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AOD 9604: Complete Research Guide to Selective Lipolysis and Where to Buy

Table of Contents

Growth hormone drives fat metabolism, but it also drives anabolic, diabetogenic, and mitogenic effects that have long limited its usefulness in metabolic research. AOD 9604 was designed at Monash University to separate those functions — isolating the lipolytic fragment of hGH while leaving the confounding activity behind. The result is a compound studied specifically for what researchers call selective lipolysis.

AOD 9604: An Engineered hGH C-Terminal Fragment

AOD 9604 (Anti-Obesity Drug 9604) is a synthetic peptide fragment corresponding to amino acids 176–191 of the C-terminus of human growth hormone (hGH), with an additional tyrosine residue added to the N-terminus to stabilize the fragment’s structure. Developed at Monash University by Professor Matthew Vickers, AOD 9604 was designed to retain hGH’s fat-metabolizing (lipolytic) properties while eliminating the anabolic, diabetogenic, and mitogenic effects associated with full-length GH — the latter of which have limited hGH’s therapeutic applicability in metabolic research.

AOD 9604 has attracted substantial research interest for “selective lipolysis” — targeted fat breakdown in adipose tissue without insulin resistance, muscle anabolism, or IGF-1 elevation. Search volume for “aod 9604 peptide” reflects consistent demand from the metabolic research community.

Mechanism of Action

  • GH Receptor Binding (Partial): AOD 9604 binds a subregion of the GH receptor (GHR) — specifically the domain responsible for lipolytic signaling — without fully activating the anabolic or proliferative pathways triggered by intact hGH
  • β3-Adrenergic Receptor Stimulation: Independent of GHR, AOD 9604 has been shown to stimulate β3-adrenergic receptors on adipocytes, activating hormone-sensitive lipase (HSL) and triglyceride lipase — the enzymes that hydrolyze stored triglycerides
  • Selective Adipose Lipolysis: The resulting fatty acid release occurs predominantly in visceral and subcutaneous adipose tissue, not in skeletal muscle — a crucial distinction for body composition research
  • No IGF-1 Elevation: Does not stimulate hepatic IGF-1 production at research doses, unlike full-length hGH — enabling cleaner mechanistic studies
  • No Insulin Resistance: Does not antagonize insulin signaling at tissue level, a key differentiator from full-length GH
  • Anti-Lipogenic Effect: Inhibits acetyl-CoA carboxylase (ACC), the rate-limiting enzyme in de novo lipogenesis (fat synthesis), simultaneously reducing fat storage while increasing fat breakdown

Clinical and Preclinical Research Data

Phase 2 Clinical Trials (TGA-approved in Australia)

  • AOD 9604 received TGA (Australian equivalent of FDA) approval for clinical trial use in obesity — a significant regulatory milestone for a research peptide
  • Phase 2a trial: Obese adults treated with oral AOD 9604 achieved statistically significant weight loss vs. placebo at 12 weeks
  • Phase 2b trial (METAOD): Demonstrated dose-dependent fat mass reduction; 1mg/day showed best benefit-to-tolerability profile
  • No diabetogenic effects observed across all dose cohorts — confirming the selective lipolysis hypothesis
  • No significant cardiovascular, renal, or hepatic adverse events

Preclinical Obesity Models

  • Obese rodents treated with AOD 9604 lost 50% more fat mass over 12 weeks vs. placebo-treated obese controls
  • Effect was fat-specific: lean mass preserved, muscle mass unchanged
  • Combination with caloric restriction produced additive fat loss effects

Cartilage and Regenerative Research

  • Emerging research (largely unpublished commercially) investigates AOD 9604 in cartilage regeneration, particularly osteoarthritis models
  • Proposed mechanism: hGH C-terminal domain involvement in chondrocyte differentiation and extracellular matrix synthesis

AOD 9604 vs. HGH Fragment 176-191 — Are They the Same?

Parameter AOD 9604 HGH Frag 176-191 (standard)
Sequence Tyr-hGH[176-191] (N-Tyr added) hGH[176-191] (no modification)
Stability Higher (Tyr disulfide cyclization) Lower (linear C-terminal fragment)
Clinical trial history Phase 2 completed (Metabolic Pharma) Primarily preclinical
Research use Clinical-grade lipolysis studies Standard lipolysis research

Dosage Reference for Research

Context Dose Route Duration
Rodent (lipolysis) 100–500 µg/kg SC or IP Daily for 4–12 weeks
Human Phase 2a (oral) 1–10 mg Oral (with food) 12 weeks
SC injection research 250–500 µg/day SC As per protocol
AOD 9604 Research Products

Frequently Asked Questions

What makes the lipolysis “selective”?

Two things. AOD 9604 binds only the GH receptor subregion responsible for lipolytic signaling, leaving anabolic and proliferative pathways largely unengaged — and it does not stimulate hepatic IGF-1 production or antagonize insulin signaling at research doses. Fatty acid release occurs predominantly in visceral and subcutaneous adipose tissue rather than skeletal muscle.

Is AOD 9604 the same as HGH Fragment 176-191?

They share the same core sequence, but AOD 9604 adds an N-terminal tyrosine residue that stabilizes the fragment through disulfide cyclization. AOD 9604 also carries a Phase 2 clinical trial history, whereas standard HGH Frag 176-191 research is primarily preclinical.

What is its regulatory status?

AOD 9604 received TGA approval in Australia for clinical trial use in obesity — a significant regulatory milestone for a research peptide — and completed Phase 2a and 2b programs with no diabetogenic effects observed across dose cohorts.

Research reference only. AOD 9604 from Core Power Peptides is intended for in vitro and laboratory use — not for human consumption, and not medical advice.

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