What the Evidence Says About Peptide Stacks for Weight Loss
The marketed peptide stacks for weight loss all run ahead of the evidence, so this article maps each compound to its actual record, from published human trials to nothing at all.
The marketed peptide stacks for weight loss all run ahead of the evidence, so this article maps each compound to its actual record, from published human trials to nothing at all.
The question underneath the article is simple, because the word “stack” now appears in weight-loss marketing everywhere while the science behind it remains scattered across registries and decades of literature, and the honest answer after reading every reachable trial and registration is that the evidence sits with single agents and with registered combinations of tested drugs, while each marketed stack carries an evidence label of its own.
I · The phrase with no literature
The word “stack” reaches weight loss from bodybuilding forums and online vendors, which means most readers meet it as a shopping list of injectable peptides long before they meet it as a scientific term, and that ordering matters because the scientific literature has no record of the concept at all.
Every marketed peptide stack discussed online today has zero human clinical evidence behind the combination itself.
A PubMed search for the phrases “peptide stack” and “peptide stacking” returns eight hits, and every one belongs to an unrelated field such as ribosome chemistry or cancer nanozymes, so the phrase carries no scientific meaning in this context. 1 The closest thing the research world has to stacking is the co-administration of tested agents inside registered trials, and those trials exist, which makes the gap between the registered versions and the marketed versions easy to measure. In REDEFINE 1, Garvey and colleagues tested cagrilintide plus semaglutide in 3,417 adults with overweight or obesity and reported a mean weight change of -20.4% at 68 weeks against -3.0% in the placebo arm, 2 whereas Heymsfield and colleagues reported in the BELIEVE trial that bimagrumab plus semaglutide produced a change of -17.8 kg at 48 weeks in 507 participants compared with -14.2 kg for semaglutide alone and -3.3 kg for placebo. 3
“from regulatory-grade randomized trial data to a complete absence of human studies” 4
Dominikowski, Frontiers in Endocrinology, 2026
The expert literature on the unregulated market reaches the same verdict from a different angle, because Villegas Meza and colleagues concluded in a 2026 sports medicine review that injectable peptides in that setting remain largely experimental, with uncertain safety profiles and product quality concerns sitting under widespread antidoping restrictions. 5 The honest census of the marketed stacks is shorter than the marketing, since the GLP-1 plus testosterone plus growth hormone trinity, the GLP-1 plus MOTS-c pairing, the GLP-1 plus tesamorelin pairing, and the retatrutide plus tesamorelin pairing each have zero registered combination studies, and the same registry and literature queries return zero for semaglutide plus ipamorelin and for tirzepatide plus tesamorelin. 6
CagriSema is itself a two-peptide combination, since cagrilintide is an amylin analogue and semaglutide is a GLP-1 receptor agonist, so “stacking” in the registered sense means pairing agents that each cleared its own trial gauntlet before the two ever met in a protocol.
II · The rationale that drives stacking
The impulse to stack grows out of a real observation, because meta-analyses of the incretin trials show that a meaningful share of the weight lost on these drugs is lean tissue, which gives the whole category a problem that a second compound might address.
The stacking impulse rests on a measured endpoint, since roughly a quarter to nearly two fifths of the weight lost on incretin therapy is lean mass, and no stack has been tested against that endpoint.
Two 2026 meta-analyses put numbers on the phenomenon: Laverde and colleagues pooled randomized controlled trials of GLP-1 receptor agonists at obesity doses, and Eisa and Barood compared lean mass changes on incretin therapy against lifestyle intervention, and the two reviews converge on the same shape, because absolute lean mass falls by a pooled -1.74 kg and by -5.44 kg for semaglutide while the lean fraction of total weight improves by 1.81 points. 7 8 The proportion of lost weight that comes from lean tissue falls between 25% and 39% on incretin therapy, which sits close to the 26.2% measured in lifestyle-based weight loss and well above the 17.5% seen when resistance training is part of the program, 8 so the muscle question is real even though the popular idea that these drugs somehow melt muscle oversimplifies a more layered picture. 7 The clinical stakes are also real, because losing skeletal muscle alongside fat changes metabolic rate, physical function, and the long-term shape of the weight lost, which is why the endpoint is worth protecting even while the tools for protecting it remain unproven. 7
The rationale for stacking follows from those numbers, because Arora and colleagues reviewed the pharmacologic options under study for preserving lean body mass during weight loss and named bimagrumab, tesamorelin, and enobosarm as the active classes, 9 which means the impulse to add a second agent has a legitimate scientific target even where the specific marketed combinations have no data. The phase 3 programs behind the incretin class, which include the STEP trials for semaglutide and the SURMOUNT-4 continuation trial for tirzepatide, established the weight-loss endpoints that these meta-analyses pool, so the lean-mass figures carry the full weight of the class’s human record, 10 and the open question is therefore which of the untested combinations could plausibly move the absolute number, a question the literature cannot answer because every candidate stack remains unstudied in humans.
The distinction matters because the two numbers describe different problems, since a stack aimed at preserving absolute lean mass is targeting something else entirely from a stack aimed at the lean fraction, and the marketed combinations rarely say which endpoint they claim to protect.
III · The trinity stack, leg by leg
The most circulated stack in the weight-loss internet is the trinity of a GLP-1 drug plus testosterone plus growth hormone, so the honest way to read it is leg by leg, because the three ingredients carry three different evidence histories and the combination carries none.
Two of the three trinity ingredients have human data individually, yet the three-way combination appears in no published randomized trial and no registered protocol.
The first leg, the GLP-1 class, carries the bulk of the human evidence in this space, since semaglutide and tirzepatide built their phase 3 records on programs such as STEP and SURMOUNT-4, 10 and the second leg, testosterone, has its own human literature in men with low testosterone, so the pairing question becomes whether combining the two has been tested, which Canal de Velasco and colleagues took up in a narrative review in Cureus.
“no randomized trials have directly evaluated the combined effects of GLP-1 RAs and TRT on body composition outcomes. The available evidence suggests a biologically plausible interaction but does not support routine combined therapy” 11
Canal de Velasco, Cureus, 2026
The human data that exists for the pairing is indirect and small, because Giagulli and colleagues reported a retrospective series of 43 obese diabetic men with overt hypogonadism in which adding liraglutide to testosterone plus metformin produced significant weight reduction over a second treatment year compared with testosterone plus metformin alone, 12 and Portillo-Canales and colleagues analyzed electronic health records from 215 men and found that incretin-based weight loss was associated with total testosterone rising from 332 to 399 ng/dL and the normal-range proportion climbing from 67% to 86%. 13 The direction of causation deserves care, since weight loss itself is associated with rising testosterone in men, which means the 332 to 399 ng/dL shift may track the weight change as much as the drugs, and a completed phase 4 trial of testosterone plus liraglutide in 30 obese hypogonadal men finished in 2015, though the reviewers who catalogued it never located its results. 14 The growth hormone leg rests on thinner ground, because the single published combination experiment, Swarbrick and colleagues in Endocrinology, Diabetes and Metabolism, found that growth hormone treatment did not augment the anti-diabetic effects of liraglutide in UCD-T2DM rats, 15 and the one registered human trial of a long-acting growth hormone with a GLP-1 drug, a phase 4 open-label study of PEG-rhGH plus semaglutide against semaglutide alone in 212 non-diabetic obese adults at Shanghai Zhongshan Hospital, has not started recruiting. 16
The 43-man cohort and the 215-man record review are associations, because a retrospective series cannot randomize who receives which treatment, so the testosterone rise may reflect the weight loss as much as the drugs, and neither dataset can speak to the three-way combination at all.
The honest label for the full trinity is “none”, since the three-way combination appears in no published trial and no registered protocol as of the verification date, and the only registered step toward any leg of it, the PEG-rhGH plus semaglutide study, has yet to enroll a single participant.
IV · Tesamorelin, the deep record in one population
Tesamorelin is the only compound in this article with phase 3 human data, so the interesting question is where that evidence was gathered, because the answer narrows the population and explains why the compound shows up in stack marketing at all.
Tesamorelin’s phase 3 record is deep and narrow, since every published result comes from HIV patients with antiretroviral-associated abdominal fat, and its combination with any GLP-1 drug appears in no trial.
Tesamorelin is a growth hormone releasing hormone analogue, which means it works by amplifying the endogenous pulse of growth hormone, and its principal data come from Julian Falutz and colleagues, whose 2007 trial in the New England Journal of Medicine treated 412 HIV patients with excess abdominal fat for 26 weeks and measured a -15.2% change in visceral adipose tissue against +5.0% on placebo, with triglycerides moving -50 versus +9 mg/dL, on the strength of which the compound gained FDA approval for HIV-associated abdominal fat accumulation. 17 A pooled analysis of two phase 3 trials by the same group, covering 806 patients of whom 543 received tesamorelin, reported a visceral fat treatment effect of -15.4% at week 26 and -17.5% at week 52 among continuous users, 18 and a separate 404-patient randomized trial with a safety extension reported changes of -10.9% against -0.6% at 6 months, with the visceral fat loss reversing when patients crossed over to placebo. 19
That evidence is locked to one population, because every phase 3 participant was living with HIV and its antiretroviral therapy, so tesamorelin’s behavior in general obesity remains an open question, 20 even though Stanley and colleagues found in JAMA that the compound also reduced liver fat in HIV patients, with a median lipid-to-water change of -2.0% against +0.9% on placebo. 21 The combination record is empty in the same way, since ClinicalTrials.gov returns zero studies pairing tesamorelin with any GLP-1 receptor agonist and PubMed shows no combination study either. 22
All of tesamorelin’s phase 3 data were collected in HIV patients with antiretroviral-associated central fat, so extrapolating the visceral fat numbers to general obesity goes beyond what the read data support, and a registered non-HIV liver fat trial has no published results as of the verification date. 20
The label for the GLP-1 plus tesamorelin stack is “none” as a combination, since each leg on its own carries human evidence while the pair appears in no registered trial and no published study.
V · Retatrutide, the phase 2 record with no combination studies
Retatrutide arrives in the stack conversation with a distinctive set of phase 2 numbers, so the natural question is whether pairing it with tesamorelin has any basis in the registry, and the search returns a clean zero.
In its phase 2 trial, retatrutide produced roughly a quarter of body weight loss at 48 weeks in the highest dose arm, and no registered or published study pairs it with any second agent.
Ania Jastreboff and colleagues published the phase 2 trial in the New England Journal of Medicine, enrolling 338 adults with obesity and reporting least-squares mean weight changes at 48 weeks of -8.7% at the 1 mg dose, -17.1% at 4 mg, -22.8% at 8 mg, and -24.2% at 12 mg against -2.1% on placebo, with dose-dependent gastrointestinal events and transient heart rate increases accompanying the response. 23 These are single-trial figures that describe what one phase 2 cohort measured, so the later phases of the program will determine whether the effect survives replication, and retatrutide runs an extensive trial program of its own, with fifteen registered studies, mostly completed early-phase work. 23
The retatrutide plus tesamorelin pairing, meanwhile, appears in no PubMed record and no ClinicalTrials.gov study, 24 which makes it a pure internet construct in the strictest sense, since neither the sponsor nor any academic group has registered a protocol for the pair, and no figure of any kind exists for the combination to compare against the phase 2 numbers. 23
The phrasing matters because -24.2% at 48 weeks in the 12 mg arm is a single-arm figure from one phase 2 trial, so describing it as roughly a quarter of body weight loss keeps the claim inside what Jastreboff and colleagues measured.
The label for this stack is “none”, since both legs carry human data separately and the pair has none at all, which means the retatrutide plus tesamorelin idea lives in marketing.
VI · MOTS-c and AOD-9604, two different evidence clocks
Two compounds often sold as GLP-1 stack partners come from opposite ends of the evidence timeline, since MOTS-c is entering human testing for the first time while AOD-9604’s human claims rest on a two-decade-old industry note.
MOTS-c has mouse data and one recruiting human trial, whereas AOD-9604 has rodent data and no published human result in its twenty-plus year history.
Changhan Lee and Pinchas Cohen’s group identified MOTS-c as a 16-amino-acid peptide encoded in a short open reading frame of the mitochondrial 12S ribosomal RNA, and their 2015 Cell Metabolism paper reported that treating mice with it prevented age-dependent and high-fat-diet-induced insulin resistance as well as diet-induced obesity, with the mechanism running through folate cycle and purine biosynthesis inhibition into AMPK activation. 25 The first human study, a phase 2 trial for improving insulin sensitivity in adults with prediabetes and overweight or obesity, opened in February 2026 and is recruiting 120 participants for daily subcutaneous dosing over 12 weeks under the sponsor Hudson Biotech, with a primary completion date in February 2027. 26 The GLP-1 plus MOTS-c pairing, meanwhile, appears in no registered trial and no published study, 27 so the stack exists only in marketing even as the single compound begins its first human readout, and the mechanistic story is what carries that marketing, because a peptide that activates AMPK sounds like a metabolic lever worth adding to a GLP-1 drug.
“prevented age-dependent and high-fat-diet-induced insulin resistance, as well as diet-induced obesity” 25
Lee, Cell Metabolism, 2015
AOD-9604 is a synthetic analogue of the lipolytic C-terminal domain of human growth hormone, sometimes written as hGH 176-191, and its entire weight-loss record is rodent, since Ng and colleagues reported in Hormone Research that oral AOD-9604 at 500 µg per kilogram per day for 19 days cut weight gain by more than half in obese Zucker rats without disturbing insulin sensitivity on euglycemic clamp, 28 and Heffernan and colleagues found in Endocrinology that 14 days of the compound reduced body weight and fat in obese mice through beta-3 adrenergic receptor signaling. 29 An industry note from 2004 said phase IIa testing was underway by February 2002, 30 and no results from that program were ever published, and no trial of the compound is registered today, 31 which leaves AOD-9604 with a two-decade-old claim and no human data trail, plus a place on the World Anti-Doping Agency prohibited list that follows from its position inside the growth hormone sequence. 32
The MOTS-c trial is run by Hudson Biotech, a commercial sponsor, so the first human data on the compound will carry industry fingerprints, and the same sponsorship question applies to 5-amino-1MQ research, which carries authors from the developing company Ridgeline Therapeutics.
The labels here divide along clear lines, because MOTS-c alone now carries a “registered human trial, no results” status while the GLP-1 plus MOTS-c stack carries “none”, and AOD-9604 carries “preclinical only” with a prohibited-in-sport flag attached.
VII · The metabolic modulators sold alongside peptides
The most telling pattern on the peptide shelves is that several of the best-selling stack ingredients are synthetic small molecules sitting outside the peptide class, so their evidence has to be read on its own terms, and all of it stops at the mouse.
SLU-PP-332, 5-amino-1MQ, and BAM-15 each have mouse data and zero human trials, and two of the three are small-molecule drugs rather than peptides.
SLU-PP-332 is a synthetic pan-agonist of the three estrogen-related receptors ERR-alpha, ERR-beta, and ERR-gamma, developed as an exercise mimetic, and the foundational work by Billon and colleagues showed in 2023 that the compound induces an ERR-alpha-dependent acute aerobic exercise response and enhances exercise capacity in mice, followed by a 2024 report that a synthetic ERR agonist alleviates metabolic syndrome in the same species. 33 A 2026 systematic review covering pan-ERR agonists such as SLU-PP-332 and SLU-PP-915 concludes on preclinical models only, 34 and ClinicalTrials.gov holds zero registered studies of the compound, 35 while doping-control laboratories are already building assays for it because exercise mimetics and metabolic modulators are prohibited in sport, 36 which means the exercise-mimetic framing that sells the molecule is also the reason it sits on the anti-doping radar.
5-amino-1MQ is a small-molecule inhibitor of the enzyme nicotinamide N-methyltransferase, and the biology behind it goes back to Kraus and colleagues, whose 2014 Nature paper showed that knocking down NNMT protected mice against diet-induced obesity. 37 The follow-up pharmacology stays in rodents, because Dimet-Wiley and colleagues reported in Scientific Reports that the inhibitor plus a low-fat diet promoted dramatic whole-body adiposity and weight loss, normalizing diet-induced obese mice to age-matched lean controls, 38 and Babula and colleagues, whose author list includes people from Ridgeline Therapeutics, found that once-daily dosing for 28 days improved body composition and metabolic variables and reduced fatty liver pathology. 39 A separate 2024 report from Dimet-Wiley and colleagues found that NNMT inhibition mimics and boosts exercise-mediated muscle improvements in aged mice, 40 no human study of 5-amino-1MQ is registered, 35 and the only human-derived data connected to the compound’s biology sit in oncology cell experiments, which is a different question entirely from weight management. 41
“promoted dramatic whole-body adiposity and weight loss” 38
Dimet-Wiley, Scientific Reports, 2022
BAM-15 is a small-molecule mitochondrial uncoupler, a compound that dissipates the proton gradient so that energy burns as heat, and Axelrod and colleagues showed in EMBO Molecular Medicine that the compound protects against obesity and improves glycemic control in high-fat-diet mice, reducing body weight and fat while improving glucose handling. 42
“BAM15-mediated mitochondrial uncoupling protects against obesity and improves glycemic control” 42
Axelrod, EMBO Molecular Medicine, 2020
The follow-up literature stays in animals and cells, with reports on breast cancer growth suppression, liver lipid metabolism through AMPK, atherosclerosis in ApoE-knockout mice, and microneedle delivery in obese mice, 43 and the human record is empty, since the only ClinicalTrials.gov hit for the name BAM-15 is a COVID-19 antibody trial of bamlanivimab, a different molecule with a similar name. 44
Searches for BAM-15 surface exactly one trial, NCT04634409, which tests the COVID-19 antibody bamlanivimab, so the compound is sometimes marketed as though human-tested on the strength of a database name collision. 44
Read the shelves against those labels and the picture resolves into a single statement: the approved and registered agents produce large weight loss on their own, the combinations that pair tested agents inside registered trials carry human numbers, and every marketed stack built from untested second compounds remains exactly that, untested, so the open question for the next few years is which registered combination trials report first, since the PEG-rhGH plus semaglutide study, the bimagrumab plus tirzepatide programs, and the first MOTS-c readout all have completion dates ahead of them, and those results may settle whether any of the marketed stacks ever earns a human evidence label. 45
- PubMed searches for “peptide stack”, “peptide stacking”, and “stacked peptides”, run live 2026-08-19: eight hits, all in unrelated fields (ribosome chemistry, biomaterials, cancer nanozymes). No indexed literature uses the phrase as a weight-loss concept.
- Garvey, W.T. et al. “Coadministered cagrilintide and semaglutide in adults with overweight or obesity (REDEFINE 1).” New England Journal of Medicine, 2025. n=3,417; mean weight change -20.4% vs -3.0% placebo at 68 weeks.
- Heymsfield, S.B. et al. “Bimagrumab plus semaglutide alone or in combination for the treatment of obesity: a randomized phase 2 trial (BELIEVE).” Nature Medicine, 2026. n=507; -17.8 kg vs -14.2 kg (semaglutide) vs -3.3 kg (placebo) at 48 weeks.
- Dominikowski, A. et al. “The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration.” Frontiers in Endocrinology, 2026.
- Villegas Meza, A.D. et al. “Injectable peptides in sports medicine: a structured narrative review of evidence, safety, and antidoping implications.” JBJS Reviews, 2026.
- Live ClinicalTrials.gov and PubMed queries, verified 2026-08-19: zero registered or published combination studies for the GLP-1+TRT+GH trinity, GLP-1+MOTS-c, GLP-1+tesamorelin, retatrutide+tesamorelin, semaglutide+ipamorelin, and tirzepatide+tesamorelin.
- Laverde, L.P. et al. “Effect of GLP-1 receptor agonists at doses for obesity management on muscle health: systematic review and meta-analysis of RCTs.” International Journal of Obesity, 2026. Absolute lean mass -1.74 kg pooled; semaglutide -5.44 kg; lean fraction +1.81 points.
- Eisa, N. and Barood, O. “Lean mass changes with incretin therapy versus lifestyle intervention: systematic review and meta-analysis of RCTs.” Diabetes, Obesity and Metabolism, 2026. Proportion lost as lean mass 25-39% (incretin) vs 26.2% (lifestyle) vs 17.5% (resistance training).
- Arora, G. et al. “Pharmacologic treatments for the preservation of lean body mass during weight loss.” Journal of Clinical Medicine, 2026. Names bimagrumab, tesamorelin, and enobosarm as the classes under study.
- Class-level human evidence for the GLP-1 receptor agonist class: multiple phase 3 randomized controlled trials, including the STEP program for semaglutide and the SURMOUNT-4 continuation trial for tirzepatide.
- Canal de Velasco, L.M. et al. “Testosterone replacement therapy as a potential strategy to preserve lean mass in men with persistently low serum testosterone receiving GLP-1 receptor agonists: a narrative review.” Cureus, 2026.
- Giagulli, V.A. et al. “Adding liraglutide to lifestyle changes, metformin and testosterone therapy boosts erectile function in diabetic obese men with overt hypogonadism.” Andrology, 2015. Retrospective, n=43.
- Portillo-Canales, S. et al. “Effect of incretin-based weight loss drugs on testosterone concentrations in men.” Endocrine Practice, 2026. Electronic health records, n=215; total testosterone 332 to 399 ng/dL; normal-range proportion 67% to 86%.
- ClinicalTrials.gov NCT03619330. Testosterone plus liraglutide vs testosterone in obese hypogonadal men, phase 4, n=30, completed 2015; results not located in this review.
- Swarbrick, M.M. et al. “Growth hormone treatment does not augment the anti-diabetic effects of liraglutide in UCD-T2DM rats.” Endocrinology, Diabetes and Metabolism, 2023. PMID 36480511.
- ClinicalTrials.gov NCT06863363. PEG-rhGH + semaglutide vs semaglutide monotherapy, phase 4, open-label, n=212, non-diabetic obese adults, Shanghai Zhongshan Hospital; status not yet recruiting.
- Falutz, J. et al. “Metabolic effects of a growth hormone-releasing factor in patients with HIV.” New England Journal of Medicine, 2007. n=412, 26 weeks; visceral adipose tissue -15.2% vs +5.0% placebo; triglycerides -50 vs +9 mg/dL. Basis for FDA approval in HIV-associated abdominal fat accumulation.
- Falutz, J. et al. “Effects of tesamorelin (TH9507), a growth hormone-releasing factor analog, in HIV-infected patients with excess abdominal fat: pooled analysis of two phase 3 trials.” Journal of Clinical Endocrinology and Metabolism, 2010. n=806 (543 tesamorelin / 263 placebo); visceral fat treatment effect -15.4% at week 26, -17.5% at week 52 in continuous users.
- Falutz, J. et al. “Effects of tesamorelin in HIV-infected patients with abdominal fat accumulation: randomized placebo-controlled trial with safety extension.” Journal of Acquired Immune Deficiency Syndromes, 2010. n=404; visceral fat -10.9% vs -0.6% at 6 months; loss reversed on switching to placebo.
- Tesamorelin’s phase 3 record is exclusively in HIV patients with antiretroviral-associated abdominal adiposity; a registered non-HIV liver fat trial (NCT07481734) has no published results as of the verification date.
- Stanley, T.L. et al. “Effect of tesamorelin on visceral fat and liver fat in HIV-infected patients with abdominal fat accumulation: a randomized clinical trial.” JAMA, 2014. Liver fat median lipid-to-water -2.0% vs +0.9% placebo, n=50.
- ClinicalTrials.gov query for tesamorelin combined with any GLP-1 receptor agonist: 0 studies; PubMed: no combination study, verified 2026-08-19.
- Jastreboff, A.M. et al. “Triple-hormone-receptor agonist retatrutide for obesity: a phase 2 trial.” New England Journal of Medicine, 2023. n=338; least-squares mean weight change at 48 weeks -8.7% (1 mg), -17.1% (4 mg), -22.8% (8 mg), -24.2% (12 mg) vs -2.1% placebo; dose-dependent gastrointestinal events and transient heart rate increases. Retatrutide trial program: 15 registered studies, mostly completed early-phase.
- PubMed “tesamorelin AND retatrutide”: 0 hits; ClinicalTrials.gov: 0 studies, verified 2026-08-19.
- Lee, C. et al. “The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance.” Cell Metabolism, 2015. 16-amino-acid peptide encoded in mitochondrial 12S rRNA short open reading frame; mechanism via folate cycle and purine biosynthesis inhibition to AMPK activation.
- ClinicalTrials.gov NCT07505745. “MOTS-c for Improving Insulin Sensitivity in Adults With Prediabetes and Overweight/Obesity.” Phase 2, recruiting, sponsor Hudson Biotech (industry), n=120, subcutaneous daily for 12 weeks, primary completion February 2027.
- ClinicalTrials.gov “MOTS-c AND (semaglutide OR GLP-1 OR tirzepatide)”: returns only an unrelated GLP-1/SGLT2 biomarker trial; PubMed: no combination study, verified 2026-08-19.
- Ng, F.M. et al. “Metabolic studies of a synthetic lipolytic domain (AOD9604) of human growth hormone.” Hormone Research, 2000. Obese Zucker rats; oral 500 µg/kg/day for 19 days cut weight gain by more than half; no adverse effect on insulin sensitivity by euglycemic clamp.
- Heffernan, M. et al. “The effects of human GH and its lipolytic fragment (AOD9604) on lipid metabolism following chronic treatment in obese mice and beta-3-AR knock-out mice.” Endocrinology, 2001. 14 days; effects tied to beta-3 adrenergic receptor expression.
- Wilding, J. “AOD-9604 metabolic.” Current Opinion in Investigational Drugs, 2004. Industry note: phase IIa trials underway by February 2002; no published human results.
- ClinicalTrials.gov queries “AOD-9604” and “AOD 9604”: 0 studies, verified 2026-08-19.
- AOD-9604 is on the WADA prohibited list: Thomas, A. et al. “Simplifying and expanding the screening for peptides <2 kDa by direct urine injection, LC, and ion mobility mass spectrometry." Journal of Separation Science, 2016; Thevis, M. et al. "Detecting peptidic drugs, drug candidates and analogs in sports doping." Expert Review of Proteomics, 2014.
- Billon, C. et al. “Synthetic ERR-alpha/beta/gamma agonist induces an ERR-alpha-dependent acute aerobic exercise response and enhances exercise capacity.” ACS Chemical Biology, 2023. PMID 36988910; and “A synthetic ERR agonist alleviates metabolic syndrome.” Journal of Pharmacology and Experimental Therapeutics, 2024. PMID 37739806. Mouse models.
- de Souza-Lima, J. et al. “Pharmacological activation of ERR-alpha/beta/gamma as an exercise mimetic: potential therapeutic applications.” Revista Medica de Chile, 2026. PMID 42024694. Systematic review limited to preclinical models.
- ClinicalTrials.gov: 0 registered studies for SLU-PP-332 and for 5-amino-1MQ, verified 2026-08-19.
- Doping-control assays for SLU-PP-332 and SLU-PP-915: Avliyakulov, N.K. et al. Drug Testing and Analysis, 2026; Möller, T. et al. Rapid Communications in Mass Spectrometry, 2026. Exercise mimetics and metabolic modulators are prohibited in sport.
- Kraus, D. et al. “Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity.” Nature, 2014.
- Dimet-Wiley, A. et al. “Reduced calorie diet combined with NNMT inhibition establishes a distinct microbiome in DIO mice.” Scientific Reports, 2022. “Promoted dramatic whole-body adiposity and weight loss”; DIO mice normalized to age-matched lean controls.
- Babula, J.J. et al. “Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction.” Diabetes, Obesity and Metabolism, 2024. DIO mice, once-daily 5-amino-1MQ for 28 days; authors from Ridgeline Therapeutics (industry).
- Dimet-Wiley, A.L. et al. “Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice.” Scientific Reports, 2024.
- Human cell work on NNMT inhibition is oncology-oriented: Akar, S. et al. “Small molecule inhibitor of nicotinamide N-methyltransferase shows anti-proliferative activity in HeLa cells.” Journal of Obstetrics and Gynaecology, 2021.
- Axelrod, C.L. et al. “BAM15-mediated mitochondrial uncoupling protects against obesity and improves glycemic control.” EMBO Molecular Medicine, 2020. High-fat-diet mice: reduced body weight and fat, improved glucose handling.
- Follow-up BAM-15 work, all preclinical: Zunica, E.R.M. et al. Cancer & Metabolism, 2021; Liu, Z. et al. FEBS Journal, 2026; Zhong, S. et al. Atherosclerosis, 2025; Zeng, F. et al. Advanced Healthcare Materials, 2026.
- ClinicalTrials.gov query “BAM-15”: exactly one study, NCT04634409, a COVID-19 antibody trial of bamlanivimab (name collision, unrelated molecule). No human trial of BAM-15 exists, verified 2026-08-19.
- Bimagrumab plus tirzepatide registrations: NCT06643728 (active, not recruiting) and NCT06890611 (completed); results not read in this review.