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SS-LUP-332 Stacking Guide: Compound Comparison
The table below compares the primary stacking compounds discussed, their mechanisms, typical research dosing ranges, and their specific role in an SS-LUP-332 protocol. SS-LUP-332 Selective PPARδ modulator; increases mitochondrial biogenesis and fatty acid oxid
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- The table below compares the primary stacking compounds discussed, their mechanisms, typical research dosing ranges, and their specific role in an SS-LUP-332 protocol.
- SS-LUP-332
- Selective PPARδ modulator; increases mitochondrial biogenesis and fatty acid oxidation gene expression
- 5–15mg daily, subcutaneous
- Foundation. Expands oxidative capacity; all other compounds address appetite, substrate availability, or energy expenditure
- ~6–8 hours (estimated)
- Required for mitochondrial expansion; stack partners convert capacity into measurable fat loss
- Tirzepatide
- Dual GIP/GLP-1 receptor agonist; slows gastric emptying, suppresses appetite, improves insulin sensitivity
- 2.5–15mg weekly, subcutaneous (titrate over 20 weeks)
- Creates caloric deficit through appetite suppression; allows SS-LUP-332 to operate in sustained energy deficit
- ~5 days
- Most effective single addition for body recomposition; SURMOUNT-1 trial: 20.9% weight loss at 72 weeks
- 5-Amino-1MQ
- NNMT inhibitor; increases NAD+ in adipose tissue, activates AMPK, promotes lipolysis
- 50–100mg daily, subcutaneous or oral
- Mobilizes stored fat (lipolysis); ensures SS-LUP-332's mitochondria have substrate to oxidize
- ~2–4 hours
- Addresses substrate availability. Fat can't be burned unless it's released from adipocytes first
- NAD+
- Coenzyme for electron transport chain; required for final step of beta-oxidation (acetyl-CoA → ATP)
- 100–250mg daily, subcutaneous, or 500mg oral (lower bioavailability)
- Prevents bioenergetic bottleneck; sustains oxidative capacity as demand increases
- ~1–2 hours (subcutaneous NAD+); NMN/NR precursors ~8–12 hours
- Critical when stacking multiple oxidative compounds; NAD+ depletion limits fat oxidation regardless of mitochondrial number
- Ipamorelin
- Selective ghrelin receptor agonist; stimulates pulsatile GH release without cortisol/prolactin elevation
- 200–300mcg, 1–3x daily, subcutaneous
- Preserves lean mass during caloric deficit; improves recovery and connective tissue integrity
- ~2 hours
- Add if training volume is high or GLP-1 agonist is suppressing protein intake below 1.6g/kg
- CJC-1295 NO DAC
- GHRH analog; extends GH half-life and increases baseline secretion
- 100–200mcg, 2–3x weekly, subcutaneous
- Sustains elevated GH between Ipamorelin pulses; mimics natural secretion pattern
- ~6–8 days
- Pair with Ipamorelin for synergistic effect. Long-acting + short-acting = baseline elevation + pulsatile peaks
- Tesofensine
- Triple monoamine reuptake inhibitor; increases thermogenesis and NEAT (non-exercise activity thermogenesis)
- 0.25–1.0mg daily, oral (start low, titrate over 4–8 weeks)
- Increases energy expenditure by 10–15%; creates larger caloric deficit without additional cardio
- ~8–10 days
- Most aggressive addition for maximum fat loss; monitor cardiovascular tolerance (increases HR/BP)
- MOTS-C
- Mitochondrial-derived peptide; improves glucose metabolism, mitochondrial respiration, and exercise capacity
- Optimizes mitochondrial function (complements SS-LUP-332's biogenesis effect); enhances endurance performance
- Best for endurance/performance stacks; less relevant for pure fat loss protocols
- Retatrutide
- Triple agonist (GLP-1/GIP/glucagon); appetite suppression + increased energy expenditure + hepatic fat oxidation
- 4–12mg weekly, subcutaneous (titrate from 2mg over 16 weeks)
- Deepest caloric deficit achievable; glucagon component adds thermogenic effect GLP-1 agonists lack
- ~5–7 days
- Strongest appetite suppression available; Phase 2 data: 24.2% weight loss at 48 weeks. Overkill for mild deficits