BAM-15
Makes mitochondria burn fuel less efficiently, so more calories are released as heat. Prevented weight gain in mice without changing food intake.
Not approved. Research use only.
Look it up on Wikipedia3 listings across 3 independently tested vendors, ranked by price per milligram after coupon codes anyone can use. Vendors you can only order from by message are hidden.
Some links here are affiliate links: if you buy through one, this site may earn a commission at no extra cost to you. Prices, rankings and plans are worked out the same way whether or not a vendor pays one.
Not an FDA-approved drug and not nominated for FDA's 503A bulks list, so US pharmacies can't legally compound it.
Daily price tracking started October 7, 2026; a price-history chart appears here once a few days have been collected.
| Vendor | Trust | Listing | Vials | Price | Per mg | |
|---|---|---|---|---|---|---|
Crush Research Affiliate #91 by metascore · US |
Metascore 76Finnrick 51%Bought vials 107% of label · 17 testsTitrateLabNo report for thisOnline checkout |
BAM15 50mg — Single Bottle | 60 × 50 mg = 3000 mg | $105.00 $1.75 per vial |
$0.035 | Buy |
NextechLabs #142 by metascore · US |
Metascore 74Finnrick 64%Bought vials 116% of label · 32 testsTitrateLabNo report for thisOnline checkout |
BAM-15 (15mg x 30 Caspsules) NEW PRODUCT | 30 × 15 mg = 450 mg | $64.99 $2.17 per vial |
$0.144 | Buy |
Modern Aminos Affiliate #125 by metascore · US |
Metascore 75 medium confidenceFinnrick 79%PepIndex 81/100Bought vials 100% of label · 5 testsTitrateLab · PeptideBase · Peptide CriticNo report for thisOnline checkout |
BAM15 $30 off through this site's link (new customers) |
1 vial, size not stated | $159.00 $30 off through this site's link (new customers) |
– | Buy |
Mixing a 15 mg vial
What each common amount of bacteriostatic water gives you on a U-100 insulin syringe. Pick a vial size above to change it.
| Water | Strength | Per 10 units (0.1 mL) | Per unit |
|---|---|---|---|
| 1 mL | 15 mg/mL | 1,500 mcg | 150 mcg |
| 2 mL | 7.5 mg/mL | 750 mcg | 75 mcg |
| 3 mL | 5 mg/mL | 500 mcg | 50 mcg |
| 5 mL | 3 mg/mL | 300 mcg | 30 mcg |
Doses studied in research Animal or lab studies only
What was given to people (or animals) in published studies and official labels, each linked to its source. This is not a recommendation: study products, purity and supervision differ from research-grade vials.
Animal studies: Mouse studies gave BAM15 orally, mixed into the diet (e.g. 0.1% and 0.2% w/w in db/db mice; 0.1% w/w in a high-fat diet in a sarcopenic-obesity model), or by injection in a mouse sepsis model; other work is in cultured cells.
No human studies of BAM15 have been published. Doses in animal studies do not translate directly to people.
What the research says
BAM15 is an experimental mitochondrial uncoupler tested only in animals and cells, where it reduced fat mass and improved glucose control in obese mice. One mouse study found it did not reduce body fat on its own. No human studies have been published.
Key papers ✓ 8~ 1? 1
-
Mitochondrial uncoupler BAM15 reverses diet-induced obesity and insulin resistance in mice.Animalssize not reportedAnimal study of orally administered BAM15 incl. hyperinsulinemic-euglycemic clamp
In diet-induced obese mice, oral BAM15 reduced body fat and liver fat and improved insulin sensitivity without changing food intake, lean mass, body temperature or toxicity markers.
Study details
- Studied
- Mice with diet-induced obesity
- Main outcome
- Body fat mass, nutrient oxidation, insulin sensitivity, toxicity markers
- Authors' conclusion
- BAM15 decreased body fat mass and hepatic fat and improved insulin sensitivity without altering food intake, lean mass or body temperature, or markers of toxicity, in mice.
- Limitations
- Mouse study; abstract gives no numbers or group sizes.
-
BAM15-mediated mitochondrial uncoupling protects against obesity and improves glycemic control.Humans + animalsPreclinical in vitro and mouse study of BAM15 against diet-induced obesity
Mice treated with BAM15 resisted diet-induced weight gain and had better body composition and glycemic control.
Study details
- Studied
- C57BL/6J mice and in vitro cell systems
- Main outcome
- Weight gain, body composition, glycemic control, energy expenditure
- Authors' conclusion
- BAM15-treated mice resisted weight gain and showed improved body composition and glycemic control independent of weight loss; authors present this as first preclinical efficacy for BAM15 in obesity.
- Limitations
- Preclinical (mouse and in vitro) study.
-
Mitochondrial uncoupling attenuates sarcopenic obesity by enhancing skeletal muscle mitophagy and quality control.Animalssize not reportedRandomized10 weeksRandomized, BAM15 (0.1% w/w in high fat diet) vs high fat diet control
In old obese mice, 10 weeks of BAM15 lowered body weight (54 to 42 g) and increased muscle mass, strength and activity.
Key resultBAM15 reduced body weight (54.0 ± 2.0 vs 42.3 ± 1.3 g, P < 0.001) and increased muscle mass (52.7 ± 0.4 vs 59.4 ± 1.0%, P < 0.001) and strength (91.1 ± 1.3 vs 124.9 ± 1.2 g, P < 0.0001).
Study details
- Studied
- Obese 80-week-old male C57BL/6J mice (sarcopenic obesity model)
- Compared with
- High fat diet control
- Main outcome
- Body weight, muscle mass and strength, mitochondrial quality control
- Authors' conclusion
- Mitochondrial uncoupling with BAM15 may mitigate age-related decline in muscle mass and function and protect against sarcopenic obesity, in mice.
- Limitations
- Mouse study; group sizes not stated in abstract.
-
Targeting negative energy balance with calorie restriction and mitochondrial uncoupling in db/db mice.Animalssize not reported4 weeksAnimal study comparing ~50% calorie restriction, BAM15 0.1% or 0.2% in diet, and 0.2% BAM15 with time-restricted feeding
In diabetic db/db mice, higher-dose BAM15 matched 50% calorie restriction for weight loss and normalised glucose tolerance; the lower dose did not change body mass.
Study details
- Studied
- Male db/db mice (severe hyperglycemia, obesity, fatty liver)
- Compared with
- Calorie restriction; lean db/+ controls
- Main outcome
- Body weight, glucose tolerance, liver steatosis
- Authors' conclusion
- High-dose BAM15 matched calorie restriction on weight loss but normalized fasting glucose and glucose tolerance; low-dose BAM15 improved glucose control independent of weight loss. Supports uncouplers as potential treatment for metabolic disease.
- Limitations
- Mouse model; abstract gives no group sizes.
-
Beneficial effects of simultaneously targeting calorie intake and calorie efficiency in diet-induced obese mice.Animalssize not reportedAnimal study of semaglutide (low or high dose) with or without BAM15
In obese mice, combining BAM15 with semaglutide reduced body fat and liver triglycerides, an effect not achieved by BAM15 or semaglutide alone.
Study details
- Studied
- Diet-induced obese mice on high-fat western diet
- Compared with
- Western diet control, BAM15 alone, semaglutide alone
- Main outcome
- Body fat, liver triglycerides, glucose homeostasis
- Sample
- Six treatment groups; group sizes not stated
- Authors' conclusion
- Combining BAM15 with either semaglutide dose decreased body fat and liver triglycerides, which no monotherapy achieved, without loss of lean mass; high-dose semaglutide plus BAM15 had the greatest effect on glucose homeostasis.
- Limitations
- Mouse study.
-
BAM15 treats mouse sepsis and kidney injury, linking mortality, mitochondrial DNA, tubule damage, and neutrophils.Humans + animalsAnimal sepsis model with BAM15 injected 0, 6 or 12 hours after CLP, plus in vitro mechanistic experiments
In a mouse sepsis model, BAM15 reduced mortality and kidney injury, even when given 12 hours after onset.
Study details
- Studied
- Mice with cecal ligation and puncture (CLP) sepsis; kidney tubule cells and neutrophils in vitro
- Compared with
- CLP mice without BAM15
- Main outcome
- Mortality, kidney damage, mitochondrial DNA release
- Authors' conclusion
- BAM15 reduced mortality, even at 12 hours, and kidney damage and splenic apoptosis, with mtDNA and mtROS mechanistically linked; authors call it an effective preventive and therapeutic candidate in experimental sepsis.
- Limitations
- Experimental mouse sepsis model.
-
BAM15 as a mitochondrial uncoupler: a promising therapeutic agent for diverse diseases.No new dataNarrative review
Review of preclinical BAM15 work: promising in obesity, diabetes, fatty liver and sepsis models, but high lipophilicity and delivery issues remain and clinical research is needed.
Study details
- Studied
- Literature on BAM15 across metabolic, liver, sepsis and cardiovascular disease
- Main outcome
- Mechanism and therapeutic potential of BAM15
- Authors' conclusion
- BAM15 shows promise in obesity, diabetes, fatty liver, sepsis and cardiovascular disease with an encouraging safety profile in preclinical work, but lipophilicity and delivery challenges remain and further research is needed.
- Limitations
- Preclinical evidence only; no human data described.
-
Diverse actions of 15 structurally unrelated mitochondrial uncouplers in cells and mice.Humans + animals4 weeks (mice)Side-by-side in vitro screen then 4-week mouse study with calorie-restriction and lean-control benchmarks
Comparing 15 mitochondrial uncouplers in cells and the best five in db/db mice, BAM15 gave the best overall result, improving body weight, fat pad weight, glucose tolerance, HbA1c and liver triglyceride at 0.2% in chow.
Key result0.2% BAM15 significantly improved body weight, fat pad weight, glucose tolerance, blood glucose, HbA1c, liver weight and triglyceride content
Study details
- Studied
- CHO-K1 cells (15 uncouplers) and male db/db mice (5 uncouplers)
- Compared with
- Chow-fed db/db control, 35% calorie restriction, lean db/+ mice
- Main outcome
- Body weight, glucose control, HbA1c, liver steatosis
- Authors' conclusion
- BAM15 had the best overall effects among the uncouplers; uncouplers should not be generalized and each needs evaluating on its own actions.
- Limitations
- Mouse and cell study; no human data.
-
Combining RNA-seq, molecular docking and experimental verification to explore the mechanism of BAM15 as a potential drug for atherosclerosis.Humans + animalsMouse treatment with RNA-seq, docking and cell experiments
In western-diet-fed ApoE-/- mice, oral BAM15 suppressed atherosclerosis and improved hyperlipidaemia and liver enzymes; in macrophages it reduced lipid accumulation.
Study details
- Studied
- Western-diet-fed ApoE-/- mice and RAW264.7 macrophages
- Main outcome
- Atherosclerosis, lipids, liver enzymes
- Authors' conclusion
- BAM15 inhibits atherosclerosis through multiple molecular targets (IL1A, SRC, CSF3) and is proposed as a potential anti-atherosclerotic drug.
- Limitations
- Animal and cell study; target mechanisms largely computational.
-
Mitochondrial uncoupler BAM15 improves skeletal muscle function and mitochondrial respiration in SarcopeniaAnimalssize not reported8 weeksBAM15-supplemented chow vs standard chow, 13-14 mice per group
Preprint (not peer-reviewed): In 24-month-old mice given BAM15 in chow for 8 weeks, muscle mitochondrial efficiency and contractile function improved in aged males.
Study details
- Studied
- 24-month-old male and female MitoQC mice (sarcopenia model) with 3-month-old reference mice
- Compared with
- Standard chow
- Main outcome
- Muscle mitochondrial respiration, contractile function, mitophagy
- Authors' conclusion
- BAM15 improved skeletal muscle mitochondrial efficiency and contractile function in aged male mice, supporting uncoupling as a strategy for sarcopenia.
- Limitations
- Preprint; mouse study; benefit seen in males only per the abstract.
Reported side effects
No human safety data in the published literature.
✓ positive · ✗ negative · ~ mixed · ? inconclusive, judged on each paper's own main outcome. Grades: A strong human evidence → D little or none. Papers and verdicts are drawn from PubMed, Europe PMC and Russian journals (CyberLeninka); not medical advice.
Discussions elsewhere
Experiences and questions about BAM-15 on other sites. Treat anecdotes with care.
Also sold in blends with BAM-15
BAM-15 + SLU-PP-332 (7). The order planner uses these automatically when a blend is cheaper than separate vials.
BAM-15: questions people ask
What is BAM-15?
Mitochondrial uncoupler (small molecule). Makes mitochondria burn fuel less efficiently, so more calories are released as heat. Prevented weight gain in mice without changing food intake.
How much does BAM-15 cost?
The cheapest BAM-15 from an independently tested vendor is $0.035 per mg (Crush Research, BAM15 50mg — Single Bottle, $105.00). Across 3 listings from 3 vendors the median is $0.144 per mg.
Where can I buy BAM-15?
3 vendors tested by Finnrick sell BAM-15. The cheapest per mg right now: Crush Research ($0.035), NextechLabs ($0.144). 0 of them publish a lab report (COA) for BAM-15; compare lab scores and reports in the table above before buying.
Is BAM-15 FDA approved?
Not approved. Research use only.
Can BAM-15 be compounded in the US?
Not an FDA-approved drug and not nominated for FDA's 503A bulks list, so US pharmacies can't legally compound it. Compounding status for every peptide.
Does BAM-15 work? What does the research say?
Evidence grade C (mostly animal studies), from 10 papers: Many mouse studies show less fat and better glucose control, but there are no human studies of BAM15 at all. BAM15 is an experimental mitochondrial uncoupler tested only in animals and cells, where it reduced fat mass and improved glucose control in obese mice. One mouse study found it did not reduce body fat on its own. No human studies have been published. See the papers.
What dose of BAM-15 was used in studies?
BAM-15 is tested only in animals or cells. Mouse studies gave BAM15 orally, mixed into the diet (e.g. 0.1% and 0.2% w/w in db/db mice; 0.1% w/w in a high-fat diet in a sarcopenic-obesity model), or by injection in a mouse sepsis model; other work is in cultured cells. These are amounts used in published studies or official labels, not a recommendation.

