Fat loss
GLP-1 + muscle preservation
A three-layer framework rather than a branded stack, and the highest-volume real-world pattern of 2026: an incretin for weight loss, a GH-axis layer for lean mass, and a recovery layer underneath. We assembled this from separate evidence and it is labelled as ours.
At a glance
- What is in it
- Sold as
- Separate vials
- The evidence
- The clinical evidence for these compounds in combination with semaglutide or tirzepatide is essentially zero. What is real is the problem the framework is trying to solve: a BMJ network meta-analysis found tirzepatide reduced fat mass most, at −25.7%, and also reduced lean mass most, at −8.3%. Resistance training and protein intake are the interventions with actual evidence behind them; the peptide layers are not.Combination-specific research is limited. Treat each compound’s evidence as separate unless a study of the combination itself is named here, and review the complete plan with a qualified clinician.
Running this stack, with the schedule, the vials it takes and a log of what you took, happens in the app: Claritide for iPhone.
Why people explore it
Common reasons for exploring it
- People already on a prescribed GLP-1 who are worried about lean mass and want to see what the evidence actually supports
- Anyone who has been sold this as a package and wants it taken apart
Where clinician input matters
- Beginners. This is four compounds.
- Anyone with heart failure. That rules out the MK-677 variant outright
- Anyone with active cancer or a cancer history
- Anyone unwilling to run baseline and mid-cycle glucose, HbA1c and IGF-1
- Pregnant, nursing or planning pregnancy within two months
The science
Read the compound mechanisms
Semaglutide mimics GLP-1, a hormone your gut releases after eating, with 94% homology to the human peptide. Activating GLP-1 receptors in the brain reduces appetite and increases fullness. It slows gastric emptying, so meals feel filling for longer. And it both increases insulin secretion and reduces glucagon secretion in a glucose-dependent way, which is why the same molecule treats type 2 diabetes. A C18 fatty di-acid chain at position 26 binds it to albumin, which is what stretches the half-life to about a week; position 8 is modified to resist the DPP-4 enzyme that clears natural GLP-1 in minutes. It is a single-receptor drug. That is the difference from tirzepatide and retatrutide, and it is why its weight-loss figure is smaller.
CJC-1295 binds the same GHRH receptors on the anterior pituitary that tesamorelin does, but with different pharmacokinetics. Without the Drug Affinity Complex, its action is short, a GH pulse of roughly 30 to 60 minutes rather than a prolonged elevation. That short window is deliberate: it is meant to be paired with a ghrelin-receptor agonist that suppresses somatostatin, so one compound presses the accelerator while the other releases the brake.
Ipamorelin activates the ghrelin receptor (GHS-R) on the pituitary. Ghrelin is the hunger hormone, and its receptor also sits on the GH release pathway, which is why this class works at all. The functional effect is suppression of somatostatin, the hormone that normally brakes GH release. Pairing it with a GHRH analog produces a larger pulse than either alone, because one compound is signalling for release while the other removes the restraint. Ipamorelin's distinguishing feature is selectivity: it hits the GH pathway without the cortisol, prolactin and appetite effects that older ghrelin mimetics produce.
BPC-157 appears to work by improving the blood supply to damaged tissue and then telling the repair machinery to switch on. It increases expression of VEGFR2, a receptor that drives angiogenesis, the growth of new blood vessels, so more oxygen and nutrients reach the injury. It also interacts with the nitric oxide system, which controls how wide blood vessels open and how strongly the inflammatory response fires, counteracting both too little and too much nitric oxide. Separately it raises growth hormone receptor expression in tendon fibroblasts and activates the FAK-paxillin pathway, the signalling route cells use to stick, crawl and divide during wound repair. It is named for a cytoprotective effect: shielding tissue from NSAIDs, alcohol and other stressors. That effect is most pronounced in the gut.
Commonly researched ranges
- SemaglutidePer labelPrescription
- CJC-1295 (no DAC)100–300 mcg
- Ipamorelin200–300 mcg
- BPC-157250–500 mcg
| Compound | Amount | Frequency | Timing |
|---|---|---|---|
| SemaglutidePrescription | Per label | Once weekly | Per label |
| CJC-1295 (no DAC) | 100–300 mcg | Per dose | Empty stomach, at least 30 minutes before food |
| Ipamorelin | 200–300 mcg | Per dose | Same window as the CJC-1295 dose |
| BPC-157 | 250–500 mcg | Once daily | Subcutaneous |
- Semaglutide: Or tirzepatide, per its own label. This layer is a prescription decision, not a self-managed one.
- CJC-1295 (no DAC): The GH layer, run as the GH stack. MK-677 at 12.5–25 mg nightly is the oral alternative and carries substantially more risk. See the cautions.
- Ipamorelin: Vendor-tier. No human trial supports this figure.
- BPC-157: The recovery layer. Supports the training that actually preserves lean mass.
- Duration
- The GLP-1 layer is ongoing and prescriber-managed. The GH layer runs in 8–12 week blocks in community practice. No source defines a duration for the three together.
Mixing each compound
Not established in available literature. Use the figures printed on your own vial.
Not established in available literature. Use the figures printed on your own vial.
Not established in available literature. Use the figures printed on your own vial.
- 10 units = 0.25 mg
- 20 units = 0.5 mg
- 30 units = 0.75 mg
- 40 units = 1 mg
- 60 units = 1.5 mg
Week by week
Semaglutide
- Week 1–16
Escalation through four steps. Nausea is most likely here and settles: it affected 44% of people against 16% on placebo, and it is the reason the schedule climbs slowly rather than starting at the target.
- Week 17
Maintenance dose reached, 2.4 mg or 1.7 mg weekly depending on what it was prescribed for.
- Week 60–68
Weight loss flattens around here. STEP 1 showed 14.9% mean reduction at 68 weeks on 2.4 mg, against 2.4% on placebo.
CJC-1295 (no DAC)
- Early weeks
Sleep improvement is the most consistently reported first benefit of the CJC-1295/ipamorelin stack in our sources.
- Week 8–12
The standard cycle length at which our sources describe reassessment for body composition and recovery.
Ipamorelin
- Early weeks
Improved sleep and recovery are the first effects our sources describe, driven by amplified GH pulses during deep sleep.
- Week 4–8
Our tesamorelin page describes stack users reporting significant fat reduction beginning in this window.
BPC-157
- Week 1–2
Subtle. Reduced inflammation, warmth or increased blood flow near the injection site, slight pain reduction. Some people feel nothing yet. The Playbook describes this as normal.
- Week 3–4
Noticeable improvement in most reports. Pain drops on movements that previously hurt, range of motion improves, swelling decreases.
- Week 5–6
People describe significant functional recovery for acute injuries in this window. Chronic injuries may need a second cycle.
- Week 6–8+
For stubborn or chronic problems, a second cycle after a 2–4 week break often brings further improvement. Chronic tendinopathy may need two full cycles.
- After stopping
Benefits generally persist. The Playbook frames this as tissue actually repairing rather than pain being masked.
What it costs
- Semaglutide: $349–1349 per month
- CJC-1295 (no DAC): Not established in available literature
- Ipamorelin: Not established in available literature
- BPC-157: $80–120 per 4–6 week cycle (two 5 mg vials)
These figures are published over different cycle lengths, so Claritide does not add them into one number. Log a vial and the cost engine will tell you what this stack costs you per week, from what you actually paid.
Cautions
- This exceeds the two-compound beginner ceiling by a wide margin. Four compounds means four variables of uncertain purity and no ability to attribute anything to anything.
- If you use MK-677 as the GH layer, read its record first. It is the only compound in this library still Category 2 under both 503A and 503B, on the basis of a randomised hip-fracture trial "terminated early due to a potential safety signal of congestive heart failure". A 2025 BMJ case report documents transaminitis in a healthy man in his early thirties after two months of use, resolving on discontinuation. The Department of Defense lists it as an unapproved drug that is "not legal for use".
- MK-677 drives hunger and water retention while the GLP-1 suppresses appetite. Those are directly competing appetite effects, and the framing comes from vendor material rather than a study, which is why we flag it to monitor rather than to avoid.
- A widely repeated claim says GH secretagogues raise insulin resistance while GLP-1s enhance insulin sensitivity, so the two partially oppose each other. It is mechanistically plausible and currently sourced only to a peptide-vendor compatibility chart. We are not publishing it as a stated antagonism until someone finds a pharmacology primary source. What we will say, from defensible sources, is that more than one compound here moves blood glucose and the combined direction is not predictable. Monitor fasting glucose and HbA1c.
- The lean-mass problem this framework addresses has a pharmacological answer in trials, bimagrumab plus semaglutide, and that answer is a quarterly intravenous antibody nobody self-administers. It is in this library as education, not as a protocol.
- Resistance training and adequate protein are the two interventions with real evidence for preserving lean mass during a caloric deficit. Track them.
Absence from this list does NOT mean safety. It means lack of research.
Every stack here is free to read, and it stays free. Your own schedule, vials and log live in the app: Claritide for iPhone.