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MK-777 (Acetamoren)

Acetamoren · MK777

C
Animal replicated
Research chemicalGhrelin Receptor AgonistGrowth Hormone SecretagogueNon-Peptide Small Molecule
RouteOralGray-market only
C
Evidence grade: Animal replicated

Effect demonstrated in multiple animal studies; human data sparse or extrapolated. Grades summarize evidence quality, not whether a compound is appropriate, legal, or risk-free.

At a glance
What it is
Non-Peptide GHS-R1a Agonist — Fourth-Generation MK-677 Analog — Novel Research Chemical — WADA S2 — Ghrelin Receptor Agonist, Growth Hormone Secretagogue, Non-Peptide Small Molecule.
Why people use it
Used primarily for muscle and performance and sleep and recovery.
What the evidence supports
Community MK-777 protocols extrapolate from MK-677 experience. Given vendor claims of higher potency (Ki = 0.8 nM vs ~1-4 nM) and longer half-life, community protocols tend toward lower doses than MK-677. Limitless: 12.5 mg capsules. Community reports: 12.5-25mg/day oral; before bed (sleep enhancement; appetite management; consistent with MK-677 timing rationale). If the claimed SSTR2/5 modulation is real, dosing might differ from MK-677 in ways the community has not yet established. Effects onset consistent with class: IGF-1 elevation detectable within 1-2 weeks; sleep quality improvement often reported in first week; appetite increase in first 2-4 weeks. Cycle length: community uses 4-12 weeks; some continuous use (mirroring MK-677 long-term trial protocols); IGF-1 monitoring recommended.
If you only read one thing

MK-777 presents the most challenging evidence evaluation problem of any compound in this chapter set: its claimed pharmacological properties are presented with numerical precision (Ki = 0.8 nM; 92% greater binding affinity; 8-10h half-life; 18-22h IGF-1 elevation) but the source of these numbers is not independent peer-reviewed research — it is vendor characterization. The GHS-R1a mechanism it claims is well-established via MK-677. The specific improvements claimed for MK-777 over MK-677 are not. A community that has already established that MK-677 works well for GH secretagogue applications now faces a choice: use the well-characterized compound with clinical data, or use the analog with vendor-claimed improvements and no published validation. The appropriate response is to treat MK-777's class mechanism (GHS-R1a agonism) as Grade C/B via MK-677 extrapolation, and MK-777's specific claimed enhancements as Grade E (vendor claim; unvalidated by independent research).

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Published literature
0human trials0human studies0animal0in vitro
Evidence reality check
Human evidence
No human studies
0 observational; RCT evidence not present in corpus.
Preclinical base
0 lab signals
0 animal; 0 in-vitro/mechanistic.
Evidence snapshot
Community MK-777 protocols extrapolate from MK-677 experience. Given vendor claims of higher potency (Ki = 0.8 nM vs ~1-4 nM) and longer half-life, community protocols tend toward lower doses than MK-677. Limitless: 12.5 mg capsules. Community reports: 12.5-25mg/day oral; before bed (sleep enhancement; appetite management; consistent with MK-677 timing rationale). If the claimed SSTR2/5 modulation is real, dosing might differ from MK-677 in ways the community has not yet established. Effects onset consistent with class: IGF-1 elevation detectable within 1-2 weeks; sleep quality improvement often reported in first week; appetite increase in first 2-4 weeks. Cycle length: community uses 4-12 weeks; some continuous use (mirroring MK-677 long-term trial protocols); IGF-1 monitoring recommended.
From the chapter quick-reference block.
Categories
Muscle & PerformanceSleep & Recovery
Properties
Active malignancy: cautionWADA S2Not injectable
Evidence
CAnimal replicated
The Evidence Situation
This is the most important thing to understand about MK-777: the claimed pharmacological properties (92% higher GHS-R1a binding affinity than MK-677, Ki = 0.8 nM; 8-10h half-life; 18-22h IGF-1 elevation; SSTR2/5 allosteric modulation) derive from vendor characterization and preclinical data, not from independent peer-reviewed published studies. No Phase 1 human trial. No published pharmacokinetic study. No dose-response study in humans. The GHS-R1a mechanism is well-established via MK-677's clinical data; MK-777's specific claimed improvements are unvalidated claims at this stage.
vs MK-677 (Ibutamoren)
MK-677 has Phase 2 clinical trials, published pharmacokinetic data in humans, and a decade of community experience. MK-777 was designed as an analog with claimed improvements in receptor selectivity, half-life, and metabolic stability. The comparison MK-677 provides the pharmacological framework that MK-777 inherits by mechanism class. Whether MK-777 actually performs better than MK-677 has not been tested in any controlled comparison.
SSTR2/5 Allosteric Modulation Claim
Vendors claim MK-777 also allosterically modulates somatostatin receptor subtypes SSTR2 and SSTR5. Somatostatin inhibits GH release; blocking SSTR2/5 would theoretically amplify the GH pulse by removing somatostatin's brake simultaneously with GHS-R1a activation. This is pharmacologically interesting but: (1) no published evidence supports this claim for MK-777; (2) if true, it would produce a larger GH pulse than GHS-R1a agonism alone — potentially with different safety implications.
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