BAM-15 Does What DNP Did, and the Margin Is Missing From the Record
Mouse dosing stopped at 200 mg per kilogram because the compound would not dissolve any further, so what the record holds is a formulation limit rather than a safety ceiling.
What it is
BAM-15 is a small molecule, PubChem CID 565708, formula C16H10F2N6O, with no amino acids in it and no peptide bonds. It sits on the peptide shelf because that is where a vendor sells it, under a title calling it a peptide.
An uncoupler puts a hole in the wall of the mitochondrion, the compartment in a cell that turns food into usable energy. Fuel keeps burning, none of it is banked, all of it leaves as heat. That is why uncouplers take weight off and why they cause fatal fevers. Same effect, two sizes.
Kenwood and colleagues named BAM-15 in 2014 (PMID 24634817), out of a screen for an uncoupler that leaves the outer boundary of the cell alone, which the older ones discharge as well. Their paper says what the older ones cost: a therapeutic index, the gap between the dose that works and the dose that harms, too narrow for the clinic.
What the trials found
Start with the part that is not there. I searched PubMed for "BAM15" and "BAM-15", retrieved all 72 records and read every title. Not one gave BAM-15 to a human being. ClinicalTrials.gov returns a single record, an Eli Lilly COVID-19 antibody trial matching on the string bamlanivimab, and the EU register returns nothing. Go and run that search yourself.
The record is animals. Alexopoulos and colleagues, Nature Communications 2020 (PMID 32409697): male C57BL/6J mice fattened on a Western diet for four weeks, then held on it five more with BAM-15 in the food at 0.1 percent by weight, 21 animals from four studies. They ate the same calories as the controls and carried 15 percent less body weight, almost all of it fat. In a separate arm, three mice given a single 10 milligram per kilogram dose down a tube into the stomach cleared half of it in 1 hour 42 minutes, which the authors call a limitation.
A second group at the Cleveland Clinic ran it separately (PMID 32519812): 10 week old obese male mice, three weeks of drug at the same concentration in the food, 16 per group, 7.5 g of body weight between the arms by day 20. Not an independent replication: Kyle Hoehn, who discovered BAM-15 and is a named inventor on its patent, is a co-author. It supplies the number everything gets scaled from, about 85 mg per kilogram per day in a mouse.
The lifespan work is in invertebrates. Fruit flies given 500 micromolar in the food, a concentration in what they ate rather than a dose per fly, lived 9 percent longer on a normal diet, 25 percent longer on a fatty one (PMID 38343281); nematode worms at 50 micromolar in the medium lived longer on average (PMID 36422268). Neither abstract gave the number of animals, and I found no lifespan study in a mammal.
What dinitrophenol did, and what it does not tell you
Dinitrophenol is why this entry exists. It worked in people: roughly nine in ten patients taking 300 mg a day by mouth lost two to three pounds a week without eating less. That figure reaches us second hand, through the introduction of the 2020 mouse paper rather than the 1930s records. Tainter estimated that by 1934 as many as 100,000 Americans had used it (NCBI Bookshelf NBK581942).
Now the other number. The lowest oral dose ever published as having killed a person is 4.3 mg per kilogram, about 300 mg in a 70 kg adult (PMID 21739343). The dose that worked and the lowest recorded fatal dose are, to within rounding, the same spoonful. Grundlingh and colleagues put it without hedging: a small margin between the beneficial and the toxic effects, and no specific antidote.
That review counted 62 published deaths as of 2011, and they did not stop. Potts and colleagues went through twelve years of poisons centre calls in the United States and the United Kingdom, 2007 to 2018 (PMID 33021407): 204 cases of systemic exposure, 86 percent of them under 40, case fatality 11.6 percent in the United States and 16.9 percent in the United Kingdom, one in six British callers. Evidence about uncoupling in people, not about this molecule.
How it compares
| Given to people? | The human record | What the evidence covers | |
|---|---|---|---|
| BAM-15 | None I could find | None found | Mice, flies, worms and cultured cells |
| 2,4-dinitrophenol | Yes, from the 1930s on | 100,000 Americans, 62 published deaths by 2011, 204 poisons centre cases 2007 to 2018 | Weight loss, and death at close to the same dose |
| SHD865, a successor | None I could find | None found | Mice. Its own paper calls it a milder uncoupler than BAM-15 (PMID 37870907) |
| SHS206, a later successor | None I could find | None found | Mice, by mouth, no adverse effects reported up to 1000 mg per kg. That number is SHS206's, not BAM-15's (PMID 39406121) |
Watch that last row. The 1000 mg per kilogram figure belongs to SHS206, a different molecule, and it is the one here most easily quoted about BAM-15. Nor does the class travel: of fifteen unrelated uncouplers compared in cells, 11 impaired maximal mitochondrial respiration, the opposite of the job, and that paper concluded each has to be judged on its own actions (PMID 40639664).
Where the dose came from
I could not find a derivation. I could not even find one number: what circulates is three incompatible sets.
A bodybuilding forum guide runs in micrograms, 10 to 50 to assess tolerance and up to 1 mg at the top, with no study or calculation behind it. A competitor dosage page runs in tens of milligrams: 5 to 10 mg a day for beginners, 15 to 30 standard, 40 to 60 advanced, on blocks of 2 to 8 weeks, the highest tier the shortest because tolerability forces cessation, its figures taken from self-report forums and vendor guidance rather than studies. The unit the market settled on is the 50 mg capsule. All of that is convention, not recommendation.
Then the arithmetic, which I could find nowhere in the literature and which is mine rather than anybody else's. Scale the 85 mg per kilogram mouse dose to a person by body surface area, dividing by the 12.3 in the conversion table of Reagan-Shaw and colleagues (PMID 17942826), and you get roughly 480 mg a day for a 70 kg adult. That does not make 480 mg safe or sensible: I could find no published study establishing a human dose, and the scaling only says where a trial would start. Every circulating number sits below it, the capsule at about a tenth and the microgram protocols between about a five hundredth and a fifty-thousandth. None came from scaling the animal work.
What could go wrong
There is no human safety data that I could find: no study of what the compound does once it is in a person's blood, how fast it rises and clears, no tolerability study, no dose ceiling, no adverse event series. And in no species could I find a maximum tolerated dose, an LD50, meaning the dose that kills half the animals given it, or a therapeutic index. Not a clean file. An empty one.
The 200 mg per kilogram figure that circulates as proof of a wide margin is not a safety finding. Single doses up to that went by tube into the stomach of male C57BL/6J mice, n = 6, and core temperature did not move. But the sentence setting that ceiling says why the experiment stopped: BAM-15 could no longer be dissolved for delivery by mouth, and the one adverse sign, transient lethargy, could not be separated from pushing paste into a stomach. That is a shelf tested by stacking bricks on it until the bricks run out. Dinitrophenol went through the same experiment, dissolved perfectly well, and did produce a ceiling: no observed adverse effect level, 25 mg per kilogram.
Those mice also lived at 22 degrees Celsius, below the roughly 30 at which a mouse is comfortable, so they had heat to spare.
The two human tissue results point opposite ways. BAM-15 cut progressive motility, the forward swimming that matters for fertilisation, in human sperm in a dish (PMID 37294625), and raised it in sperm being frozen and thawed (PMID 42295994).
It is also on the 2026 World Anti-Doping Agency Prohibited List, banned at all times.
What we do not know
Whether that absence of fever survives ordinary warmth, and what happens in an animal that sheds heat less easily than a mouse; I found no dog, pig or primate study, and surface area to volume is central to the safety argument. And why I can find no record of BAM-15 going into a person, twelve years after it was named.
My take
The margin is the whole compound and the file on it is blank. I could not find the experiment. What bothers me is the 200 mg per kilogram figure: a solubility limit wearing a safety label, quoted as though somebody had gone looking for a toxic dose and failed to find one.
The other thing is the direction of travel. The people who found this molecule spent a decade building gentler successors, and the friendliest number in the programme, no adverse effects in mice given up to 1000 milligrams per kilogram by mouth, belongs to SHS206 and not to BAM-15. It is the number I would expect to see moved. That reads less like a drug candidate waiting its turn than like a laboratory tool that got a shelf.
If you have seen BAM-15 for sale, I want to know which unit the page used, micrograms or a 50 mg capsule, and whether dinitrophenol was named anywhere on it.
Frequently asked
Has BAM-15 been tested in humans?
I could find no published study that gave BAM-15 to a person, at any dose. I searched PubMed for BAM15 and BAM-15, retrieved all 72 records and read every title, and they are cell, animal, chemistry and review papers. ClinicalTrials.gov returns one record for the term, an Eli Lilly COVID-19 antibody trial that matches on the string bamlanivimab, and the EU Clinical Trials Register returns nothing.
Is BAM-15 the same thing as DNP?
They are chemically unrelated molecules that do the same thing to a mitochondrion, which is carry protons across it so fuel burns as heat instead of making usable energy. DNP has a human record and it is a bad one: about 100,000 Americans used it in the 1930s, the lowest oral dose published as having killed a person is 4.3 mg per kilogram, about 300 mg in a 70 kg adult, and 62 deaths had been published by 2011. That record belongs to DNP and not to BAM-15.
Is BAM-15 safe to take?
There is no human safety data I could find: no tolerability study, no dose ceiling and no adverse event series. In mice, single doses by tube into the stomach up to 200 mg per kilogram did not raise body temperature, but that experiment stopped because the compound would not dissolve any further rather than because a toxic dose was reached, and I could find no published maximum tolerated dose for BAM-15 in any species, no dose that kills half the animals given it, and no measured gap between the dose that works and the dose that harms.
How much BAM-15 do people take?
What circulates runs from 10 micrograms to 60 milligrams a day depending on the page, a six thousandfold spread for the same molecule, and none of those pages shows a derivation. Capsules are commonly sold at 50 mg. These are conventions reported as conventions rather than recommendations, and no human dose has been established in any published study I could find.
Did BAM-15 work in animals?
In mice it did. Male C57BL/6J mice eating drug mixed into the food at 0.1 percent by weight for five weeks, 21 animals pooled from four studies, ate the same calories as the untreated mice and ended up 15 percent lighter than them, almost all of the difference being fat. Fruit flies and nematode worms fed it lived longer. I could find no lifespan study in a mammal and no study in a person.
Is BAM-15 banned in sport?
It is named on the 2026 World Anti-Doping Agency Prohibited List, which took effect on 1 January 2026, under section S4.4.1 as an activator of AMPK, the fuel gauge a cell switches on when it runs short of energy. That section is prohibited at all times, in and out of competition, and its substances are non-Specified, which is the more serious sanctioning category. WADA states that it added the compound because it has been found in supplements.
This content is for educational and informational purposes only and is not medical advice. Peptides discussed are research compounds and may not be approved for human use. Nothing here should be used to diagnose, treat, cure, or prevent any disease. Always consult a qualified healthcare professional before starting any peptide, supplement, or protocol. Individual responses vary. Do not self-administer compounds without proper medical supervision.
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