BAM-15 — Research, Dosing & Price Guide

BAM-15 is a next-generation mitochondrial uncoupling agent that dissipates the proton gradient across the inner mitochondrial membrane, converting stored energy directly into heat rather than ATP. Unlike the notorious uncoupler DNP (2,4-dinitrophenol), BAM-15 selectively targets mitochondrial membranes without depolarizing the plasma membrane, providing a dramatically wider therapeutic window. In preclinical studies, it reduces body fat by up to 20%, improves insulin sensitivity, and reverses fatty liver disease — all without affecting food intake or lean mass.

BAM-15 functions as a protonophore, a molecule that shuttles protons across biological membranes. It selectively inserts into the inner mitochondrial membrane and facilitates the passage of protons from the intermembrane space back into the mitochondrial matrix, bypassing ATP synthase (Complex V). This short-circuits oxidative phosphorylation — the proton-motive force is dissipated as heat rather than being used to generate ATP. The cell responds to this ATP deficit by increasing substrate oxidation — burning more fats and sugars to regenerate the proton gradient. This creates a futile cycle that elevates metabolic rate and energy expenditure without physical activity. BAM-15 also activates AMPK downstream (sensing the reduced ATP/AMP ratio), which further promotes fatty acid oxidation, glucose uptake, and mitochondrial biogenesis. The critical safety distinction from DNP is membrane selectivity. DNP is a non-selective protonophore that depolarizes both mitochondrial and plasma membranes, disrupting cellular ion gradients and causing dangerous hyperthermia with a narrow margin between effective and lethal doses. BAM-15 shows >100-fold selectivity for mitochondrial membranes over the plasma membrane, meaning it uncouples mitochondria at doses that leave cellular membrane potential intact. Additionally, it reduces reactive oxygen species (ROS) production by keeping the electron transport chain in a more oxidized state, providing antioxidant benefits.

• A 2020 study published in Nature Communications demonstrated BAM-15 reduced body fat mass by 20% in diet-induced obese mice over 6 weeks without affecting food intake, lean mass, or core body temperature — addressing DNP's primary safety concern.
• The same study showed BAM-15 improved glucose tolerance and insulin sensitivity independently of weight loss, suggesting direct metabolic benefits on skeletal muscle and liver.
• Toxicology studies found no observed adverse effects at 50x the effective dose in mice, confirming an exceptionally wide therapeutic window compared to DNP.
• BAM-15 reduced hepatic steatosis (fatty liver) by 45% in high-fat-diet-fed mice, with histological confirmation of reduced lipid droplets and inflammatory infiltrates.
• Mitochondrial selectivity confirmed: BAM-15 showed >100-fold preference for depolarizing mitochondrial membranes vs. plasma membranes in isolated cell studies.
• Reduced reactive oxygen species (ROS) production in treated tissues, suggesting antioxidant-like benefits alongside metabolic enhancement.
• A follow-up study showed BAM-15 improved cardiac function in a heart failure model, indicating tissue-protective effects beyond fat loss.

• Oral liquid formulation: typically supplied at 30–50 mg/mL. Standard dose is 0.5–1 mL daily (15–50 mg depending on concentration and individual response).
• Research dose in mice: 10 mg/kg/day orally, which produced 20% fat mass reduction over 6 weeks without toxicity.
• Human-equivalent dose estimation: approximately 0.8–1.5 mg/kg/day based on allometric scaling from murine data. Start conservatively.
• Dose titration recommended: begin with half the target dose for 1–2 weeks to assess tolerance before increasing. Monitor subjective body temperature and energy levels.
• Take with food to improve oral absorption and reduce GI side effects. Morning dosing is preferred to align with daytime metabolic activity.
• Cycle: 8–12 weeks on, 4 weeks off. Monitor body composition, fasting glucose, and liver enzymes.
• Can be combined with SLU-PP-332 for complementary metabolic effects (mitochondrial uncoupling + exercise mimetic). Some vendors offer pre-made BAM-SLU blends.

Known Side Effects

• Mild increase in body temperature — most users report feeling slightly warmer, particularly during the first week. Unlike DNP, this does not progress to dangerous hyperthermia at recommended doses.
• Gastrointestinal discomfort — nausea, loose stools, or mild cramping, especially when taken on an empty stomach. Taking with food mitigates this.
• Increased sweating — consistent with elevated metabolic rate and thermogenesis. Stay well-hydrated.
• Fatigue during initial adaptation — the shift in cellular energetics can cause temporary tiredness as the body adjusts to reduced ATP efficiency. Usually resolves within 5–7 days.
• Theoretical concern of reduced exercise performance at very high doses — if too much proton gradient is dissipated, ATP production during intense exercise could be impaired. Stay within recommended doses.
• Long-term human safety data does not exist — all safety data is preclinical. Proceed with appropriate caution.

Safety Profile

BAM-15 represents a major safety improvement over historical mitochondrial uncouplers. Its >100-fold membrane selectivity means it lacks the narrow therapeutic window and hyperthermia risk that made DNP infamous. In mouse studies, no toxicity was observed at 50 times the effective dose — an extraordinary safety margin for an uncoupling agent. Core body temperature remained normal at effective doses, and no organ damage was detected on histological examination. However, all safety data is preclinical. No human clinical trials have been conducted, and the long-term effects of sustained mitochondrial uncoupling in humans are unknown. Contraindications include mitochondrial diseases, cardiac arrhythmias, hyperthyroidism (already elevated metabolic rate), and pregnancy/breastfeeding. Individuals taking medications that affect mitochondrial function (metformin, statins) should exercise caution. Monitoring liver enzymes, thyroid function, and fasting glucose during use is prudent.

Days 1–5: Slight increase in body temperature and warmth, particularly after dosing. Energy levels may fluctuate as cells adjust to altered energetics. GI effects are most likely during this adaptation period. Weeks 1–2: Metabolic adaptation stabilizes. Energy returns to normal or improves. Increased sweating during activity. Subtle fat loss may begin, particularly noticeable in morning appearance before eating. Weeks 3–6: Primary fat loss window. Body composition changes become visible — reduced abdominal fat, improved definition. Appetite remains stable (not suppressed). Improved glucose and insulin markers may be detectable on blood work. Weeks 7–12: Continued fat loss with gradual plateau. Liver function improvements (reduced hepatic fat) may be reflected in ALT/AST normalization. Total fat mass reduction of 10–15% is achievable with concurrent exercise and dietary awareness.

Prices sourced from peptides.gg marketplace. Prices may vary.