⚡ Upcoming Titration
Sep 14
SS-31 → 10mg · Tesa → 2mg · Ipa → 200mcg
Sep 20
BPC-157 → 500mcg (10u)
Sep 27
Reta → 5mg (42u) — Sunday
Oct 11
TB-500 → maintenance Mon only
Oct 25
Reta → 6–8mg maintenance
Nov 29
MOTS-c C1 ends — reassess 5mg vs 10mg
Today's Protocol
💉 5:15 AM — Fasted
MOTS-c 5mg
25u · train days
🏋️ 6:00 AM — Train
Post-WO Shake
Collagen + Vit C + Creatine
☀️ Sunday Only
Retatrutide 3mg
25u · weekly
🌙 10 PM+ — Min 2–3hrs Fasted
Tesamorelin 1mg
10u → 20u Sep 14
Ipamorelin 100mcg
3u → 6u Sep 14
12-Week Cycle Cost
12-Week Total
MOTS-c held at 5mg ★
More
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PAIRINGS & ECOSYSTEM
How the 8 compounds work together
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Reference Library
Mechanisms · Evidence · Monitoring
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💰
Full Cost & Reconstitution
Vial breakdown · BAC water · Concentrations
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Active Stack — 8 Compounds
Retatrutide
Fat Loss · Triple GLP-1/GIP/GCGR
GHK-Cu
Skin & Collagen · Copper Peptide
SS-31
Mitochondrial · Cardiolipin
MOTS-c
AMPK · Fat Oxidation
Tesamorelin
GH Axis · Visceral Fat
Ipamorelin
GH Pulse · GHS-R1a
BPC-157
Injury Repair · Angiogenesis
TB-500
Cell Migration · Tendon Repair
Titration Schedule
✅ Aug 2
Reta starts · 2.5mg
✅ Aug 31
SS-31 · Tesa · Ipa start
🟢 Sep 6
BPC-157 starts · 250mcg
🟢 Sep 7
MOTS-c + TB-500 loading start
📅 Sep 14
SS-31→10mg · Tesa→2mg · Ipa→200mcg
📅 Sep 20
BPC-157 → 500mcg (10u)
Sep 27
Reta → 5mg (42u) Sunday
Oct 11
TB-500 → Mon maint only
Nov 29
MOTS-c C1 ends · reassess 5 vs 10mg
Visual Timeline
Why Each Schedule Is Different
💪 Tesa + Ipa — 5 On / 2 Off
Both bind receptors that desensitize with continuous stimulation. GHRH-R (Tesa) and GHS-R1a (Ipa) undergo β-arrestin recruitment and receptor internalization when activated daily. Surface receptor density drops and the GH pulse diminishes. Weekend break restores receptor density so Monday hits with full amplitude. Continuous daily dosing defeats the pulsatile mechanism entirely.
🧬 GHK-Cu — 5 On / 2 Off (Different Reason)
Not receptor desensitization — GHK-Cu clears in 30 min regardless. The reason is MMP/TIMP balance. GHK-Cu upregulates both MMPs (break down old collagen) and TIMPs (protect new matrix). Continuous daily copper tips the balance toward net collagen breakdown. Two-day break allows new collagen to consolidate without constant MMP activity.
⚡ SS-31 — Daily 7 Days
Structural cardiolipin binding — not receptor signaling. No receptor to rest. The moment SS-31 clears (within hours), cardiolipin loses protection, cytochrome c converts to peroxidase, ETC degrades. Taking weekends off = two full days of unprotected mitochondria per week. Daily is not optional.
🩹 BPC-157 — Daily 7 Days
Continuous angiogenesis — new capillary formation into avascular rotator cuff tissue is an ongoing biological process. Injured tissue does not pause on weekends. No receptor desensitization concern — growth factor pathways, not GPCRs. Daily maintains the repair stimulus without interruption.
⚡ MOTS-c — Training Days Only (Not 5/2)
Not a 5 on/2 off protocol — training-day specific. MOTS-c AMPK activation is most potent when converging with exercise-induced AMPK. Two signals > either alone. On rest days: no co-stimulus, blunted effect. Rule: training days, not weekdays. Train Saturday → inject Saturday.
🩹 TB-500 — Mon+Thu → Mon (Not Standard)
G-actin sequestration and cell migration density protocol — not receptor-based. Mon+Thu loading establishes repair cell flux at the injury site over 5 weeks. Maintenance sustains it. Completely different logic from receptor desensitization.
Phase Dates
C1 ON: Jul 29–Sep 22OFF: Sep 23–Oct 6C2 ON: Oct 7–Dec 1OFF: Dec 2–15C3 ON: Dec 16–Feb 9
C1 ON: Aug 31–Nov 22OFF: Nov 23–Dec 20C2 ON: Dec 21–Mar 14OFF: Mar 15–Apr 11
C1 ON: Sep 7–Nov 29OFF: Nov 30–Dec 27C2 ON: Dec 28–Mar 21
C1 ON: Sep 6–Nov 28OFF: Nov 29–Dec 26C2 ON: Dec 27–Mar 20
Load: Sep 7–Oct 10Maint: Oct 11–Dec 5OFF: Dec 6–Jan 2C2 Load: Jan 3–Feb 6
8 Compounds · One Ecosystem
Reta + Tesa + MOTS-c
Fat loss through 5 independent mechanisms — appetite, thermogenesis, hepatic oxidation, GH lipolysis, adipose beiging
Tesa + Ipa
Two G-proteins on same pituitary cell → 3–8× GH pulse → muscle preservation + overnight repair overnight
GHK-Cu + Collagen + Vit C
Skin tight as fat disappears — fibroblast signal + substrate + crosslinking enzyme all present simultaneously
SS-31 + MOTS-c
Mitochondria protected structurally (SS-31) and multiplied (MOTS-c) — powers the 6 AM sessions
BPC-157 + TB-500
BPC-157 builds the repair environment. TB-500 physically moves repair cells into it — most logical pairing in the stack
BPC-157 + Tesa/Ipa
GH receptors upregulated at shoulder up to 7× — nightly GH pulse hits the injury site directly
GHK-Cu + Reta
Reta suppresses fibroblast collagen via GLP-1R. GHK-Cu counteracts via TGF-β/Wnt. Running both is pharmacologically necessary — not optional
TB-500 + GHK-Cu
Independent NF-κB suppression through two different pathways — additive anti-inflammatory effect at shoulder
Pairings — Deep Dive
What They Do
Tesamorelin binds GHRH-R (Gs → cAMP → PKA) — loads GH pulse amplitude. Ipamorelin binds GHS-R1a (Gq → PLC → IP₃ → Ca²⁺) — fires the pulse AND suppresses somatostatin simultaneously. Two different G-proteins on the same pituitary somatotroph cell. Two different calcium sources. Non-competing pathways converging on GH exocytosis. Combined: 3–8× baseline GH vs 2–5× each alone.
Why Pre-Bed Is Non-Negotiable
Somatostatin (the GH brake) is at its daily nadir during slow-wave sleep. 10 PM injection aligns with this permissive window. Morning cortisol directly counteracts GH at the pituitary level — morning dosing is not slightly less effective, it is physiologically opposed.
What you feel: Faster overnight recovery, preserved lean muscle during fat loss, deeper sleep quality, visceral fat reduction, skin collagen via IGF-1 → fibroblast stimulation.
What They Do
SS-31 stabilizes cardiolipin in the inner mitochondrial membrane — protects ETC supercomplexes, prevents cytochrome c peroxidase formation, maintains cristae architecture. More ATP per O₂ consumed. MOTS-c activates AMPK via AICAR → PGC-1α → mitochondrial biogenesis, GLUT4 translocation, adipose beiging. SS-31 protects what exists. MOTS-c builds more.
Why Complementary (Not Redundant)
SS-31 is structural — infrastructure protection. MOTS-c is signaling — biogenesis and metabolic switching. They operate on completely different layers of mitochondrial function and reinforce each other.
What you feel: Stronger energy at 6 AM, less fatigue between sets, faster session-to-session recovery, better fat burning during training.
What They Do
GHK-Cu activates TGF-β and Wnt on dermal fibroblasts, delivers Cu²⁺ to lysyl oxidase for collagen crosslinking, resets 4,000+ genes toward younger tissue states. Critically counteracts Reta's GLP-1R-driven collagen suppression. Collagen peptides supply procollagen amino acids (glycine, proline, hydroxyproline) as raw substrate. Vitamin C hydroxylates proline/lysine — without it, GHK-Cu's signal produces collagen amino acids that cannot form stable structural collagen.
The Complete Pathway
GHK-Cu = signal · Collagen peptides = substrate · Vitamin C = crosslinking enzyme cofactor. All three are required. Any one missing breaks the chain.
What you feel: Skin staying tight as fat disappears. Improved firmness at the 3–5 month mark. Reduced joint soreness. Counteracting the loose skin risk of aggressive GLP-1-driven weight loss.
Five Independent Mechanisms
Reta activates GLP-1R (appetite/satiety suppression), GIPR (brown adipose thermogenesis, GI buffer), GCGR (hepatic fat oxidation + resting energy expenditure — the mechanism tirzepatide lacks). Tesamorelin drives pulsatile GH → preferential visceral fat lipolysis. MOTS-c activates AMPK → fat oxidation during training + adipose beiging/thermogenesis. None of these five pathways compete or overlap.
What you feel: Reduced appetite, consistent scale movement toward 200 lbs, waist circumference reduction, improved resting metabolic rate.
What They Do
BPC-157 drives VEGFR2 angiogenesis into the avascular rotator cuff zone, upregulates GH receptors at the injury site up to 7-fold (amplifying the nightly Tesa+Ipa GH pulse directly at the shoulder), drives EGR-1 tenocyte identity for organised collagen vs scar. TB-500 binds G-actin → mobilises repair cells to physically migrate into the injury zone, drives independent VEGF angiogenesis through endothelial cell migration, suppresses chronic NF-κB inflammation.
Why They're Paired — The Key Insight
BPC-157 builds the repair environment and vascular highway. TB-500 physically moves the repair cells into it. BPC-157 without TB-500: the infrastructure exists but cells aren't moving in. TB-500 without BPC-157: cells mobilise but the environment isn't primed. Together: complete repair cascade.
What you feel: Reduced shoulder pain on push/pull movements within 2–4 weeks. Structural tendon repair over 3–6 months for a chronic multi-year injury.
Compound Reference — Tap to Expand
12-Week Cycle Cost
12-Week Total
MOTS-c held at 5mg ★
Reconstitution Quick Reference
MOTS-c Stock Plan
✅ 5mg held — C1
3 more × 40mg needed
Order before Oct 19
Stock: 3×40mg + 6×10mg = 180mg
C1 needs: 300mg (5mg × 5 days × 12 wks)
Shortfall: 120mg — order 3 × 40mg = $375
Saving vs 10mg: $875/cycle
Vial Inventory — Tap +/- to Update