HGH Fragment 176-191 Price Comparison — Compare 4 Vendors

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Growth hormone researchSafety Rating 7/10

Price Comparison

Compare vendors · per 5mg

4 vendors competing

VendorPrice$ / mgUpdated
SomaChems7/10$39.99$49.99−20% · code PEPTIDEPRICES$8.00May 14, 2026Buy →
Biotech Peptides6/10$44.00$8.80May 14, 2026Buy →
Core Peptides5.5/10$44.00$8.80Apr 16, 2026Buy →
Modern Aminos9/10$48.00$9.60May 14, 2026Buy →

Research details

HGH Fragment 176-191 — research data

Research-literature reference data, NOT patient instructions. Not for human use. Consult a licensed clinician for any human application.

Research dose range250–500 mcg SC daily, injected into abdominal fat, fasted state (morning or pre-workout). Cycle 8–12 weeks.
AdministrationSubcutaneous injection
Safety7/10 · Not FDA-approved
NCAA D1Banned

Overview

About HGH Fragment 176-191

Mechanism of action

C-terminal fragment of HGH (amino acids 176–191); selectively activates fat cell beta-3 adrenergic receptors to stimulate lipolysis; inhibits lipogenesis without affecting IGF-1 or causing hyperglycemia.

Safety profile

Minimal. Injection site redness, rare headache. No glucose dysregulation. No cancer risk from IGF-1 elevation. · Similar to AOD-9604; designed to avoid full GH side effects; no IGF-1 elevation; well-tolerated anecdotally

Storage

Stability & handling

❄️Lyophilized (powder)2–8°Cper labeling (often refrigerated)
💉Reconstituted2–8°Cwithin 14 days
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Research

Studies & key findings

  • HGH Fragment 176-191 (AOD9604), a 16-amino-acid C-terminal fragment of hGH with a Tyr→Phe substitution at position 177, produces fat-selective lipolytic effects without binding the hGH receptor, without stimulating IGF-1 production, and without affecting insulin sensitivity or promoting tissue growth — demonstrating that the growth and metabolic functions of hGH are structurally separable.
  • Chronic treatment with AOD9604 in obese mice reduced body weight, increased in vivo fat oxidation, and elevated plasma glycerol (index of lipolysis); crucially, beta-3 adrenergic receptor knockout mice were unresponsive to AOD9604, identifying beta-3 AR upregulation as an obligate downstream mechanism for long-term lipolytic effects.

5 peer-reviewed sources cited — clinical, preclinical, and regulatory.

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