HGH Fragment 5mg

HGH Fragment 176–191 is a synthetic peptide corresponding to the C-terminus of human growth hormone. Unlike full-length GH, the 176–191 fragment does not activate the GH receptor or raise IGF-1. Preclinical work suggests adipocyte-selective actions—enhancing lipolysis and inhibiting lipogenesis—without classical GH-like anabolic or diabetogenic effects.

Description

HGH Fragment 176–191

Benefit Key take-aways
1 Selective adipose lipolysis Rodent and cell studies show increased hormone-sensitive lipase activity and glycerol/FFA release in white adipocytes, with preferential reduction of abdominal/visceral fat versus lean tissue.
2 Anti-lipogenic effects Downstream signalling reduces de novo lipogenesis markers (e.g., FAS/ACC) and can blunt LPL-mediated lipid uptake in adipose tissue.
3 Energy-expenditure signals In diet-induced obese mice, treatment increases UCP-1/UCP-3 expression and fatty-acid oxidation genes, hinting at browning/thermogenic shifts.
4 Glucose neutrality (short-term) Small human studies report no meaningful change in fasting glucose or HbA1c over weeks; insulin and IGF-1 remain near baseline.
5 No IGF-1 elevation Because the fragment lacks GH-receptor activity, IGF-1 levels typically do not rise, potentially lowering mitogenic and edema risks seen with GH.
6 Joint/tendon exploratory signal Preclinical work shows increased collagen gene expression and improved histology after tendon injury; human data are insufficient.
7 Liver-fat hypothesis By reducing ectopic lipid flux from adipose tissue, models suggest downward pressure on hepatic steatosis; confirmatory human trials are lacking.
8 Lifestyle synergy Pairing with caloric restriction and exercise amplifies fat-loss signals in animal models; human trials to date did not show large standalone weight loss.
9 Tolerability Across short-term studies, AE rates near placebo (GI upset, headache most common); no consistent edema, arthralgia, or IGF-1-related effects. Long-term safety remains uncertain.

2. Molecular Mechanism of Action

2.1 Receptor Pharmacodynamics

The 176–191 fragment does not bind or activate the GH receptor and does not stimulate IGF-1. Proposed actions are adipocyte-selective, with evidence for cAMP/PKA-HSL pathway activation and suppression of lipogenic transcriptional programs. The precise upstream receptor remains unresolved.

2.2 Down-stream Biology

Pathway Functional outcome Context
cAMP–PKA–HSL ↑ lipolysis, FFA mobilization White adipose tissue
AMPK/PPAR cross-talk ↑ fatty-acid oxidation, ↓ lipogenesis Liver/adipose
Mitochondrial/thermogenic genes (UCPs) ↑ energy expenditure (preclinical) Brown/brite adipocytes

3. Pharmacokinetics

  • Absorption/route: Investigated as parenteral peptide; some programs explored oral formulations, but oral bioavailability appears low and formulation-dependent.

  • Half-life: Short plasma half-life (minutes to ~1 h) typical of small peptides; pharmacodynamic effects depend on frequent dosing or specialized delivery.

  • Distribution/Clearance: Primarily extracellular distribution; proteolytic degradation and renal clearance; no CYP interactions expected.

4. Pre-clinical and Translational Evidence

4.1 Obesity/Adiposity

Multiple rodent studies show reductions in fat mass and improvements in lipid oxidation with minimal effect on lean mass. Human RCTs have been mixed and several failed to meet primary weight-loss endpoints, though tolerabilitywas generally favorable.

4.2 Metabolic Health

Short-term human data show neutral glycaemia and no IGF-1 rise; lipid changes are modest and inconsistent. In animals, hepatic lipid handling and thermogenic gene expression improved.

4.3 Musculoskeletal Tissue

Exploratory preclinical data suggest collagen synthesis support and improved histology after tendon injury; clinical relevance is unproven.

5. Emerging Clinical Interests

Field Rationale Current status
Adjunct in obesity care Adipocyte-selective lipolysis without IGF-1 Early human signals; no approvals
NAFLD/MASH (theoretical) Reduced adipose lipid spillover to liver Preclinical rationale; no pivotal trials
Sports-injury recovery Collagen gene up-regulation in models Preclinical only
Cardiometabolic risk Possible TG/HDL improvements if fat mass drops Requires robust human data

6. Safety and Tolerability

  • Common AEs: Mild GI discomfort, headache, injection-site reactions (parenteral).

  • Endocrine: IGF-1 unchanged; no GH-like edema/arthralgia pattern reported in short studies.

  • Glycaemia: Generally neutral; no systematic hypoglycaemia signal.

  • Unknowns: Long-term safety, carcinogenicity, and effects in special populations remain insufficiently characterized.

Comparative safety matrix

Concern rHGH 176–191 fragment Tesamorelin (GHRH analog) Somatropin (GH)
IGF-1 elevation No Yes (physiologic) Yes (dose-dependent)
Edema/arthralgia Low (short-term) Moderate Moderate–higher
Glycaemic impact Neutral (short-term) Neutral → mild ↑ Neutral → mild ↑
Evidence for fat loss Preclinical > human Robust in HIV VAT Mixed in non-GHD adults

7. Regulatory Landscape

  • Approval status: Not approved by FDA/EMA or other major regulators for any indication.

  • Sporting bodies: Classified under non-approved substances by anti-doping authorities; use in sport is prohibited.

  • Supply: Frequently marketed online as a “research chemical”; quality, purity, and dosing not assured.

8. Future Directions

  • Mechanistic clarity: Identify the proximal receptor/target and confirm on-target biomarkers in humans.

  • PK engineering: Half-life extension (e.g., lipidation, depot, or pegylation) to enable practical dosing.

  • Phenotype targeting: Trials in visceral-predominant obesity or NAFLD with imaging (MRI-PDFF) and metabolic endpoints.

  • Combination therapy: Pairing with GLP-1/GIP agonists or SGLT2 inhibitors to evaluate additive fat- and liver-fat reductions.

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