Dual GIP/GLP-1 receptor agonist. Delivers potent appetite suppression and improved insulin sensitivity via two complementary pathways. SURMOUNT-1 (NEJM, 2022) demonstrated mean 22.5% total body weight reduction at the 15mg dose over 72 weeks.
Starting Dose
2.5mg weekly
Rest Period
Protocol dependent
⚠️ Full escalation ladder — +2.5mg every 4 weeks minimum: 2.5 → 5 → 7.5 → 10 → 12.5 → 15mg (20 weeks to maximum). Do not skip intermediate steps. GI side effects (nausea, vomiting, diarrhoea) are most common during dose increases. Titrate to the highest tolerated dose. Monitor for hypoglycaemia in extended fasted protocols.
GLP-1 receptor agonist with the most extensive clinical evidence base in this class. STEP 1 (NEJM, 2021) demonstrated mean 14.9% body weight reduction at 68 weeks. The SELECT trial (NEJM, 2023) confirmed a 20% relative reduction in major cardiovascular events in overweight non-diabetic patients.
Starting Dose
0.25mg weekly
Rest Period
Protocol dependent
⚠️ Full escalation schedule: 0.25mg × 4 wks → 0.5mg × 4 wks → 1mg × 4 wks → 1.7mg × 4 wks → 2.4mg (maintenance). Do not skip the 4-week hold at 1.7mg. Do not use where there is a personal or family history of medullary thyroid carcinoma or MEN2 syndrome.
Triple GIP/GLP-1/Glucagon receptor agonist — the most potent metabolic peptide currently in research. Phase 2 (NEJM, 2023) demonstrated mean 24.2% body weight loss at 48 weeks in the 12mg arm. Phase 3 trials (TRIUMPH programme) are ongoing.
Rest Period
8+ weeks (convention)
⚠️ Glucagon receptor activity produces greater thermogenic effect but also dose-dependent heart rate elevation (~6.7bpm above baseline at 12mg in Phase 2). Titration in the Phase 2 trial took approximately 24 weeks to reach 12mg via gradual increments through 2mg → 4mg → 8mg → 12mg. Do not compress escalation — allow adequate time at each step before advancing.
BPC-157 + TB-500
Tissue Repair
Synergistic blend combining BPC-157's localised tissue repair (tendon, ligament, muscle, gut mucosa) with TB-500's systemic healing via thymosin β4 analogue activity — promoting angiogenesis, cell migration and anti-inflammation throughout the body.
BPC-157 Dose
250–500mcg daily
TB-500 Dose
2.5–5mg 2× weekly
TB-500 Maintenance
2.5mg weekly
💡 For musculoskeletal injury research: inject SC or IM as close to the target site as practical. BPC-157 can also be administered orally (dissolved in distilled water) for gastrointestinal research — GI stability in animal models is well-documented. TB-500 loading: 2.5–5mg total per week, split across two injections, for 4–6 weeks; then 2.5mg weekly maintenance. Note: neither compound has completed a published human RCT — all dosing is extrapolated from animal research.
CJC-1295 + Ipamorelin
Growth Hormone
Combined GHRH/GHRP peptide stack designed to amplify natural GH pulsatility. CJC-1295 (with DAC) extends GHRH activity over several days; Ipamorelin provides selective GH pulse stimulation with minimal off-target cortisol, prolactin or appetite effects.
💡 Timing is critical. Once-daily pre-sleep injection is the most common protocol and aligns with the largest natural nocturnal GH pulse. More intensive protocols use twice daily (pre-sleep + fasted pre-exercise). Three-times-daily offers no clear additional benefit over twice-daily in current research. Elevated insulin from a carbohydrate meal will blunt GH secretion — wait at least 2 hours post-meal before injecting.
Tesamorelin
Growth Hormone
Stabilised synthetic GHRH analogue with an N-terminal trans-3-hexenoic acid group that protects it from DPP-4 degradation. FDA-approved for HIV-associated lipodystrophy. Among the best-characterised GHRH peptides in controlled clinical trials for visceral fat reduction. Note: visceral fat re-accumulates toward baseline on cessation.
Alt. Protocol
1mg daily (off-label)
Rest Period
4–8 weeks (convention)
💡 The FDA-approved dose is 2mg daily SC. Some research protocols use 1mg daily as a cost-reduction measure, though this is not the validated clinical dose. Morning administration preferred. Significant visceral fat reduction documented at 12 and 26 weeks in controlled trials. A randomised trial (Baker et al.) also demonstrated improvements in executive function and verbal memory in older adults at 20 weeks.
Copper tripeptide naturally present in human plasma, urine and saliva — declining with age. Genomic analysis shows GHK-Cu influences over 4,000 human genes, activating tissue remodelling, antioxidant defence, collagen synthesis and nerve repair pathways.
Route
Subcutaneous / Topical
💡 Subcutaneous injection preferred for systemic anti-ageing, organ regeneration and neurological protocols. Can be compounded to 0.1–1% concentration for topical skin research (wound healing, elasticity, hair growth). The "4,000 gene" figure derives from an in vitro fibroblast study (Pickart et al., 2015) — in vivo human data is limited but the compound is well-tolerated with no significant reported adverse effects in the research literature.
SS-31 (Elamipretide)
Longevity
Mitochondria-targeted antioxidant tetrapeptide. Selectively concentrates in the inner mitochondrial membrane where it binds cardiolipin, stabilising cristae structure, reducing electron leak and restoring ATP synthesis in aged or metabolically stressed cells. FDA-approved (2025) for Barth syndrome.
Clinical Dose
4–40mg daily
Rest Period
4 weeks (convention)
💡 Phase II/III trials have used 4mg/day SC (PROGRESS-HF) up to 40mg/day SC (MMPOWER-3, Barth syndrome). Conservative community protocols often start lower but 4mg/day is the lowest validated clinical dose. Research applications: cardiac ischaemia-reperfusion, chronic kidney disease, skeletal muscle dysfunction, retinal degeneration. Storage: −20°C until reconstitution; stable 28 days at 2–8°C after reconstitution. Do not refreeze.
Mitochondrial-derived peptide encoded within the 12S rRNA gene of mitochondrial DNA — the first peptide shown to translocate from the cytoplasm to the nucleus during metabolic stress, directly regulating nuclear gene expression and metabolic homeostasis.
💡 Well-documented exercise-mimetic effects: improves skeletal muscle glucose uptake and insulin sensitivity independently of insulin via AMPK activation (Cell Metabolism, 2015; 2019). Circulating MOTS-c declines with age in human plasma. Pre-clinical data shows improved insulin sensitivity, reduced adipogenesis and extended healthspan. No published human clinical trial yet — all dosing is community convention extrapolated from animal studies. Administer on training days for best results in metabolic research.
Nicotinamide adenine dinucleotide — the essential coenzyme for cellular energy production (NADH→ATP via oxidative phosphorylation), DNA repair (substrate for PARP enzymes) and sirtuin activation (SIRT1–7 longevity genes). Tissue NAD+ declines significantly with age, with estimates of 40–50% reduction in adipose tissue between ages 40 and 60.
SC Starting Dose
50mg, 2–3× weekly
SC Peak Dose
100mg per session
IV Dose
250–500mg per session
Rest Period
Cycle or ongoing
⚠️ IV: flushing, chest tightness, nausea and tingling can occur even at low infusion rates — symptoms are rate-dependent and idiosyncratic. Start slow and titrate rate upward. Standard safe practice: begin at 25mg/hr and increase cautiously. Subcutaneous injection is significantly better tolerated. IV and SC have different pharmacokinetic profiles. Oral NMN/NR are indirect precursors with lower bioavailability compared to direct NAD+ administration.
Small-molecule inhibitor of NNMT (nicotinamide N-methyltransferase) — an enzyme highly expressed in adipose tissue that consumes SAM and suppresses NAD+ biosynthesis. By inhibiting NNMT, 5-Amino-1MQ promotes fat cell metabolism and elevates intracellular NAD+ and SAM availability.
Frequency
Once daily (oral)
💡 Unlike all other compounds in this guide, oral administration is the established research route — oral bioavailability is sufficient for a small molecule. NNMT inhibition redirects nicotinamide toward NAD+ synthesis rather than methylation disposal, raising intracellular NAD+ independently of precursor supply — mechanistically synergistic with direct NAD+ supplementation (human trial confirmation pending). Animal research (Small et al., 2021) shows preferential reduction of white adipose tissue with preservation of lean mass. No published human clinical trial yet.
All compounds listed are for in vitro research purposes only. Dosage information is derived from published preclinical and clinical research literature and is provided for reference. Nova Biolabs does not provide medical advice.
