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Specimen Atlas of Research Peptides81 plates · MIT
Side-by-side · Research reference

HGH Fragment 176-191vsMelanotan-II

Side-by-side comparison across mechanism, dosage, evidence, side effects, administration, and stack synergies. Citations on every claim where available.

AAnimal-StrongHUMAN-REVIEWED28/59 cited
BPhase 1HUMAN-REVIEWED9/43 cited
HGH Fragment 176-191
GH Fragment · Pre-Clinical
50%Weight gain reductionNg 2000
~26 minHalf-life (est.)
No IGF-1 ↑GH axis impact
SQ · IP (animal) · Oral (tested)
Melanotan-II
MC1R + MC4R agonist · Tanning + sexual response
0.25–1.0 mgPer doseDorr 1996
Phase 1Evidence levelDorr 1996
~1 hrHalf-life
SQ · Abdomen · Loading 5–7 days, then maintenance

01Mechanism of Action

Parameter
HGH Fragment 176-191
Melanotan-II
Primary target
Beta-3 adrenergic receptors on adipocytesHeffernan 2001
MC1R (skin) + MC3R + MC4R (CNS sexual / appetite)Dorr 1996
Pathway
Fragment → β3-AR upregulation → Enhanced lipolytic sensitivityHeffernan 2001
MC1R agonism → melanocyte tyrosinase → eumelanin synthesis. MC4R → autonomic sexual arousal centresDorr 1996Simerly 2023
Downstream effect
Increased lipolysis and beta-3 AR mRNA expression without IGF-1 axis activation
Skin darkening, photo-protection, increased sexual desire / spontaneous erectionDorr 1996
Feedback intact?
N/A — does not interact with GH/IGF-1 axis
Origin
Synthetic peptide derived from hGH residues 176-191; AOD9604 includes N-terminal tyrosine (177-191)Cox 2015
Cyclic 7-AA modified α-MSH analog; designed at University of ArizonaDorr 1996
Antibody development
Not reported in available studies

02Dosage Protocols

Parameter
HGH Fragment 176-191
Melanotan-II
Animal dose (oral)
500 mcg/kg body weightNg 2000
Obese Zucker rats, 19 days.
Animal dose (IP)
Not specified (14-day chronic administration)Heffernan 2001
Obese mice, daily IP injection.
Human equivalent dose
Not established — no published human RCTs
Frequency
Once daily (animal models)
Daily during loading; 1–2× per week maintenance
Evidence basis
Animal studies only
Phase 1 + anecdotalDorr 1996
Duration tested
Detection window
50 pg/mL LOD in urine; stable metabolite extends detectionCox 2015
WADA-banned; anti-doping testing available.
Oral bioavailability
Demonstrated efficacy in animal oral administrationNg 2000
Potential for oral therapeutic development.
Loading phase
0.25–0.5 mg/day SQ × 5–7 daysDorr 1996
Builds up to visible tan.
Maintenance
0.5–1.0 mg 1–2×/week
After visible tan develops; supports with UV exposure.
Lower / starter dose
0.1 mg / day
Conservative starter — assess tolerability for nausea.
Duration
8–12 weeks per cycle
Reconstitution
Bacteriostatic water; protect from light
Timing
Evening preferred (24h tan-development cycle)
Half-life
~1 hour plasma; effects on melanocytes persist days

03Metabolic / Fat Loss Evidence

Parameter
HGH Fragment 176-191
Melanotan-II
Primary fat target
Adipose tissue (general) — beta-3 AR mediated lipolysisHeffernan 2001
Weight gain reduction
50% reduction vs control (15.8 ± 0.6 g vs 35.6 ± 0.8 g)Ng 2000
Obese Zucker rats, 19 days oral administration.
Body fat reduction
Significant decrease in body weight and body fat in obese mice (14 days)Heffernan 2001
Lipolytic activity
Increased adipose tissue lipolytic activityNg 2000
Direct measurement in treated animals.
Beta-3 AR expression
Upregulated β3-AR mRNA in obese mice to lean-comparable levelsHeffernan 2001
Insulin sensitivity
No adverse effect — euglycemic clamp confirmedNg 2000
Contrasts with intact hGH diabetogenic effects.
IGF-1 impact
No elevation — fragment does not activate GH/IGF-1 axis
Beta-3 AR dependency
Effect abolished in β3-AR knockout miceHeffernan 2001
Confirms β3-AR as primary mechanism.
Route of administration
Efficacy demonstrated via oral and IP routesNg 2000Heffernan 2001
Human evidence
None published — pre-clinical only

04Side Effects & Safety

Parameter
HGH Fragment 176-191
Melanotan-II
Insulin sensitivity
No adverse effects observed in euglycemic clamp (animal)Ng 2000
GH/IGF-1 axis
No activation — avoids diabetogenic effects of full GHNg 2000
Human safety data
Not available — no published human trials
WADA status
Banned as performance-enhancing drugCox 2015
Metabolic profile
Six metabolites identified; CRSVEGSCG most stableCox 2015
Detection window implications for doping control.
Nausea
Common, especially loading phase
Flushing
Common transient
Spontaneous erection
Common in men — MC4R cross-effectDorr 1996
Increased mole / freckle pigmentation
Existing moles darken; new lesions possible
Melanoma risk
Theoretical concern — increased melanocyte activity; CAUTION in melanoma history
Appetite suppression
MC4R-mediated; mild
Pregnancy / OB
Contraindicated
Absolute Contraindications
HGH Fragment 176-191
  • ·Competitive athletes (WADA-banned)Cox 2015
Melanotan-II
  • ·History of melanoma or atypical mole syndrome
  • ·Pregnancy / breastfeeding
  • ·Active uncontrolled hypertension
Relative Contraindications
HGH Fragment 176-191
  • ·Absence of human safety data — experimental use only
Melanotan-II
  • ·Significant freckling / dysplastic nevus
  • ·Personal or family melanoma history

05Administration Protocol

Parameter
HGH Fragment 176-191
Melanotan-II
1. Route
Subcutaneous injection primary route in research context. Oral administration demonstrated efficacy in animal models at 500 mcg/kg.
Add 2 mL bacteriostatic water to 10 mg vial → 5 mg/mL = 500 mcg per 0.1 mL. Light-protected.
2. Frequency
Once daily dosing used in animal studies. Timing not specified; GH-independent mechanism suggests flexibility.
SQ — abdomen. Rotate sites.
3. Duration
Animal protocols: 14–19 days. Human duration not established — no published trials.
Evening preferred. UV exposure (sunlight or tanning bed) helps develop tan.
4. Storage
Lyophilized peptide storage per standard peptide protocols. Metabolite stability suggests refrigerated reconstituted solution viable.
Lyophilised: refrigerate, light-protected. Reconstituted: refrigerate ≤30 days.
5. Detection
Detectable in urine via SPE-LC-MS at 50 pg/mL LOD. Extended detection window via stable metabolite CRSVEGSCG.Cox 2015
29–31G insulin syringe.