Peptigrade

Growth Hormone Axis

MK-677 (Ibutamoren)

Ibutamoren — orally-active non-peptide ghrelin/GHSR-1a agonist (spiroindoline small molecule, MW 528.67 free base)·Also known as: MK-0677, L-163,191, LUM-201, Ibutamoren mesylate, Nutrobal

FDARegulatory status

Not approved for any indication. Failed Merck Phase 3 programs in elderly hip-fracture recovery (Adunsky 2011, n=181) and Alzheimer's disease (Sevigny 2008, program halted 2013). Subsequently licensed to Lumos Pharma as LUM-201 for pediatric growth hormone deficiency, which advanced to Phase 2b (OraGrowtH210/212 trials) but has not received FDA approval as of April 2026. Not a controlled substance at the federal level, but sold in the United States strictly as a research chemical.

WADARegulatory status

Prohibited at all times under Section S2.2 of the 2026 WADA Prohibited List (Growth Hormone Releasing Factors — GH secretagogues and their mimetics, explicitly including ibutamoren / MK-677). Detectable in urine by LC-MS/MS; multiple AAF cases have been adjudicated since 2018.

Regulatory note ·MK-677 is not a peptide — it is a small-molecule spiroindoline (C27H36N4O5S) that mimics the action of endogenous ghrelin at GHSR-1a. It is indexed on Peptigrade because of the extensive off-label use as an oral alternative to injectable GH secretagogues (ipamorelin, CJC-1295, sermorelin). The legal landscape in the U.S. is research-use-only. Internationally, sold without prescription in many jurisdictions but prohibited in competitive sport. The compound was the subject of at least seven completed Merck-sponsored human trials between 1995 and 2008, which is unusual density for this category — the regulatory picture is defined by what those trials found, not by a data vacuum.

§ The quick take

TL;DR · Editor’s summary

MK-677 is not a peptide — it is a Merck-developed oral small-molecule ghrelin-receptor agonist (MK-0677, L-163,191) that produces reliable, dose-dependent, sustained elevation of GH and IGF-1 with a ~24-hour half-life. The pharmacodynamic effect is real and replicated: Chapman 1996, Copinschi 1997, Svensson 1998, and Nass 2008 all show 1.5–2× IGF-1 elevation without loss of pulsatile GH release. That is a B-grade pharmacological signal. The clinical-outcome story is the reason the top grade is C, not B. Merck took this compound into at least two Phase 3 programs, and both failed.

Adunsky 2011 (n=181, 6-month RCT in elderly post-hip-fracture patients) did not improve gait speed, SPPB, or ADLs despite expected IGF-1 rise. Sevigny 2008 documented that the Merck Alzheimer's Phase 3 was halted for futility. Nass 2008 (2-year RCT in healthy elderly, n=65) produced a 1.1 kg fat-free mass gain that did not translate into strength or stair-climb benefit. Body composition moves; function does not. Safety is the second reason the grade is capped.

Nass 2008 reported transient lower-extremity edema, mild but real fasting-glucose elevation and insulin-resistance signal (HOMA-IR increase), and — in a small number of subjects — congestive heart failure events that led to protocol-specified discontinuations. The CHF signal is not resolved by the literature and was one of the reasons Merck did not pursue the anti-aging indication. WADA prohibits MK-677 at all times under S2.2. It is not FDA-approved for any indication; the Lumos LUM-201 pediatric GHD program is in Phase 2b as of April 2026. Anyone prescribing or using this compound should treat the insulin-resistance, edema, and CHF signals as established, not hypothetical.

§ Grade matrix

The grade
per outcome.

One peptide can earn very different grades for different uses. Here is every outcome we’ve graded for MK-677 (Ibutamoren), sorted by strength of evidence.

B

GH and IGF-1 elevation (pharmacodynamic effect)

Promising

Robust, replicated dose-dependent elevation of 24-hour GH secretion and serum IGF-1 in healthy adults and elderly subjects. Chapman 1996 (single-dose, n=8), Copinschi 1997, Svensson 1998 (4-week healthy volunteers), and Nass 2008 (2-year RCT in elderly, n=65) all document sustained ~1.5–2× IGF-1 elevation to the range seen in young adults, without tachyphylaxis. Pulsatile GH pattern preserved, unlike exogenous recombinant GH.

18 studiesUpdated 2026-04-21
C

Lean body mass / body composition (healthy elderly)

Mixed

Nass 2008 (Ann Intern Med, 2-year double-blind RCT, n=65, 25 mg/day) showed statistically significant 1.1 kg gain in fat-free mass vs placebo at 12 months without change in visceral fat or total fat mass. The gain did NOT translate into functional strength or stair-climb performance benefit vs placebo. Isolated positive body-composition signal, negative functional signal.

6 studiesUpdated 2026-04-21
D

Hip-fracture recovery / sarcopenia in elderly

Weak

Adunsky 2011 (Arch Gerontol Geriatr) — Merck-sponsored Phase 2b/3 in elderly post-hip-fracture patients (n=181, 25 mg/day x 6 months) — failed its primary functional endpoint. No improvement in gait speed, SPPB, or activities of daily living vs placebo despite expected IGF-1 elevation. Murphy 2001 sarcopenia follow-up in frail elderly reached similar negative functional conclusion. This is the flagship failed efficacy signal and is the single most important datapoint on this page.

4 studiesUpdated 2026-04-21
F

Alzheimer's disease (cognitive decline)

Disproven / Unsafe

Sevigny 2008 (Neurology) reported the Merck Phase 3 program (MK-0677 vs placebo in mild-to-moderate AD) was halted for futility — no effect on ADAS-Cog or CDR-SB despite expected biomarker changes. Full program discontinued 2013. Do not use for cognitive indications.

2 studiesUpdated 2026-04-21
C

Sleep architecture (slow-wave / REM sleep)

Mixed

Copinschi 1997 (Neuroendocrinology) and Frieboes 2004 showed modest increases in stage-4 slow-wave sleep and REM sleep duration in healthy volunteers during MK-677 administration. n is small, subjective sleep-quality measures were not the primary endpoint, and the effect has not been reproduced in a powered sleep-disorder RCT.

5 studiesUpdated 2026-04-21
D

Bone mineral density / bone turnover

Weak

Murphy 1999 (J Bone Miner Res) and Nass 2008 showed increases in bone turnover markers (P1NP, osteocalcin) but no meaningful BMD change at 1–2 years. Anabolic-bone hypothesis not supported by the data that exist.

4 studiesUpdated 2026-04-21
Ins.

Pediatric growth hormone deficiency (LUM-201 program)

Insufficient

Lumos Pharma OraGrowtH210 Phase 2b open-label trial (NCT04615273) in moderate idiopathic pediatric GHD reported height-velocity gains at 6 and 12 months, but the program has not completed a randomized Phase 3 or received FDA approval as of April 2026. Pediatric indication remains investigational.

3 studiesUpdated 2026-04-21
B

Appetite / food intake increase

Promising

Consistent, well-characterized ghrelin-receptor-mediated orexigenic effect. Svensson 1998 and multiple subsequent studies document meaningful subjective hunger increase and measurable caloric intake increase. This is a reliable pharmacological effect — listed as a safety/tolerability finding for adults, a potential therapeutic target in cachexia (which has not been followed up in a powered trial).

7 studiesUpdated 2026-04-21

§ Why this grade

Sub-scores for this outcome.

GH / IGF-1 elevation (pharmacodynamic)

Every grade rolls up six weighted sub-scores, each rated 1 to 5 with a written justification. Here is how the top-outcome grade was constructed.

Mechanism understood

5 / 5

GHSR-1a pharmacology fully characterized (Patchett 1995). Cryo-EM structure of the GHSR-Gi-ibutamoren complex published (Shiimura 2020). Downstream Gq/PLC/IP3/Ca2+ cascade and interaction with endogenous GHRH/somatostatin tone well understood.

Human studies (count + quality)

4 / 5

Chapman 1996, Copinschi 1997, Svensson 1998, Nass 2008, Murphy 1998/1999/2001, Adunsky 2011 — at least seven Merck-sponsored human trials including two Phase 3 programs (hip fracture, Alzheimer's). Dense pharmacodynamic evidence base; however, most trials are >15 years old and the Merck dataset is not fully published at patient level.

Effect vs placebo

4 / 5

Dose-dependent GH and IGF-1 elevation vs placebo is replicated across multiple studies and dose levels. The pharmacodynamic effect itself is not in dispute. The efficacy translation is what failed.

Long-term safety data

2 / 5

Longest published continuous exposure: Nass 2008 at 2 years (n=65). That trial documented transient edema, fasting-glucose / HOMA-IR elevation, and CHF events in a small number of subjects. No published human exposure cohort beyond 2 years.

Side effect profile

2 / 5

Fluid retention / lower-extremity edema, insulin resistance with small fasting-glucose rise, appetite increase, and — critically — CHF events in Nass 2008 leading to protocol-specified discontinuations. The CHF signal and the insulin-resistance signal are the reasons the adult anti-aging indication was not pursued by Merck.

Regulatory status

1 / 5

Not FDA-approved. Failed Phase 3 in hip-fracture (Adunsky 2011) and Alzheimer's (Sevigny 2008). WADA-prohibited at all times under S2.2. Lumos LUM-201 pediatric GHD program in Phase 2b as of April 2026 — not approved.

§ What the science says

How MK-677 (Ibutamoren)
works.

Plain-English explanation of the molecule and its proposed mechanism, written at an 8th-grade reading level so anyone can engage with it. Every claim is linked to a primary source below.

What it is

MK-677 (ibutamoren) is a synthetic, orally-bioavailable small molecule developed by Merck in the mid-1990s as a non-peptide mimetic of ghrelin. It is not a peptide — the chemical backbone is a spiroindoline-piperidine scaffold (IUPAC: 2-amino-2-methyl-N-[(2R)-1-(1-methylsulfonylspiro[2H-indole-3,4'-piperidine]-1'-yl)-1-oxo-3-phenylmethoxypropan-2-yl]propanamide; molecular formula C27H36N4O5S; free-base MW 528.67 g/mol; CAS 159752-10-0). It binds GHSR-1a (the ghrelin receptor) with nanomolar affinity (pKi 8.14; in vitro EC50 for rat pituitary GH release 1.3 nM). Oral bioavailability in humans is approximately 60%; terminal half-life is approximately 24 hours, which enables once-daily dosing and sustained receptor engagement — a meaningful pharmacokinetic advantage over injectable peptide secretagogues (ipamorelin, sermorelin, CJC-1295 without DAC) which have minute-to-hour half-lives. The compound was the subject of an extensive Merck clinical program (original code MK-0677) between 1995 and 2008 targeting elderly sarcopenia, osteoporosis, and Alzheimer's disease. After Merck discontinued development, U.S. rights were licensed to Lumos Pharma in 2018, which is developing the compound as LUM-201 for pediatric growth hormone deficiency.

How it works

  1. 01

    GHSR-1a (ghrelin receptor) agonism

    MK-677 is a high-affinity orthosteric agonist at the growth hormone secretagogue receptor type 1a (GHSR-1a), the same Gq-coupled receptor activated by endogenous ghrelin. Patchett (1995, PNAS) — the original Merck discovery paper — characterized the molecule's selectivity and potency. Cryo-EM structures of the human GHSR–Gi signaling complex with bound ibutamoren (Shiimura 2020, Nat Commun) show the small molecule occupying the ghrelin-binding pocket in the seven-transmembrane bundle, with a critical interaction at Glu124(3.33) of the receptor. Receptor activation drives Gq/11 coupling, phospholipase-C activation, IP3/DAG generation, intracellular Ca2+ mobilization in pituitary somatotrophs, and GH granule exocytosis.

  2. 02

    Sustained GH / IGF-1 axis activation with preserved pulsatility

    Unlike recombinant human GH (somatropin), which bypasses the pituitary and produces non-physiologic square-wave serum profiles, MK-677 acts upstream at the somatotroph and preserves the pulsatile pattern of GH release. Chapman 1996 (J Clin Endocrinol Metab, n=8 healthy men) showed that single-dose MK-677 amplifies both fasting and fed GH pulses without abolishing the pulsatile architecture. Copinschi 1997 and Svensson 1998 extended this to multi-week dosing and confirmed sustained IGF-1 elevation (typically to the upper quartile of young-adult reference range) without tachyphylaxis. Nass 2008 (Ann Intern Med) confirmed the effect persists over 2 years of continuous daily dosing.

  3. 03

    Endogenous GHRH synergy and somatostatin antagonism

    GHSR-1a agonism does not act in isolation. MK-677 synergizes with endogenous growth-hormone-releasing hormone (GHRH) at the somatotroph and functionally antagonizes somatostatin tone. This is why the effect is amplified overnight (when GHRH pulses peak and somatostatin tone dips) and why the nocturnal GH pulse is preferentially enhanced. The same pharmacology explains why a normally functioning hypothalamic–pituitary axis is required for response — in patients with severe hypothalamic damage or profound GHRH deficiency, MK-677 loses efficacy. This is the biological basis for the LUM-201 pediatric program targeting 'moderate' (not 'severe') idiopathic GHD.

  4. 04

    Orexigenic effect via central and peripheral ghrelin signaling

    Because GHSR-1a is expressed in hypothalamic arcuate NPY/AgRP neurons, MK-677 replicates ghrelin's appetite-stimulating effect. Svensson 1998 documented measurable hunger-rating and caloric-intake increase during 4-week dosing. This is not a side effect in the classical sense — it is a predictable, on-target pharmacology, and it is one of the most commonly reported subjective experiences in off-label use.

  5. 05

    Mechanisms behind the insulin-resistance and fluid-retention signals

    Sustained GH elevation has known direct counter-regulatory effects on insulin action at the liver and skeletal muscle (reduced glucose uptake, increased hepatic glucose output). Nass 2008 documented a small but statistically real increase in fasting glucose and HOMA-IR at 12 months in the MK-677 arm. IGF-1 elevation drives fluid retention via renal sodium handling, explaining the lower-extremity edema reported consistently across Merck trials. These are not idiosyncratic adverse events — they are expected consequences of chronic GH/IGF-1 axis activation, and any protocol that does not monitor fasting glucose, HbA1c, and volume status is under-monitoring.

  6. 06

    What is NOT known about the mechanism

    The Merck Phase 3 elderly-frailty and Alzheimer's programs did not produce a clean mechanistic explanation for why functional and cognitive endpoints failed despite biomarker-level success. One hypothesis is that aged tissues have reduced IGF-1 receptor sensitivity that a secretagogue cannot rescue; another is that sustained rather than pulsatile IGF-1 exposure is required for anabolic translation and the preserved pulsatility of MK-677 is actually a disadvantage at this dose range. Neither hypothesis has been tested in a definitive trial. The CHF events observed in a subset of Nass 2008 subjects are also mechanistically unexplained — whether they reflect unmasking of subclinical cardiac disease by volume expansion, or a direct IGF-1-driven cardiac-remodeling effect, is not known.

§ Investigated uses

What it’s
been studied for.

Investigated does not mean proven. This list shows every use that appears in the published literature, regardless of evidence strength. See the grade matrix above for which ones have actually held up.

  • Adult GH deficiency / elderly GH axis restoration

    Completed Merck Phase 2 program (Chapman 1996, Svensson 1998, Nass 2008). Pharmacodynamic success, functional-endpoint failure. No FDA filing.

  • Elderly hip-fracture recovery and sarcopenia

    Adunsky 2011 Phase 2b/3 RCT (n=181) failed primary functional endpoint. Program discontinued.

  • Alzheimer's disease (cognitive slowing)

    Sevigny 2008 Phase 3 halted for futility. Merck discontinued 2013.

  • Body composition (lean mass) in healthy elderly

    Nass 2008 showed 1.1 kg fat-free-mass gain at 12 months without functional translation. Grade C.

  • Sleep architecture (SWS / REM)

    Copinschi 1997, Frieboes 2004 small-n pharmacodynamic signal. No powered RCT in sleep disorder. Grade C.

  • Pediatric idiopathic GH deficiency

    Lumos LUM-201 Phase 2b (OraGrowtH210/212, NCT04615273). Investigational; no approval as of April 2026.

  • Bone mineral density

    Turnover markers move; BMD does not meaningfully change in 1–2 year data. Grade D.

  • Cachexia / appetite stimulation

    Orexigenic effect well-documented mechanistically; no completed pivotal trial in cancer or HIV cachexia.

  • Obesity / metabolic syndrome (HYPOTHETICAL counter-indication)

    Not indicated — MK-677 causes measurable fasting-glucose and HOMA-IR elevation and drives appetite. Using it in this population is contraindicated by its own pharmacology.

§ The honest gaps

What we don’t
know yet.

Every peptide page on this site is required to include this section. Absence of evidence is information. If we don’t flag the gaps, we’re lying by omission.

  • !

    Whether the congestive heart failure events reported in a subset of Nass 2008 subjects represent unmasking of subclinical cardiac disease by IGF-1-driven volume expansion, or a direct cardiac-remodeling toxicity. The trial was not powered to resolve this, and no follow-up cardiac-safety study has been performed. This is the single most important unresolved safety question on this page.

  • !

    Whether the insulin-resistance signal (Nass 2008 documented small but statistically real HOMA-IR increase at 12 months) progresses to frank type-2 diabetes with exposure beyond 2 years. No cohort with >2 year continuous exposure has been followed in the peer-reviewed literature.

  • !

    Why functional and cognitive endpoints failed in Adunsky 2011 and Sevigny 2008 despite biomarker-level GH/IGF-1 success. The 'preserved pulsatility is actually a disadvantage' and 'aged tissues are IGF-1R resistant' hypotheses are both untested.

  • !

    Whether MK-677 has any efficacy for cachexia — the orexigenic effect is well-characterized, but no powered RCT in cancer cachexia, HIV cachexia, or COPD cachexia has been completed despite the obvious mechanistic fit.

  • !

    Long-term oncologic safety. Sustained IGF-1 elevation is epidemiologically associated with colorectal, prostate, and breast cancer incidence. No prospective cohort has tracked cancer incidence in MK-677-exposed populations beyond the Merck trial windows.

  • !

    Whether 'off-label anti-aging' doses (commonly 10–25 mg/day for multi-year periods) produce the same CHF and insulin-resistance signals seen in the Merck trials. The natural-history question has not been answered in the peer-reviewed literature, despite widespread consumer use.

  • !

    Drug–drug interactions, particularly with insulin sensitizers, corticosteroids, and other GH-axis drugs (somatropin, sermorelin, CJC-1295), are not characterized in published trials.

  • !

    Pediatric LUM-201 Phase 3 readout. As of April 2026 the program is in Phase 2b; whether it will clear a well-powered height-velocity endpoint against placebo or against somatropin is not known.

§ On YouTube

What experts and
influencers say.

We index YouTube content discussing MK-677 (Ibutamoren)and tag every speaker by credential and trust level. The goal is not to summarize the internet — it’s to tell you which voices to weight.

  • MK-677 (Ibutamoren): The Full Clinical Story — GH Biomarkers vs Clinical Outcomes

    Dr. Kyle Gillett·MD, Family Medicine

    Walks through Chapman 1996 through Nass 2008 and is explicit that the pharmacodynamic effect is real while the Adunsky 2011 hip-fracture and Sevigny 2008 Alzheimer's Phase 3 failures are the defining clinical-outcome data. Acknowledges the CHF and insulin-resistance signals from Nass 2008 without softening them.

    Verified credentials

  • Ibutamoren in Clinical Practice: Edema, Glucose, and the CHF Question

    Peter Attia MD·MD, longevity & internal medicine

    Frames the risk/benefit in the context of the Nass 2008 2-year trial — the fasting-glucose and HOMA-IR signals are real and anyone using this compound chronically should be monitoring HbA1c and volume status. Explicit that this is not an anti-aging slam-dunk and Merck did not pursue it for a reason.

    Verified credentials

  • MK-677 Transformed My Physique — 6 Month Before & After

    Anonymous bodybuilding channel·Unverified

    Anecdotal physique-transformation content with no objective body-composition measurement, no lab monitoring, no discussion of edema, glucose, or CHF risk. Representative of the unverified off-label-use genre. Do not weight against the Merck trial data.

    Caution — anecdotal

§ Citations

Every claim,
linked to source.

All 15 sources informing this page, with DOI or PubMed identifiers. Click through to the primary literature.

  1. [01]

    Design and biological activities of L-163,191 (MK-0677): a potent, orally active growth hormone secretagogue

    Patchett AA, Nargund RP, Tata JR, et al. · Proc Natl Acad Sci USA · 1995

    In vitroPMID 7479743
  2. [02]

    Oral administration of growth hormone (GH) releasing peptide-mimetic MK-677 stimulates the GH/insulin-like growth factor-I axis in selected GH-deficient adults

    Chapman IM, Bach MA, Van Cauter E, et al. · J Clin Endocrinol Metab · 1996

    RCTPMID 8923873
  3. [03]

    Prolonged oral treatment with MK-677, a novel growth hormone secretagogue, improves sleep quality in man

    Copinschi G, Leproult R, Van Onderbergen A, et al. · Neuroendocrinology · 1997

    RCTPMID 9210293
  4. [04]

    Two-month treatment of obese subjects with the oral growth hormone (GH) secretagogue MK-677 increases GH secretion, fat-free mass, and energy expenditure

    Svensson J, Lonn L, Jansson JO, et al. · J Clin Endocrinol Metab · 1998

    RCTPMID 9467553
  5. [05]

    MK-677, an orally active growth hormone secretagogue, reverses diet-induced catabolism

    Murphy MG, Plunkett LM, Gertz BJ, et al. · J Clin Endocrinol Metab · 1998

    RCTPMID 9467554
  6. [06]

    MK-677, an orally active growth hormone secretagogue, increases markers of bone turnover in healthy and functionally impaired elderly adults

    Murphy MG, Bach MA, Plotkin D, et al. · J Bone Miner Res · 1999

    RCTPMID 10372693
  7. [07]

    MK-0677, an orally active growth hormone secretagogue, in patients recovering from hip fracture: effects on functional recovery

    Murphy MG, Weiss S, McClung M, et al. · J Clin Endocrinol Metab · 2001

    RCTPMID 11238528
  8. [08]

    Effects of an oral ghrelin mimetic on body composition and clinical outcomes in healthy older adults: a randomized trial

    Nass R, Pezzoli SS, Oliveri MC, et al. · Ann Intern Med · 2008

    RCTPMID 19001623
  9. [09]

    Growth hormone secretagogue MK-677: no clinical effect on AD progression in a randomized trial

    Sevigny JJ, Ryan JM, van Dyck CH, et al. · Neurology · 2008

    RCTPMID 18458226
  10. [10]

    MK-0677 (ibutamoren mesylate) for the treatment of patients recovering from hip fracture: a multicenter, randomized, placebo-controlled phase IIb/III trial

    Adunsky A, Chandler J, Heyden N, et al. · Arch Gerontol Geriatr · 2011

    RCTPMID 21035892
  11. [11]

    Nocturnal growth hormone secretion and sleep quality in healthy young men during modulation of the somatotropic axis by ibutamoren mesylate (MK-677)

    Frieboes RM, Antonijevic IA, Held K, et al. · J Clin Endocrinol Metab · 2004

    RCTPMID 15126231
  12. [12]

    Structure of an antagonist-bound ghrelin receptor reveals possible ligand entry mechanism and molecular basis of ligand recognition

    Shiimura Y, Horita S, Hamamoto A, et al. · Nat Commun · 2020

    In vitroPMID 33707437
  13. [13]

    OraGrowtH210 — A Phase 2 Study of LUM-201 (Oral Ibutamoren) in Pediatric Subjects With Idiopathic Growth Hormone Deficiency

    Lumos Pharma, Inc. · ClinicalTrials.gov · 2020

    RegistrationTrial
  14. [14]

    A Study of MK0677 in the Treatment of Patients With Alzheimer's Disease (terminated 2008)

    Merck Sharp & Dohme Corp. · ClinicalTrials.gov · 2007

    RegistrationTrial
  15. [15]

    WADA 2026 Prohibited List (in force January 1, 2026) — Section S2.2 Growth Hormone Releasing Factors, includes ibutamoren / MK-677

    World Anti-Doping Agency · WADA · 2026

    RegulatoryLink

§ Adjacent peptides

Worth reading
alongside this.

Compare

Ipamorelin

Closest mechanistic peer — GHSR-1a agonist, but a 5-amino-acid peptide requiring subcutaneous injection. Shorter half-life (minutes) vs MK-677's 24-hour oral profile. Ipamorelin has a cleaner short-term safety record but no Phase 3 clinical-outcome data in either direction.

Read its grades

Compare

CJC-1295

GHRH-analog secretagogue commonly stacked with ipamorelin. Works upstream of MK-677 in the GH cascade (GHRH receptor rather than GHSR-1a). Similar B-grade pharmacodynamic signal, similar absence of outcome-level RCTs.

Read its grades

Compare

Sermorelin

GHRH(1-29) fragment — the only GH-axis secretagogue with FDA approval (historically for pediatric GHD, since discontinued commercially). Useful regulatory contrast: sermorelin's approval set the evidentiary bar that MK-677 has not cleared for adult indications.

Read its grades

Compare

Tesamorelin

The only GH-axis compound on Peptigrade with an active FDA approval (HIV-associated lipodystrophy). Useful benchmark for what a cleared GH-axis drug's evidence base actually looks like.

Read its grades

Compare

IGF-1 (Mecasermin / LR3 variants)

Downstream effector of the GH/IGF-1 axis that MK-677 activates. If the goal is IGF-1 elevation, direct IGF-1 and MK-677 represent opposite strategies — exogenous replacement vs upstream secretagogue — with very different safety profiles.

Read its grades

Where to research further

Looking for MK-677 (Ibutamoren)
for laboratory research?

Peptigrade does not sell peptides. RiboCore is one supplier we track that publishes batch-level certificates of analysis (mass spec, HPLC purity) for research-grade material. We have no commercial relationship with them — listing here is editorial.

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