Peptide Schedule
BAM-15Small moleculeNo amino acid sequence. Icon reflects category theme only.BAM-15 Dosage Calculator
BAM-15 (N5,N6-bis(2-fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine) is a small-molecule mitochondrial uncoupler that has attracted significant attention in metabolic research circles.
5mcg · Daily
Summary: Add 0mL BAC water to your 5mg vial. Draw to < 0.1 units on a U-100 syringe for a 5mcg dose. This vial will last 0 doses.
Cycle Planner
BAM-15 Pharmacokinetics
Pharmacokinetics — Active Dose Over Time
t½ = ~1.7 hoursDisclaimer: This curve is a simplified first-order exponential decay model. Actual pharmacokinetics vary based on injection site, individual metabolism, body composition, and other factors. Half-life values are approximate and based on available preclinical and clinical literature. Many research peptides lack formal human pharmacokinetic studies. This is for educational purposes only — not medical advice.
BAM-15 Dosing Protocol
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 5mg | Daily |
| Moderate | 10mg | Daily |
| Aggressive | 20mg | Daily |
Note: Oral small molecule — no reconstitution or injection required. BAM-15 is a mitochondrial protonophore uncoupler, not a peptide, but is included because it is widely discussed in peptide and metabolic optimization communities. CAS number 210302-17-3. Chemical formula C16H10F2N6O. Low water solubility aids mitochondrial membrane penetration. The short half-life (~1.7 hours) is a known limitation — split dosing or extended-release formulations may improve sustained exposure. All efficacy and safety data are from cell culture and rodent studies. No human clinical trials have been conducted.
About BAM-15
BAM-15 (N5,N6-bis(2-fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine) is a small-molecule mitochondrial uncoupler that has attracted significant attention in metabolic research circles. Although it is not a peptide, BAM-15 is frequently discussed alongside peptide-based metabolic agents because of its potent effects on energy expenditure and fat oxidation in preclinical models. Mitochondrial uncouplers work by dissipating the proton gradient across the inner mitochondrial membrane, forcing cells to burn more fuel to maintain their electrochemical potential. What makes BAM-15 stand out from older uncouplers like DNP (2,4-dinitrophenol) and FCCP is its selectivity: BAM-15 depolarizes mitochondrial membranes without affecting plasma membrane potential. This selectivity translates to substantially lower cytotoxicity at effective doses. In cell-based assays, BAM-15 can sustain maximal mitochondrial respiration rates without triggering apoptosis — something classical uncouplers cannot do safely. The landmark 2020 study published in Nature Communications demonstrated that mice fed a high-fat western diet supplemented with BAM-15 had significantly reduced body fat mass, improved insulin sensitivity across multiple tissue types, and decreased hepatic lipid accumulation — all without any reduction in food intake, lean body mass, or body temperature. Hyperinsulinemic-euglycemic clamp studies confirmed whole-body insulin sensitization. Importantly, hematological and biochemical markers of toxicity remained normal throughout the study. BAM-15 is orally bioavailable at approximately 67% in mice, with a Cmax of 8.2 micromolar and a half-life of 1.7 hours. It primarily accumulates in the liver and clears from tissues within four hours. The short half-life is a recognized limitation that researchers are working to address through formulation strategies and structural derivatives like SHM115. Beyond obesity, BAM-15 has shown preclinical activity in sepsis-associated kidney injury, acute myeloid leukemia, and Toxoplasma gondii infection, underscoring the broad therapeutic potential of targeted mitochondrial uncoupling.