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

HGH Fragment 176-191vsTB-500

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 2HUMAN-REVIEWED8/46 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)
TB-500
Thymosin β4 fragment · Healing
2 mgPer doseGoldstein 2012
Phase 2Evidence levelGoldstein 2012
~2 hrHalf-life
SQ or IM · Multiple sites · 2–3×/week

01Mechanism of Action

Parameter
HGH Fragment 176-191
TB-500
Primary target
Beta-3 adrenergic receptors on adipocytesHeffernan 2001
G-actin (sequestering) + cell-surface integrinsGoldstein 2012
Pathway
Fragment → β3-AR upregulation → Enhanced lipolytic sensitivityHeffernan 2001
Actin remodelling → cell migration; integrin-linked signaling → angiogenesis; anti-inflammatory cytokine modulationGoldstein 2012Malinda 1999
Downstream effect
Increased lipolysis and beta-3 AR mRNA expression without IGF-1 axis activation
Accelerated wound healing, endothelial migration, hair follicle regeneration, cardiac repair (preclinical)Goldstein 2012
Feedback intact?
N/A — does not interact with GH/IGF-1 axis
Endogenous protein at baseline; supplementation amplifies
Origin
Synthetic peptide derived from hGH residues 176-191; AOD9604 includes N-terminal tyrosine (177-191)Cox 2015
17-AA active fragment of endogenous 43-AA thymosin β4 (TMSB4X gene)Goldstein 2012
Antibody development
Not reported in available studies

02Dosage Protocols

Parameter
HGH Fragment 176-191
TB-500
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× per week (loading); then 1× per week (maintenance)
Evidence basis
Animal studies only
Animal-strong + Phase 2 dermal/ocular trialsGoldstein 2012
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
2 mg per injectionGoldstein 2012
Anecdotal community range; clinical Phase 2 trials used 70–840 mcg/kg IV.
Lower / starter dose
1 mg per injection
Duration
4–8 weeks loading; longer maintenance for chronic injury
Reconstitution
Bacteriostatic water, 1–2 mL per 5 mg vial
Timing
Evening or pre-rest preferred (anecdotal)
Half-life
~2 hours (estimated; tissue uptake longer)

03Metabolic / Fat Loss Evidence

Parameter
HGH Fragment 176-191
TB-500
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
TB-500
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.
Injection site reaction
Mild erythema, transient pain
GI symptoms
Rare nausea (anecdotal)
Cancer risk
Theoretical via angiogenesis pathway
Lethargy / fatigue
Reported anecdotally during loading phase
Antibody formation
No data (no long-term human trials)
Pregnancy / OB
Avoid
Long-term safety
Unknown beyond Phase 2
Absolute Contraindications
HGH Fragment 176-191
  • ·Competitive athletes (WADA-banned)Cox 2015
TB-500
  • ·Active malignancy (theoretical angiogenesis concern)
  • ·Pregnancy / breastfeeding
Relative Contraindications
HGH Fragment 176-191
  • ·Absence of human safety data — experimental use only
TB-500
  • ·Cancer history
  • ·Concurrent VEGF inhibitor therapy

05Administration Protocol

Parameter
HGH Fragment 176-191
TB-500
1. Route
Subcutaneous injection primary route in research context. Oral administration demonstrated efficacy in animal models at 500 mcg/kg.
Add 1–2 mL bacteriostatic water to 5 mg vial → 2.5–5 mg/mL. Roll gently.
2. Frequency
Once daily dosing used in animal studies. Timing not specified; GH-independent mechanism suggests flexibility.
SQ near injury site (preferred), or systemic SQ (abdomen). Rotate sites.
3. Duration
Animal protocols: 14–19 days. Human duration not established — no published trials.
Evening or pre-sleep is most common anecdotal timing.
4. Storage
Lyophilized peptide storage per standard peptide protocols. Metabolite stability suggests refrigerated reconstituted solution viable.
Lyophilised: room temp, 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
27–31G, 4–8 mm insulin syringe.

06Stack Synergy

HGH Fragment 176-191
— no documented stacks
TB-500
+ BPC-157
Strong
View BPC-157

TB-500 and BPC-157 cover complementary halves of tissue repair: BPC-157 upregulates VEGFR2-driven angiogenesis and fibroblast outgrowth; TB-500 sequesters G-actin to enable endothelial / epithelial migration. The anecdotal canonical "healing stack" — pairs especially well for tendon and ligament injuries.

TB-500
2 mg SQ · 2× per week
BPC-157
250–500 mcg SQ · daily
Primary benefit
Combined angiogenesis + cell migration for tendon/ligament/muscle repair