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BAM-15Small moleculeNo amino acid sequence. Icon reflects category theme only.Also known as: BAM15, BAM 15
Mice on a high-fat western diet lost body fat without eating less, exercising more, or losing lean mass. BAM-15 (CAS 210302-17-3) is the mitochondrial uncoupler behind that result, a small molecule that forces cells to burn extra fuel by short-circuiting the proton gradient in mitochondria. No human clinical trials exist yet, and all dosing comes from allometric scaling of rodent studies. Bodybuilders and metabolic optimization communities discuss it as a mechanistically cleaner alternative to DNP, with the critical caveat that community doses sit 5 to 30 times below the estimated therapeutic range.
BAM-15 (N5,N6-bis(2-fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine, CAS 210302-17-3) is a small-molecule mitochondrial protonophore, not a peptide. It shows up in peptide communities because the target audience overlaps. Mice on a western diet lost body fat, improved insulin sensitivity, and showed lower hepatic lipid levels after eight weeks of BAM-15 (Axelrod et al.)[1]. Lean mass, body temperature, and food intake all stayed the same. BAM-15 is a selective uncoupler. It shows up in peptide communities because the target audience overlaps. The molecule dissipates the proton motive force across the inner mitochondrial membrane. Cells respond by oxidizing more glucose and fatty acids to restore their electrochemical gradient, burning additional calories in the process. The key selling point over older uncouplers like DNP: BAM-15 depolarizes mitochondria without touching the plasma membrane. That selectivity means lower cytotoxicity at working concentrations (Kenwood et al., Mol Metab 2014)[2]. Real-world use sits in a gray area. Community protocols run 50 to 300 mg per day split across two or three oral doses. Allometric scaling from mouse data puts the estimated therapeutic range at 500 to 1,500 mg per day. That gap has never been bridged by a human trial. Oral bioavailability lands around 67% in mice with a 1.7-hour half-life, meaning plasma levels drop to near zero within four hours of each dose. Research status: preclinical only. WADA added BAM-15 to the prohibited list under S4.4.1 effective January 1, 2026. The compound holds an "emerging-research" classification with a safety grade of C.
The electron transport chain pumps protons from the mitochondrial matrix into the intermembrane space, building a proton motive force that drives ATP synthase. BAM-15 bypasses ATP synthase entirely. It carries protons back across the inner mitochondrial membrane through a non-enzymatic pathway, collapsing the electrochemical gradient. The aniline nitrogen on the oxadiazolopyrazine scaffold handles proton shuttling. On planar bilayer lipid membranes and in liposomes, BAM-15 drives proton conductance at potency comparable to the classical uncoupler CCCP (Antonenko et al.)[3]. In isolated rat liver mitochondria, it collapses membrane potential, accelerates respiration rate, and triggers calcium efflux. Selectivity matters here. DNP and FCCP depolarize both the inner mitochondrial membrane and the plasma membrane. BAM-15 only depolarizes mitochondria. Cells ramp up oxygen consumption and substrate oxidation to compensate for the lost gradient, burning extra glucose and fatty acids, but the plasma membrane stays intact. That distinction explains the lower cytotoxicity profile. In cell-based assays, BAM-15 can sustain maximal mitochondrial respiration without triggering apoptosis. DNP cannot do that safely. The downstream metabolic result: increased whole-body energy expenditure and fat oxidation without sympathomimetic stimulation. No catecholamine release. No CNS activation. No heart rate increase. The calorie burn happens at the mitochondrial level, which is why body temperature stayed normal even at supratherapeutic mouse doses.
Reduces body fat mass, improves whole-body insulin sensitivity, and increases energy expenditure in mouse models without hyperthermia or lean mass loss at any tested dose. No human trials exist.
Axelrod et al. Nature Communications 2020 (PMID 32409697): 8-week western-diet C57BL/6J mouse study with hyperinsulinemic-euglycemic clamp confirmation; primary efficacy reference
All efficacy and safety data from rodent studies only; 1.7-hour half-life limits sustained exposure; gram-scale allometric doses untested in humans; no Phase 1 safety trial; WADA-prohibited as of January 1, 2026; no human PK data
Experimental metabolic agent positioned as mechanistically safer DNP alternative. Cautiously interested community; no structured n-of-1 outcome data with biomarker confirmation.
Science establishes mechanism and mouse-level dose range (~500–1,500 mg/day allometric); community uses 50–300 mg/day based on vendor capsule sizing with no efficacy validation. Two-orders-of-magnitude gap is unresolved. No human trial bridges them. Community use may reflect sub-therapeutic dosing or a conservative safety stance given complete absence of human data.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 200mg | Daily |
| Moderate | 400mg | Daily |
| Aggressive | 600mg | Daily |
BAM-15 is an oral small molecule. No reconstitution, no bacteriostatic water, no syringes. Buy it as powder or pre-made capsules. The short half-life (1.7 hours) means once-daily dosing is near-pointless. You need at least two doses per day spaced six hours apart. Three is better if you can manage it. Morning, early afternoon, and late afternoon with food works for most schedules. Skip the evening dose if it affects sleep. Powder sourcing matters here. Research-grade suppliers like Cayman Chemical or Sigma-Aldrich provide HPLC-verified material with proper CAS verification (210302-17-3). Gray-market capsule vendors don't offer the same quality accountability; dosing accuracy in DIY capsules is suspect because BAM-15 has low water solubility, making even powder distribution inside gelatin caps inconsistent. Store powder at negative 20 degrees Celsius, desiccated, away from light. If you dissolve it in DMSO for research use, that solution stays stable at negative 20 degrees Celsius for up to six months. Avoid repeated freeze-thaw cycles. The community dose range (50 to 300 mg per day) sits 5 to 30 times below what allometric scaling predicts as therapeutic. That might mean sub-therapeutic dosing or conservative safety reasoning. Nobody knows yet.
No established human cycling protocol exists. In the primary mouse study, BAM-15 was administered continuously via diet for the study duration. An 8-week-on, 4-week-off schedule is a conservative extrapolation commonly discussed in research communities. The short half-life means pharmacological effects cease within hours of the last dose, so extended washout periods are likely unnecessary from a pharmacokinetic standpoint. Cycling rationale is based on general precaution rather than observed tolerance or tachyphylaxis.
No receptor desensitization, tachyphylaxis, or hormonal axis suppression has been documented with BAM-15 in any published study. The 1.7-hour half-life means pharmacological action ceases within hours of the last dose. Cycling is recommended exclusively as a precautionary measure given the complete absence of human long-term safety data, not because of established tolerance or observed toxicity with continuous use.
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Expected: Unknown in humans. Mouse model: significant fat mass reduction and insulin sensitivity improvement detectable at weeks 3–6 at 0.10% dietary doses. Human outcome at community doses (sub-allometric) is unvalidated: benefits may be absent or unmeasurable.
Monitor: Liver function panel (ALT, AST, ALP) at baseline and 4 weeks: BAM-15 primarily accumulates in liver. Fasting glucose and insulin at baseline and end of cycle. Body temperature spot-checks if any warmth sensation occurs.
Obtain BAM-15 powder from a research-grade supplier with a certificate of analysis showing HPLC purity of 98% or above. Verify the CAS number (210302-17-3) matches.
If using bulk powder, weigh individual doses on a milligram scale (0.001 g precision minimum). For a 50 mg starting dose, that is 0.050 g. Transfer into size 4 gelatin capsules, or dissolve in a lipophilic carrier if preferred.
Food reduces potential GI discomfort and may improve absorption given the compound's low water solubility.
Take the second dose approximately six hours later, also with food. This timing strategy maintains detectable plasma levels across roughly 8 of 16 waking hours; the 1.7-hour half-life makes single daily dosing ineffective for sustained exposure.
Avoid evening dosing if you notice any sleep disruption.
Start at 50 mg per dose (100 mg per day total) for weeks one and two. If tolerated, increase to 100 to 200 mg per dose during weeks three through eight, for a total daily intake of 200 to 600 mg.
Monitor body temperature daily for the first two weeks (oral thermometer). Any reading above 38.0 degrees Celsius (100.4 degrees Fahrenheit) that correlates with dosing is an absolute stop signal.
Run a liver function panel (ALT, AST, ALP) at baseline, week four, and the end of the eight-week cycle. Stop if transaminases exceed 1.5 times the upper limit of normal.
Oral bioavailability ~67% in mice; no human PO bioavailability data
All mouse efficacy studies used dietary administration. BAM-15 has low water solubility: formulation in lipophilic carrier or encapsulation improves absorption. Standard capsule form is the community route.
IP administration bypasses first-pass metabolism; not valid for human extrapolation
Some mouse mechanistic studies used IP injection. Do not extrapolate IP mouse doses to oral human protocols.
Both target mitochondrial energy metabolism via different mechanisms (MOTS-c activates AMPK; BAM-15 directly uncouples). Theoretically complementary but additive mitochondrial stress is unstudied.
AMPK activator with overlapping fat-loss mechanism. Both discussed in metabolic optimization communities. No combination protocol established; additive metabolic stress possible.
Additive mitochondrial uncoupling: both compounds dissipate the proton gradient. Combined use creates dangerous risk of excessive energy depletion and potentially fatal hyperthermia.
Do not combineDirect pharmacodynamic overlap: additive uncoupling of inner mitochondrial membrane. No therapeutic window at combined doses.
Do not combineMetformin inhibits Complex I while BAM-15 dissipates the proton gradient: theoretical risk of excessive mitochondrial stress and lactic acidosis. Not studied.
Thyroid hormones naturally increase metabolic rate via mitochondrial mechanisms. Additive thermogenic and energy expenditure effect is plausible; could cause excessive energy depletion.
No human has ever taken BAM-15 in a controlled clinical setting. Every safety claim about this compound traces back to cell culture dishes and mice. That context matters more than any individual finding. In preclinical experiments, mice receiving BAM-15 intraperitoneally for over seven days showed no obvious clinical toxicity at any tested dose. Hematological and biochemical markers stayed within normal ranges [1]. Body temperature remained unchanged, which is a meaningful signal because the defining danger of classical uncouplers like DNP is fatal hyperthermia. BAM-15 did not trigger apoptosis at effective concentrations in cell-based assays. At very high concentrations, slight inhibition of mitochondrial respiration was observed, but substantially less than what FCCP produces at comparable levels. The short 1.7-hour half-life cuts both ways. If something goes wrong, the compound clears within hours. But it also means any adverse effect from a single dose would be transient, making chronic toxicity harder to detect without long-term studies that haven't been done. Theoretical risks based on mechanism: excessive energy depletion with overdose. Mitochondrial uncoupling forces cells to burn more fuel. Push that too hard and energy-demanding tissues (heart, brain, liver) could become fuel-starved. This has not been observed in published BAM-15 studies, but it is the established lethality mechanism of DNP. Liver accumulation deserves attention. BAM-15 concentrates in hepatic tissue based on mouse pharmacokinetics. Liver function monitoring (ALT, AST) at baseline, mid-cycle, and end of cycle is the minimum standard. Stop immediately if transaminases exceed two times the upper limit of normal. Pregnancy and breastfeeding: no reproductive safety data exists. Avoid completely. Individuals with known mitochondrial disorders (mitochondrial myopathy, MELAS) should not use BAM-15 because uncoupling can worsen the energy deficit those conditions already produce. WADA added BAM-15 to the prohibited substance list under S4.4.1 effective January 1, 2026. Any athlete or military personnel subject to testing faces sanctions. Quality control is a genuine concern. BAM-15 has been found as an undeclared adulterant in dietary supplements. The reverse (labeled BAM-15 containing a different compound) is also a documented quality risk. Require a certificate of analysis with HPLC purity of 98% or above from any source before use.
Verify BAM-15 dosing and safety with a second opinion
Research chemical with no GMP manufacturing standard applicable to human use, no pharmaceutical-grade compounding availability, confirmed presence as undeclared adulterant in supplement products, and no regulatory oversight of purity or potency. HPLC-verified powder from established research vendors (Carolina Chemical, Cayman Chemical, Sigma-Aldrich) is substantially different in quality accountability from capsule-form gray-market products.
| Test | When | Target |
|---|---|---|
| Liver function panel (ALT, AST, ALP, bilirubin) | Baseline, week 4 (mid-cycle), end of 8-week cycle | ALT/AST within 1.5x ULN; stop immediately if >2x ULN |
| Fasting glucose and insulin (HOMA-IR) | Baseline and end of cycle | Fasting glucose <100 mg/dL; HOMA-IR <2.0 as general metabolic health marker |
| Body temperature (oral or axillary) | Daily for first 2 weeks; weekly thereafter | Normal: 36.1–37.2°C (97–99°F). Stop if >38.0°C (100.4°F) with BAM-15 as likely cause. |
| Basic metabolic panel (electrolytes, creatinine, BUN) | Baseline and end of cycle | — |
BAM-15 primarily accumulates in the liver in mouse pharmacokinetics (Cmax hepatic). Hepatic safety signal is the most likely first indicator of any human toxicity.
Primary efficacy endpoint in mouse studies; also monitors for hypoglycemia risk if stacking with insulin sensitizers.
Hyperthermia is the defining safety concern for mitochondrial uncouplers (fatal with DNP). No temperature elevation observed in mice even at supratherapeutic doses; monitoring confirms this translates to human use.
BAM-15 showed protective effects in sepsis-associated kidney injury in mice (PMID 36757801) but human renal effects are unknown. Electrolyte status relevant given increased mitochondrial substrate oxidation.
Initial dosing phase. Due to the short 1.7-hour half-life, plasma levels do not accumulate significantly between doses. Some users report a subtle increase in warmth or metabolic rate within hours of dosing. No visible body composition changes expected.
Consistent daily dosing establishes a pattern of transient mitochondrial uncoupling. Increased energy expenditure may become noticeable during active dosing windows. No measurable fat loss expected yet in most individuals.
Based on mouse model data, fat mass reduction becomes measurable with sustained daily administration. Insulin sensitivity improvements were detectable by this timeframe in preclinical studies. Hepatic lipid levels may begin to decrease.
In the mouse obesity study, significant reductions in body fat mass and improved glycemic control were well established by this point. Body temperature and lean mass remained unchanged throughout. Effects are expected to reverse within days of discontinuation given the short half-life.
Days 1 through 7: Titration with no observable effect. Each dose hits peak plasma levels within one to two hours and clears within four. At community doses of 50 to 200 mg per day, mitochondrial uncoupling probably stays below the threshold for measurable metabolic change. No accumulation happens between doses with a 1.7-hour half-life. Most users report nothing perceptible. Some describe mild warmth or slight sweating during the active dosing window. No body composition changes show up in week one. GI discomfort is possible if you skip the food; headache sometimes shows up during early dosing. Weeks 2 through 4: Possible early metabolic signal. Mouse models at therapeutic dietary doses (0.10%) showed detectable insulin sensitivity improvements by weeks three and four. Whether sub-allometric human community doses produce any measurable metabolic shift is unverified. Anecdotal reports mention slightly more sweating during exercise and a mild reduction in appetite. No biomarker-confirmed human outcomes exist. GI effects fade for most people if dosing stays consistent. Weeks 5 through 8: This is the window where mouse data gets interesting. Axelrod's group confirmed fat mass reduction and whole-body insulin sensitization by week eight at 0.10% dietary dosing in C57BL/6J mice [1]. Hepatic lipid levels dropped. Body temperature stayed normal. Lean mass was preserved. On the human side, no structured outcome reports with biomarker confirmation exist. Individual anecdotes describe one to three kilograms of fat loss over eight weeks, but without controls, imaging, or bloodwork to confirm the mechanism. Post-cycle (off weeks): Given the 1.7-hour half-life, pharmacological activity stops within four to eight hours of the last dose. No pharmacokinetic basis exists for a long washout period. Any fat loss you keep depends on diet. Users describe effects as reversible within days of stopping. No persistent metabolic adaptation has been reported.
Plasma exposure occurs within 1–2 hours of each dose but clears within 4 hours. At community doses (50–200 mg/day), mitochondrial uncoupling is likely sub-threshold for measurable metabolic effect. No accumulation between doses at 1.7-hour half-life.
Most users report nothing perceptible. Some describe a very mild increase in warmth or sweat during dosing window. No body composition changes detectable in week 1.
In mouse models at therapeutic dietary doses (0.10%), insulin sensitivity improvements were detectable by week 3–4. At sub-allometric human community doses, any metabolic effect is unverified.
Anecdotal reports of slightly increased sweat during workouts and minor reduction in appetite. No biomarker-confirmed outcomes available.
In Axelrod 2020, significant fat mass reduction and confirmed whole-body insulin sensitization were established by week 8 at 0.10% dietary dosing in mice (equivalent to ~500 mg/day allometrically). Hepatic lipid accumulation decreased. No body temperature change. Lean mass preserved.
No structured human outcome reports with biomarker confirmation. Individual anecdotes describe 1–3 kg fat loss over 8 weeks but without controls or imaging to confirm.
Given 1.7-hour half-life, pharmacological effects cease within 4–8 hours of last dose. No pharmacokinetic basis for extended washout period. Any fat loss maintenance would depend on dietary adherence.
Effects described as reversible within days of cessation. No persistent metabolic adaptation reported.
Source: Axelrod et al. Nature Communications 2020 (PMID: 32409697): oral PK in C57BL/6J mice
Loading the interactive decay curve.
BAM-15 is classified as a research chemical. It has no FDA approval for any human indication. No IND application or clinical trial registration appears in public databases. The compound cannot be legally sold as a dietary supplement, drug, or food ingredient for human consumption in the United States. WADA (World Anti-Doping Agency) added BAM-15 to the prohibited substance list under category S4.4.1 (Metabolic Modulators) effective January 1, 2026. Athletes and military personnel subject to anti-doping testing face sanctions if BAM-15 is detected. Purchasing BAM-15 for personal research use from chemical suppliers is legal in most jurisdictions, but no regulatory body oversees purity, potency, or manufacturing quality for human-use scenarios. Compounding pharmacy availability does not exist. This content is provided for educational and research reference purposes only. It does not constitute medical advice, and Peptide Schedule does not endorse the use of research chemicals for human self-administration. Consult a qualified healthcare provider before making any decisions about investigational compounds.
Peptide Schedule Research TeamReviewed Apr 20266 Citations
