Shred Stack: mechanism, evidence and research limits

A supplier-defined, formulation-specific research mixture rather than a single compound or an approved medicine. In this site context it is labelled as AOD-9604 (a synthetic 16-amino-acid growth-hormone fragment) plus 5-amino-1MQ (a methylquinolinium small-molecule NNMT inhibitor). It is therefore not ‘a peptide’ in the singular: one proposed component is a peptide and the other is not. AOD-9604: Tyr-hGH177-191, a stabilised C-terminal fragment related to human growth hormone 5-amino-1MQ (5-amino-1-methylquinolinium): an experimental small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT) No named Shred Stack formulation, product information or regulator-reviewed combined-use protocol was identified in the sources reviewed. AOD-9604 was the subject of a 2015 Australian scheduling decision, but scheduling is a control classification, not evidence that a particular product is ARTG-included or approved. The ARTG is the appropriate public register to check a specific product, sponsor or active ingredient at the time of enquiry.

‘Shred Stack’ is best understood as a marketing or supplier label, not as the name of a defined medicine. In the formulation considered here, it combines two very different research materials: AOD-9604, a synthetic peptide fragment derived from the C-terminal region of human growth hormone, and 5-amino-1MQ, which is a small-molecule NNMT inhibitor rather than a peptide. The component studies do not add up to evidence for the mixture. AOD-9604 reduced weight and fat measures in obese mice, while a historical oral human development programme was primarily summarised as tolerability data and did not deliver a meaningful population-level weight-loss result. 5-amino-1MQ changed adipocyte metabolites in vitro and reduced weight and white-fat measures during an 11-day experiment in diet-induced-obese mice. Neither evidence base tests the labelled mixture in people.

Shred Stack is not an international non-proprietary name, an active ingredient or a standardised combination medicine. It is a label that must be tied to the actual ingredients and strengths on a particular product. For this record, the label denotes AOD-9604 plus 5-amino-1MQ. That distinction is fundamental: a study of either component alone, in a different formulation, cannot establish the benefit, safety, quality or administration of their combination. [3] [4] [5] [6]

The word ‘peptide’ is only partly accurate here. AOD-9604 is described in the human safety paper as Tyr-hGH177-191, a synthetic C-terminal human-growth-hormone fragment with an added N-terminal tyrosine. In contrast, the 5-amino-1MQ research programme describes methylquinolinium-scaffold NNMT inhibitors as small molecules. Treating both as interchangeable ‘peptides’ obscures differences in chemistry, absorption, pharmacology and evidence. [2] [3] [5]

AOD-9604 is related to the lipid-metabolism region at the C-terminus of human growth hormone, but it is not full-length 191-amino-acid growth hormone. In the human trial summary, AOD-9604 did not significantly change circulating IGF-1 in the reported studies, which is consistent with it not behaving as a substitute for standard growth-hormone therapy. That observation does not itself prove fat loss, safety in every setting, or equivalence to a supplier vial. [3]

In a primary mouse study, chronic intraperitoneal AOD-9604 treatment for 14 days reduced body weight and body fat in obese mice and was associated with higher beta-3-adrenergic-receptor RNA expression. The same study found that long-term treatment did not produce the weight/lipolysis change in beta-3-receptor knockout mice, yet acute AOD-9604 still increased energy expenditure and fat oxidation in those knockout mice. The authors therefore concluded that the lipolytic actions were not directly mediated through beta-3 receptors, even though receptor expression may contribute to later lipolytic sensitivity. This is careful mouse mechanistic evidence, not a demonstrated human pathway. [4]

NNMT is an enzyme involved in nicotinamide metabolism. In the primary 5-amino-1MQ study, the compound inhibited NNMT in differentiated adipocytes, lowered intracellular 1-methylnicotinamide, increased intracellular NAD+ and S-adenosylmethionine, and suppressed lipogenesis in cell experiments. Those are direct measurements in defined laboratory systems; they do not show that raising NAD+ is a proven fat-loss mechanism in people, nor do they make NAD+ and 5-amino-1MQ interchangeable. [5]

The compound’s small-molecule identity matters clinically and practically. It should not be described as a growth-hormone fragment, a hormone or a coenzyme. Nor does its presence beside AOD-9604 turn the pair into a single mechanism: one component was developed around a growth-hormone-fragment hypothesis, whereas the other targets an intracellular methyltransferase in preclinical work. [3] [5]

The AOD-9604 experiment was an obese-mouse and beta-3-adrenergic-receptor-knockout-mouse study. Its outcomes were body weight, body fat, lipolytic sensitivity, receptor RNA and acute energy/fat-oxidation measures. It did not test people, a mixed AOD-9604/5-amino-1MQ preparation, appetite outcomes in ordinary clinical care, or long-term morbidity and mortality. [4]

The 5-amino-1MQ in-vivo proof-of-concept used 17-week-old male C57BL/6 diet-induced-obese mice that had received a high-fat diet. After 11 days of systemic treatment, the treated group lost about 5.1% of baseline weight while controls gained about 1.4%; food intake was not significantly different. The researchers also reported roughly 35% lower epididymal white-fat mass, smaller adipocytes and lower total cholesterol. This was a small, short mouse experiment (nine animals per group), not a human weight-management trial. [5]

A later mouse study examined 5-amino-1-methylquinolinium together with a switch from a Western to a low-fat diet, focusing on the cecal microbiome and adipose-related metabolites. Because the intervention combined a dietary change with the inhibitor, it cannot isolate a human effect of 5-amino-1MQ or validate adding it to AOD-9604. The authors frame the work as proof-of-concept and a basis for future mechanistic exploration. [6]

A 2013 paper summarised six randomised, double-blind, placebo-controlled AOD-9604 studies: early intravenous and oral safety studies, a 12-week oral phase IIb study in 300 clinically obese adults, and a 24-week oral phase IIb study in 502 obese adults. The 24-week study used oral tablets and a placebo run-in; it was not an injection study and did not contain 5-amino-1MQ. A route, dosage form and investigational supply chain are part of what was studied, not details that can be carried across to a blend vial. [3]

The safety report found adverse-event distributions broadly similar to placebo, no statistically significant between-group differences in IGF-1 or oral-glucose-tolerance measures, and no anti-AOD-9604 antibodies in the tested subset. However, the TGA’s 2015 scheduling reasons state that the obesity programme was discontinued in 2007 because clinical trials did not show a meaningful weight-loss outcome across the trial population. A tolerability finding and an unsuccessful efficacy programme must be read together. [3] [9]

No published controlled human trial of the exact AOD-9604 plus 5-amino-1MQ mixture was identified in the primary studies and regulator records reviewed for this article. There is likewise no formulation-specific human evidence demonstrating additive or synergistic fat loss, lean-mass preservation, appetite effects, adverse-event profile, injection route, dilution method, storage window or administration schedule. [3] [4] [5] [6]

The animal findings cannot establish the safety of long-term exposure, pregnancy use, interactions, cardiovascular outcomes, organ-specific toxicity or rare adverse events in people. The TGA’s scheduling decision specifically noted limited evidence on repeated intravenous or subcutaneous AOD-9604 use and on long-term oral use above clinical-trial amounts. Those are evidence gaps, not proof that every proposed risk will occur. [5] [9]

For a supplier-defined mixture, uncertainty extends beyond pharmacology. Without an evaluated final formulation, individual-component evidence does not establish physical compatibility, stability after preparation, concentration accuracy or sterility of a combined product. TGA guidance warns that unapproved therapeutic goods have not been assessed for quality, safety or effectiveness; its peptide advisory also highlights uncertainties about manufacture, sterility, contents and labelling for unapproved products, especially injectables. [1] [7]

In Australia, a therapeutic good not included in the Australian Register of Therapeutic Goods (ARTG) has not been assessed by the TGA for safety, quality or effectiveness. Defined pathways can allow certain health practitioners to access some unapproved goods after ARTG options have been considered, but such a pathway is not a blanket approval and does not create a standard consumer protocol for Shred Stack. [7]

The public ARTG can be searched by product name, active ingredient, sponsor, licence details or ARTG identifier. A label, a certificate presented by a seller, or the phrase ‘research use only’ is not an ARTG entry. The TGA expressly says that a ‘research use only’ disclaimer does not change a product’s regulatory status or itself permit importation, supply or advertising. [1] [8]

AOD-9604 was placed in Schedule 4 and Appendix D Item 5 in the TGA delegate’s 2015 decision. This historical scheduling decision reflects a recommended level of control; it is not approval of a named AOD-9604 or Shred Stack formulation. Current product and jurisdictional status should be checked from the ARTG and current medicines/poisons information rather than inferred from a 2015 document. [8] [9]

Do not compare an AOD-9604 mouse result, an oral historical AOD-9604 trial and a 5-amino-1MQ mouse result as though they were three dose options for one treatment. Ask first whether the material, model, route, comparator, endpoint and duration match the claim. A mouse change in epididymal fat, for example, is not the same endpoint as clinically meaningful body-weight management in people. [3] [4] [5]

For athletes subject to anti-doping rules, AOD-9604 is explicitly listed by WADA among growth-hormone fragments prohibited at all times. This anti-doping classification is not evidence that it improves performance or fat loss, but it is a separate practical consequence from medical approval. The 2026 list’s S0 category also covers pharmacological substances without current approval by a governmental regulatory health authority for human therapeutic use. [10]

Is Shred Stack an approved medicine in Australia?

No regulator-reviewed Shred Stack formulation or product information was identified in the reviewed materials. The relevant test for a particular product is whether it appears in the ARTG; products outside the ARTG have not been assessed by the TGA for safety, quality or effectiveness. A scheduling decision for AOD-9604 is not an approval of a mixture. [7] [8] [9]

Is Shred Stack actually a peptide?

Not as a whole. In the formulation considered here, AOD-9604 is a synthetic peptide fragment, while 5-amino-1MQ is a small-molecule methylquinolinium NNMT inhibitor. Calling the whole mixture ‘a peptide’ is chemically incomplete. [3] [5]

Do AOD-9604 studies prove that the blend causes fat loss in people?

No. The positive AOD-9604 mechanistic study was in obese mice, and the historical human programme tested oral AOD-9604 alone, not this blend. The TGA’s scheduling reasons report that the obesity programme did not show a meaningful weight-loss outcome across the trial population. [3] [4] [9]

Is there human research on 5-amino-1MQ for weight management?

The primary evidence reviewed here is adipocyte work and short diet-induced-obese mouse experiments. No controlled human trial of 5-amino-1MQ, or of the exact AOD-9604/5-amino-1MQ mixture, was identified in the reviewed primary studies and regulator records. [5] [6]

Can a component study be used to choose a route, dose, dilution or storage method for Shred Stack?

No. The human AOD-9604 studies summarised oral and intravenous trial products, while the 5-amino-1MQ mouse studies used experimental systemic treatment. Neither establishes compatibility, sterility, stability, route or a human administration schedule for the combined supplier-labelled mixture. [3] [5] [6]

Shred Stack is a formulation label, not a fixed pharmacological entity. The reviewed component studies do not establish the contents, quality, compatibility, stability, route or relative exposure of every product using that label. [1] [3] [5] [7]

AOD-9604’s positive mechanistic findings are from mouse work, and its historical human development evidence was for oral or intravenous AOD-9604 alone—not a mixed vial. The cited Australian scheduling rationale reports no meaningful weight-loss outcome across the clinical programme’s overall population. [3] [4] [9]

5-amino-1MQ evidence reviewed here is confined to enzyme/cell work and brief diet-induced-obese mouse experiments. These models cannot determine human effectiveness, optimal exposure, long-term safety or interaction with AOD-9604. [5] [6]

No controlled human study of the exact AOD-9604/5-amino-1MQ mixture was identified in the reviewed sources. This record therefore supplies no administration, dilution, storage, injection, efficacy or combined-use protocol. [3] [4] [5] [6]

Regulatory information can change. The cited TGA scheduling document is a 2015 historical decision; ARTG inclusion and applicable state/territory controls should be checked at the point of use. [7] [8] [9]

1. [1] Understanding your responsibilities when importing, compounding and supplying unapproved peptide products. TGA regulatory and safety guidance, published 13 April 2026.
2. [2] Safety and Metabolism of AOD9604, a Novel Nutraceutical Ingredient for Improved Metabolic Health. Narrative report of AOD9604 genotoxicology, toxicology, pharmacokinetics and historical clinical-development data; Journal of Endocrinology and Metabolism (2014), doi:10.14740/jem213w.
3. [3] Safety and Tolerability of the Hexadecapeptide AOD9604 in Humans. Summary of six randomised, double-blind, placebo-controlled AOD9604 clinical studies, including 12-week (n=300) and 24-week (n=502 randomised) oral phase IIb obesity studies; Journal of Endocrinology and Metabolism (2013), doi:10.4021/jem157w.
4. [4] 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. Obese-mouse and beta-3-adrenergic-receptor knockout-mouse experiment; 14 days of chronic intraperitoneal treatment plus acute metabolic testing; Endocrinology (2001), 142(12):5182-5189, doi:10.1210/endo.142.12.8522.
5. [5] Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Enzyme, permeability and cultured-adipocyte assays plus an 11-day systemic-treatment proof-of-concept in male diet-induced-obese C57BL/6 mice (n=9 per group); Biochemical Pharmacology (2018), 147:141-152, doi:10.1016/j.bcp.2017.11.007.
6. [6] Reduced calorie diet combined with NNMT inhibition induces changes in the intestinal microbiota of diet-induced obese mice. Diet-induced-obese male C57BL/6 mouse study comparing Western-diet/low-fat-diet transitions with or without 5-amino-1-methylquinolinium, with cecal microbiome and metabolic measures; Scientific Reports (2022), doi:10.1038/s41598-021-03670-5.
7. [7] Unapproved therapeutic goods. TGA guidance on goods not included in the ARTG and defined access pathways.
8. [8] Searching the Australian Register of Therapeutic Goods (ARTG). TGA guidance on the public ARTG database and its search fields.
9. [9] Delegates’ final decisions and reasons for decisions — March 2015. TGA delegate’s final scheduling decision and rationale, dated 19 March 2015.
10. [10] 2026 Prohibited List. World Anti-Doping Agency prohibited-substances list, effective 1 January 2026.