Metatrutide (GLP-4)

A name that no registry carries

Five databases were queried for this name on 18 August 2026 and four of them answered. PubChem returned PUGREST.NotFound for metatrutide in both the compound and the substance database. The FDA Global Substance Registration System returned a total of zero records; the identical query run against retatrutide returned two, so the endpoint was working. PubMed returned zero, logging the term as a quoted phrase not found. The ClinicalTrials.gov version 2 API returned a totalCount of zero. ChEMBL returned HTTP 500 to every request including control queries for substances that certainly exist, so it contributed nothing here and its silence is not evidence of anything.

Registries do capture names of this class once they are assigned. The retatrutide entry in the FDA system carries CAS 2381089-83-2, INN 12350, USAN JK-35 and UNII NOP2Y096GV, the full apparatus that accumulates around a molecule as it moves through the naming process. Metatrutide carries none of it. Resemblance to retatrutide, mazdutide and the rest of that family is orthographic: the word was built to sit beside them rather than issued by the body that issues those names. Every field in the identity block on this page is therefore null.

The name attaches instead to a small number of product listings and two discussion threads. Those sources describe a lyophilised two-component blend rather than a single molecule, which accounts for the empty registry result. A mixture prepared to order has no reason to hold a registry number. It also means that sequence, formula and molecular mass have no answer in principle, since any answer would depend on which vial was measured.

What the listings describe

Product listings give a composition of 10 mg of a retatrutide-type peptide, written as GLP3-Reta, plus 2 mg of PEG-MGF per vial. A forum thread on the same product describes it as combining GLP-1, GIP, glucagon and PEG-MGF into one blend. One thread participant stated there were no available studies on the blend; that is consistent with what the database searches returned. A further claim in the same thread, that the material had been examined in rabbit and mouse work, traces to nothing and is logged in the unsourced table below. The commercial pages give molecular weight and CAS number as reference dependent, which is not an identifier.

The marketing name presents the blend as GLP-4, the next term in a series. No such term exists. Proglucagon, catalogued by UniProt as P01275, is cleaved into glicentin, glicentin-related polypeptide, oxyntomodulin, glucagon, glucagon-like peptide-1 and glucagon-like peptide-2. The series stops at two. A symbol search of the HGNC gene database returns exactly two approved human genes beginning with GLP: GLP1R and GLP2R. Neither a GLP3 receptor nor a GLP4 receptor is on the human gene register, so the numeral in the name counts nothing that has been described.

A PubMed query for GLP-4 returns 28 records, 20 of them indexed under Caenorhabditis elegans. The nematode gene glp-4 encodes a valyl aminoacyl transfer-RNA synthetase, characterised in a 2015 paper in G3, and is used across the worm literature as a germline-proliferation mutant. Most of the remaining records are string matches inside unrelated abbreviations. A query for glucagon-like peptide-4 returns ten records, none of which describes such a peptide; the matches are token collisions across the incretin and dipeptidyl peptidase-4 literature, together with a 1990 guinea-pig gallbladder study of a glucagon-secretin-like peptide and a GPR119 agonist pharmacology paper. The only GLP-4 in the indexed literature is a worm gene.

The incretin component, as tested on its own

Retatrutide has a published human record and this site logs it separately. In the phase 2 obesity trial reported by Jastreboff and colleagues in the New England Journal of Medicine, 338 adults with a body-mass index of 30 or higher, or 27 to under 30 plus a weight-related condition, received subcutaneous retatrutide or placebo once weekly for 48 weeks. Least-squares mean change in body weight at 48 weeks was −24.2% in the 12 mg group against −2.1% on placebo. Dose-dependent increases in heart rate peaked at 24 weeks and declined afterwards.

In the phase 2 type 2 diabetes trial reported by Rosenstock and colleagues in The Lancet, 281 adults with HbA1c between 7.0% and 10.5% were randomised across placebo, dulaglutide 1.5 mg and six retatrutide regimens. Least-squares mean change in HbA1c at 24 weeks was −2.02% in the 12 mg group, against −0.01% on placebo and −1.41% on dulaglutide. Both trials administered retatrutide as a single molecule, alone, under a fixed escalation schedule, in a monitored setting.

Those conditions matter for what may be carried across. A figure measured on one molecule administered alone describes that molecule administered alone. PubMed returns zero records for retatrutide combined with mechano growth factor and zero for retatrutide combined with IGF-1, so no published work has examined the two together in any system. Trial numbers reproduced beneath a blend name are being moved outside the experiment that produced them.

The growth-factor component, and a replication that failed

Mechano growth factor is the name Goldspink's laboratory gave to a splice variant of IGF-1, IGF-1Ec in humans, whose unique carboxy-terminal E domain yields a 24-residue peptide. The FDA registry holds it as a protein substance under UNII Q86M4KXC2P with sequence YQPPSTNKNTKSQRRKGSTFEERK, formula C121H197N41O40 and a calculated mass of 2868.17. That record carries no CAS number, and the registry holds no entry for any PEGylated form. What the abbreviation MGF denotes therefore shifts between sources: the full splice variant, the 24-residue E peptide, a 25-residue synthetic variant used in tendon work, and a PEGylated derivative that no registry describes.

Kandalla and colleagues reported in Mechanisms of Ageing and Development that the 24-residue E peptide increased the proliferative lifespan of primary human muscle satellite cells and delayed their senescence in cultures from neonatal and young adult donors, but not in cultures from old adult donors. That result sits behind most of the tissue-remodelling language attached to this component on commercial pages. The work was done in culture, on cells taken from donors of different ages, and it measured proliferation, senescence and fusion index rather than anything at the level of a tissue or an animal.

Fornaro and colleagues then attempted to reproduce it. Working across two pharmaceutical companies, they applied the peptide at concentrations up to 500 ng/mL to C2C12 myoblasts, primary human skeletal muscle myoblasts and primary mouse muscle stem cells, and recorded no increase in proliferation and no delay of myotube fusion. Mature IGF-1 and full-length IGF-1Eb produced a proliferative response in the same assays. A separate readout, ERK phosphorylation in cardiac myocytes, also failed to respond to either the native or a stabilised peptide. Their paper closes by questioning whether the E peptide has a physiological role at all.

In vivo rodent work is more favourable and more heterogeneous. Peña and colleagues delivered the E-domain peptide from polymeric microrods injected into mouse myocardium after coronary artery ligation and recorded reduced mortality, an amelioration of the decline in haemodynamics and delayed decompensation against empty microrods; the untreated groups declined by two weeks and decompensated further by ten weeks post-infarct. Riddoch-Contreras and colleagues delivered MGF as a plasmid rather than a peptide into the hindlimb muscles of SOD1(G93A) mice and recorded greater motoneuron survival than with an IGF-I plasmid. One frequently surfaced MGF paper, on nucleus pulposus cell apoptosis, was retracted by Bioscience Reports in August 2024 and remains indexed with its abstract intact.

The half-life figures, and where they come from

Two numbers circulate for this component and they are not compatible. One family of pages states that PEGylation extends the half-life of MGF from minutes to several hours. Another states that it extends it to two or three days, and a forum participant repeated the second figure while reasoning about how it would sit against a weekly incretin. A third figure, five to seven minutes for the unmodified peptide, appears alongside both.

None of the three traces to a measurement. A PubMed search for PEG-MGF returns exactly one record, a 2026 narrative review in Frontiers in Endocrinology that surveys performance-enhancing peptides and describes self-administration practice rather than reporting pharmacokinetics. Searching for pegylation combined with mechano growth factor returns the same single record. Searching mechano growth factor combined with half-life returns one paper, a 2001 review by Goldspink and Yang stating qualitatively that MGF has a shorter half-life in the unbound state than liver-type IGF-1, and giving no figure.

PEGylation is also underspecified everywhere it appears here. Polymer chain length and attachment residue determine what a PEGylated peptide weighs and how it clears, and no listing states either. Thevis and colleagues characterised one grey-market MGF product by mass spectrometry for doping-control purposes and found a protein of 12264.9 Da whose sequence was close to IGF-1Ec but missing the terminal lysine and carrying histidine instead of arginine at position 109. That is the one time material of this kind has been independently analysed in the literature, and it was not the reference sequence.

Nothing has administered the combination

No study has given these two components together. PubMed returns nothing for the pairing, ClinicalTrials.gov holds no registered study of it under any of the names in use, and no preclinical model, cell system or pharmacokinetic characterisation of the mixture appears in the indexed record. The claim implicit in the product name, that four pathways are engaged in a coordinated way, has not been tested in any organism.

Co-formulation raises questions the public record cannot answer. The incretin component is a single 39-residue peptide in the FDA registry record cited here as r14, whose systematic name places a twenty-carbon diacid chain on the lysine at position 17 through a glutamyl-AEEA linker; that peptide and a PEGylated growth-factor derivative lyophilised into one vial have no published compatibility, stability or degradation data as a mixture, and the identity of the second component is not established by any certificate in the public domain. Whether the material in a given vial matches the stated composition is unknown, and the Thevis analysis is the only precedent for checking.

Regulatory position

Retatrutide is investigational. It has not been approved by any regulator for any indication, and the trials above were conducted under investigational supply with controlled identity and purity. Mechano growth factor has never been approved anywhere either, and no registered human trial has administered the E peptide to people. The ClinicalTrials.gov version 2 API, queried on 18 August 2026, returned 487 studies for query.term 'mechano growth factor' and 105 for query.intr; inspection of the interventional records found none administering MGF, IGF-1Ec or the E peptide, the matches being keyword collisions on 'growth factor' across unrelated growth hormone, IGF-1 and exercise trials.

Sport governance treats the two differently. The 2026 WADA Prohibited List, in force from 1 January 2026, names mechano growth factors under S2.3 among growth factors prohibited at all times, alongside IGF-1 and its analogues and thymosin-beta-4 derivatives, and closes the section with a residual clause reaching other growth factors and growth factor modulators that affect muscle, tendon or ligament protein synthesis or degradation, vascularisation, energy utilization, regenerative capacity or fibre type switching. Thevis and colleagues record that the MGF peptide has been prohibited under those regulations since 2005. Neither retatrutide nor any other incretin receptor agonist appears anywhere in the 2026 list; the words glucagon, GLP-1 and incretin do not occur in the document.

Material sold under this name sits outside both frames. It is not an approved medicine, not an investigational supply governed by a protocol, and not a registry-identified substance. The published record establishes nothing about the mixture as sold: not its composition, not its stability, not its behaviour in any organism. Its two named components have never been studied in each other's presence, and one of them has never been given to a person in a registered trial at all.

What is not known

Nothing about this blend as a blend is established. No study has administered its two named components together in any species, cell system or assay; PubMed returns zero records for retatrutide combined with mechano growth factor, and ClinicalTrials.gov holds no registered study under any name in use. There is no published compatibility, stability or degradation data for a 39-residue fatty-acylated incretin peptide and a PEGylated growth-factor derivative lyophilised into one vial, and no pharmacokinetic characterisation of either component in the other's presence. The identity of the growth-factor component is unresolved even in principle: the abbreviation MGF is applied across the literature to the full IGF-1Ec splice variant, a 24-residue E peptide, a 25-residue synthetic variant, and PEGylated derivatives that no registry describes, and no listing states the polymer's chain length or attachment site. Whether any given vial matches its stated composition is unknown, and the only published independent analysis of grey-market material of this kind found a sequence that was close to the reference but not identical to it. The MGF E peptide has never been administered to a person in a registered trial, so no human safety or exposure data exist for it at all. Retatrutide's own record is 48 weeks at longest and comes from investigational supply under a protocol. Neither component is an approved medicine in any jurisdiction, and mechano growth factors are prohibited at all times under the 2026 WADA Prohibited List.

Questions