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

HGH Fragment 176-191vsSelank

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
BHuman-MechanisticAUTO-DRAFTED11/40 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)
Selank
Anxiolytic + Cognitive · Russian Pharma
150–300 mcg/doseIntranasalZaderej 2014
~30 minOnset
Intranasal · 2–3×/day during stress / cognitive demand

01Mechanism of Action

Parameter
HGH Fragment 176-191
Selank
Primary target
Beta-3 adrenergic receptors on adipocytesHeffernan 2001
Monoamine system (serotonin / GABA modulation) + immunomodulation via tuftsin domainZaderej 2014
Pathway
Fragment → β3-AR upregulation → Enhanced lipolytic sensitivityHeffernan 2001
Tuftsin-derived immune signaling + CNS monoamine modulation → reduced anxiety + improved mood / cognitionMedvedev 2007
Downstream effect
Increased lipolysis and beta-3 AR mRNA expression without IGF-1 axis activation
Anxiolytic + cognitive enhancement; immunomodulation via increased IL-6 + IFN-γMedvedev 2007Zaderej 2014
Feedback intact?
N/A — does not interact with GH/IGF-1 axis
No GABA-receptor binding; no dependence reportedMedvedev 2007
Origin
Synthetic peptide derived from hGH residues 176-191; AOD9604 includes N-terminal tyrosine (177-191)Cox 2015
Synthetic 7-AA peptide derived from human tuftsin (immune-system tetrapeptide)Zaderej 2014
Antibody development
Not reported in available studies

02Dosage Protocols

Parameter
HGH Fragment 176-191
Selank
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)
2–3× per day during stress
Evidence basis
Animal studies only
Human-mechanistic + Russian clinical trialsMedvedev 2007
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.
Standard dose
150–300 mcg / dose intranasalZaderej 2014
Lower / starter dose
75 mcg / dose
Duration
10–14 day cycles, repeated as needed
Reconstitution
Pre-formulated nasal spray (commercial); research vial: bacteriostatic water
Timing
Morning + early afternoon preferred
Half-life
Short (minutes plasma); CNS effect lasts ~3 hr

03Metabolic / Fat Loss Evidence

Parameter
HGH Fragment 176-191
Selank
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
Selank
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.
Nasal irritation
Mild burning or congestion (transient)
Sedation
None — distinct from benzodiazepinesMedvedev 2007
Dependence / withdrawal
None reported in clinical useZaderej 2014
Cognitive impairment
None — opposite effect (enhancement)
Allergic reaction
Rare hypersensitivity
Long-term safety
Limited Western RCT data
Pregnancy / OB
Avoid — insufficient data
Absolute Contraindications
HGH Fragment 176-191
  • ·Competitive athletes (WADA-banned)Cox 2015
Selank
  • ·Pregnancy / breastfeeding
  • ·Hypersensitivity to peptide
Relative Contraindications
HGH Fragment 176-191
  • ·Absence of human safety data — experimental use only
Selank
  • ·Active autoimmune disease (theoretical via immunomodulation)

05Administration Protocol

Parameter
HGH Fragment 176-191
Selank
1. Route
Subcutaneous injection primary route in research context. Oral administration demonstrated efficacy in animal models at 500 mcg/kg.
Pre-formulated nasal spray (commercial) or research vial reconstituted with bacteriostatic water.
2. Frequency
Once daily dosing used in animal studies. Timing not specified; GH-independent mechanism suggests flexibility.
Intranasal — 1–3 sprays per nostril per dose. Tilt head slightly back.
3. Duration
Animal protocols: 14–19 days. Human duration not established — no published trials.
Morning + early afternoon for cognitive demand; PRN for acute anxiety.
4. Storage
Lyophilized peptide storage per standard peptide protocols. Metabolite stability suggests refrigerated reconstituted solution viable.
Refrigerate after reconstitution; ≤30 days. Light-protected.
5. Detection
Detectable in urine via SPE-LC-MS at 50 pg/mL LOD. Extended detection window via stable metabolite CRSVEGSCG.Cox 2015
Avoid co-administration with strong sedatives or other anxiolytics initially.