Lean Stack (HGH Fragment + IGF-1)
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Lean Stack (HGH Fragment + IGF-1)

Original price was: €109,90.Current price is: €96,17.

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HGH Fragment 176-191
1 × HGH Fragment 176-191

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Original price was: €39,95.Current price is: €34,96.
IGF-1 LR-3
1 × IGF-1 LR-3

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Original price was: €69,95.Current price is: €61,21.

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Description

Lean Stack — HGH Fragment 176-191 + IGF-1 LR3 Bundle

De Lean Stack is the scientific designation for the HGH Fragment 176-191 + IGF-1 LR3 bundle — a research kit targeting two complementary pathways of body composition. HGH Fragment 176-191 stimulates selective lipolysis without IGF-1 elevation or insulin resistance. IGF-1 LR3 directly activates the IGF-1 receptors on muscle tissues for muscle growth and fat oxidation. As a result, the Lean Stack both fat regulation research and muscle mass preservation via two separate biological pathways.

Moreover, the combination rationale is strongly scientifically substantiated. HGH Fragment 176-191 decouples the lipolytic action of growth hormone from the anabolic and glucose-metabolic effects — allowing researchers to study fat burning without IGF-1 elevation confounders. IGF-1 LR3 complements this by activating direct anabolic signaling in muscle tissue — precisely the pathway that the fragment does not stimulate. Thus, the two peptides together offer a unique dual-pathway research model for body composition.

What is the Lean Stack?

The Lean Stack combines two peptides that each address a different aspect of body composition. HGH Fragment 176-191 focuses exclusively on fat metabolism — it stimulates lipolysis in fat cells without the growth and glucose effects of full growth hormone. IGF-1 LR3 focuses on the anabolic side — it activates IGF-1 receptors directly in muscle tissue for cell growth, protein synthesis, and fat oxidation. In this way, the two peptides complement each other without mechanistic overlap.

Specifically, this is the most relevant distinction of the Lean Stack from other GH-related stacks. Complete growth hormone (HGH) increases both IGF-1 and fat burning, but also causes insulin resistance and hyperglycemia. HGH Fragment 176-191 offers the lipolytic action without those metabolic side effects. As a result, researchers can study lipolysis and muscle preservation independently of IGF-1 signaling.

HGH Fragment 176-191: Selective Lipolysis without IGF-1 Elevation

HGH Fragment 176-191 is a synthetic peptide that replicates the C-terminal region of the human growth hormone molecule (amino acids 176–191). Researchers identified that this region harbors the fat-burning properties of GH — without the primary GH receptor binding sites required for IGF-1 induction and cell proliferation.

At the molecular level, HGH Fragment 176-191 acts via beta-3 adrenergic receptors on fat cell membranes. Activation of these receptors triggers hormone-sensitive lipase (HSL) and adipose triglyceridenase (ATGL) via the cAMP-dependent protein kinase A pathway. As a result, fat cells break down stored triglycerides into free fatty acids and glycerol for energy consumption. Simultaneously, the peptide inhibits lipogenesis—the production of new adipose tissue.

Furthermore, the safety rationale is particularly relevant for research. Full GH increases IGF-1, causes hyperglycemia, and activates cell proliferation. HGH Fragment 176-191 does not do any of that. As a result, it offers researchers an isolated fat metabolism model — without the confounders of full GH use.

Research applications HGH Fragment 176-191

  • Selective lipolysis via beta-3 adrenergic receptor activation in fat cells
  • Inhibition of lipogenesis — study of fat storage prevention
  • Fat metabolism study without IGF-1 elevation or insulin resistance
  • Isolation of lipolytic GH pathways from proliferative and glucose effects
  • Comparative study: Fragment vs. full GH in metabolic models

Scientific References — HGH Fragment 176-191

  • Heffernan MA, et al. Increase of fat oxidation and weight loss in obese mice caused by treatment chronic with human growth hormone or a modified C-terminal fragment. Int J Obes Relat Metab Disord. 2001;25(10):1442–9. PubMed PMID 11673762
  • Ng FM, et al. Metabolic studies of a growth hormone-releasing peptide (AOD9604) with anti-obesity effects in humans. Arch Biochem Biophys. 2000;380(2):256–62. PubMed PMID 10933079
  • Alpha Carbon Labs. HGH Fragment 176-191 vs. Adipotide: Targeted Adipose Reduction Comparative Mechanisms. 2025. Alpha Carbon Labs 2025

IGF-1 LR3: Direct Anabolic Signaling in Muscle Tissue

IGF-1 LR3 (Insulin-like Growth Factor 1 Long Arg3) is a synthetic variant of human IGF-1, modified with a 13-amino acid N-terminal extension (including Arg3) that significantly reduces binding to IGF-binding proteins (IGFBPs). As a result, IGF-1 LR3 remains unbound and active in circulation — with a half-life of 20–30 hours compared to only 15–20 minutes for native IGF-1.

At the molecular level, IGF-1 LR3 binds directly to IGF-1 receptors on muscle tissues. To do so, it activates the PI3K/Akt and MAPK signaling pathways—pathways that are essential for cell growth, protein synthesis, and lipid oxidation. Furthermore, IGF-1 LR3 stimulates satellite cell activation and muscle hypertrophy via two routes: hyperplasia (increase in muscle cells) and mitogenesis (production of new muscle fibers).

Furthermore, the favorable binding pharmacology of IGF-1 LR3 is scientifically relevant. Native IGF-1 has a high affinity for IGFBPs, which limit its activity. IGF-1 LR3 largely bypasses this limitation—resulting in a more direct and controlled anabolic response. This offers researchers a precise tool for IGF-1 receptor biology research.

Research applications IGF-1 LR3

  • Direct IGF-1 receptor activation in skeletal muscle tissue
  • PI3K/Akt and MAPK signaling pathways for protein synthesis and cellular growth
  • Satellite cell activation, hyperplasia and muscle fiber mitogenesis
  • Fat oxidation and nutrient partitioning in body composition models
  • Comparative study: IGFBP evasion vs. native IGF-1

Scientific References — IGF-1 LR3

  • Clemmons DR. Metabolic actions of insulin-like growth factor-I in normal physiology and diabetes. Endocrinol Metab Clin North Am. 2012;41(2):425–43. PubMed PMID 22682638
  • Glass DJ. Skeletal muscle hypertrophy and atrophy signaling pathways. Int J Biochem Cell Biol. 2005;37(10):1974–84. PubMed PMID 16087388
  • Svensson J, et al. Liver-derived IGF-I regulates mean life span in mice. PLoS ONE. 2011;6(2):e16817. PubMed PMID 21347421

Why HGH Fragment 176-191 and IGF-1 LR3 Form the Ideal Lean Stack

The power of the Lean Stack lies in mechanistic complementarity. HGH Fragment 176-191 activates fat burning via beta-3 adrenergic lipolysis — without IGF-1 elevation, without insulin resistance, and without cell proliferation. In doing so, it completely isolates the lipolytic pathway of GH.

IGF-1 LR3 complements this by directly activating anabolic signaling in muscle tissue. It bypasses the liver and acts directly on skeletal muscle receptors — the pathway that HGH Fragment 176-191 specifically does not stimulate. In doing so, the combination provides researchers with simultaneous coverage of fat metabolism and muscle anabolism via completely separate molecular pathways.

In concrete terms, this is scientifically unique. Full GH activates both pathways together—thereby creating confounders. The Lean Stack, on the other hand, separates them. As a result, it offers researchers the opportunity to modulate and study lipolysis and muscle anabolism independently of each other—a mechanistic advantage that no single peptide or full GH preparation offers.

Research applications of the Lean Stack

  • Dual-pathway body composition analysis — fat burning and muscle preservation simultaneously
  • Isolated lipolysis study without IGF-1 confounders
  • IGF-1 receptor biology and PI3K/Akt signaling in muscle models
  • Comparative metabolic studies: Fragment vs. full GH
  • Nutrient partitioning and insulin sensitivity models
  • Fat oxidation and adipogenesis inhibition combined with muscle mass analysis

Who Is the Lean Stack Intended For?

  • Metabolism researchers who study lipolysis and fat storage mechanisms
  • Sports science teams conducting body composition and muscle mass research
  • Endocrinologists studying IGF-1 receptor biology and GH fragment pharmacology
  • Biochemists who model dual-pathway fat metabolism and muscle anabolism

Bundle Contents

  • HGH Fragment 176-191 — research-grade lyophilized peptide (≥98% purity, HPLC-verified)
  • IGF-1 LR3 — research-grade lyophilized peptide (≥98% purity, HPLC-verified)

Both peptides are supplied as lyophilized powder. HPLC certificates are available upon request.

Frequently Asked Questions about the Lean Stack

What is the difference between HGH Fragment 176-191 and full HGH?

Full HGH increases IGF-1, stimulates cell proliferation, promotes insulin resistance, and activates fat burning. HGH Fragment 176-191 retains only the lipolytic activity — via beta-3 adrenergic receptors — without IGF-1 elevation, without insulin effects, and without cell proliferation. As such, it offers a cleaner and more isolated research model for fat metabolism.

Why is IGF-1 LR3 better than native IGF-1 for research?

Native IGF-1 has a half-life of only 15–20 minutes and binds strongly to IGFBPs, which inhibit its activity. Due to its Arg3 modification, IGF-1 LR3 has a half-life of 20–30 hours and low IGFBP affinity. As a result, it remains active in circulation and offers researchers more stable and reproducible anabolic signaling in experimental models.

Scientific References

  1. Heffernan MA, et al. Fat oxidation and weight loss caused by HGH C-terminal fragment. Int J Obes. 2001;25(10):1442–9. PubMed PMID 11673762
  2. Ng FM, et al. Metabolic studies of AOD9604 with anti-obesity effects in humans. Arch Biochem Biophys. 2000;380(2):256–62. PubMed PMID 10933079
  3. Clemmons DR. Metabolic actions of IGF-I in normal physiology and diabetes. Endocrinol Metab Clin North Am. 2012;41(2):425–43. PubMed PMID 22682638
  4. Glass DJ. Skeletal muscle hypertrophy and atrophy signaling pathways. Int J Biochem Cell Biol. 2005;37(10):1974–84. PubMed PMID 16087388
  5. Svensson J, et al. Liver-derived IGF-I regulates mean life span in mice. PLOS ONE. 2011, 6 (2): e16817. PubMed PMID 21347421

⚠ For research purposes only — Disclaimer: This product is intended exclusively for in vitro and laboratory researchIt is not intended for use in humans or animals, self-administration, diagnosis, treatment or prevention of any disease or medical condition. HGH Fragment 176-191 and IGF-1 LR3 possess not regarding approval from the FDA, EMA or any equivalent regulatory authority for therapeutic use in humans. Researchers must comply with all applicable local laws and regulations. Keep out of reach of children. Handle in accordance with Good Laboratory Practice (GLP) guidelines.

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