison control immediately; treatment is aggressive cooling and supportive intensive care only.
Tip: Chronic harms that ended its 1930s medical use — cataracts (some causing blindness) and agranulocytosis. There is no safe-use mitigation; the compound should not be taken.
Tip: Illicit material has no identity, purity or dose guarantees, and individual metabolism varies widely — a dose survived by one person can kill another.
Timing is flexible for DNP (2,4-Dinitrophenol) — consistent daily use matters more than the time of day. There is no safe or endorsed dosing schedule for a lethal uncoupler with no antidote.
DNP (2,4-Dinitrophenol) should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are fatal hyperthermia / acute poisoning, cataracts / agranulocytosis, harm from an unregulated, inaccurately dosed product. Use caution if any of these apply to you: Anyone — DNP is lethal in overdose with no antidote and a razor-thin, unpredictable margin; there is no safe dose; Not an approved medicine and not a regulated dietary supplement — an illicit, unregulated industrial chemical; do not self-source; Anyone with cardiac disease, hyperthermia risk, or exertion in heat (additive thermogenic strain).
Bimagrumab
Mostly mechanism / observationalAn investigational monoclonal antibody that blocks the activin type II receptor (ActRII) — the receptor through which myostatin and activin restrain muscle — producing a striking body recomposition (fat DOWN, lean muscle UP) but NO proven functional benefit. In a phase 2 trial in adults with type 2 diabetes and obesity, bimagrumab caused a large loss of fat mass and a real gain in lean mass over 48 weeks, which is why it is now being developed as a metabolic / obesity drug. But the muscle-disease story is a cautionary one: its pivotal phase 2b trial in inclusion-body myositis (RESILIENT) added muscle yet FAILED its primary walking endpoint, and a 2025 systematic review concluded it had no effect on disease progression. It is NOT an approved drug, NOT a dietary supplement, and NOT a longevity drug — gaining muscle on a scan is not the same as moving or living better. This entry exists to inform, not to recommend.