Side-by-side · Research reference

HGH Fragment 176-191vsLivagen

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

BAnimal-StrongHUMAN-REVIEWED20/32 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)

Livagen

Khavinson Bioregulator · Hepatoprotective Tetrapeptide

50%Dipeptidase inhibitionTimofeeva 2005

Oral / SQRoutes tested

LiverTarget tissueKhavinson 2001

Oral or SQ · Tissue-specific to liver

01Mechanism of Action

Parameter

HGH Fragment 176-191

Livagen

Primary target

Beta-3 adrenergic receptors on adipocytesHeffernan 2001

Hepatocyte protein synthesis machineryBrodskiĭ 2001

Pathway

Fragment → β3-AR upregulation → Enhanced lipolytic sensitivityHeffernan 2001

Tissue-specific bioregulator → Hepatocyte stimulation → Protein synthesis normalizationBrodskiĭ 2001 Khavinson 2001

Downstream effect

Increased lipolysis and beta-3 AR mRNA expression without IGF-1 axis activation

Age-dependent enzyme normalization, hepatoprotection in fibrosis/hepatitis models, elevated protein synthesis in senescent hepatocytes

Feedback intact?

N/A — does not interact with GH/IGF-1 axis

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Origin

Synthetic peptide derived from hGH residues 176-191; AOD9604 includes N-terminal tyrosine (177-191)Cox 2015

Directed chemical synthesis from amino acid analysis of liver polypeptide preparations (Ventvil)

Antibody development

Not reported in available studies

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02Dosage Protocols

Parameter

HGH Fragment 176-191

Livagen

Animal dose (oral)

500 mcg/kg body weightNg 2000

Obese Zucker rats, 19 days.

Not specified in abstracts; 2-week administration protocolTimofeeva 2005

Per os administration in rats.

Animal dose (IP)

Not specified (14-day chronic administration)Heffernan 2001

Obese mice, daily IP injection.

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Human equivalent dose

Not established — no published human RCTs

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Frequency

Once daily (animal models)

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Evidence basis

Animal studies only

Animal models (rats, 1–24 months age); in vitro hepatocyte cultureTimofeeva 2005 Brodskiĭ 2001 Khavinson 2002

Duration tested

14–19 daysHeffernan 2001 Ng 2000

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Detection window

50 pg/mL LOD in urine; stable metabolite extends detectionCox 2015

WADA-banned; anti-doping testing available.

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Oral bioavailability

Demonstrated efficacy in animal oral administrationNg 2000

Potential for oral therapeutic development.

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Duration (experimental)

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2 weeks (enzyme study); up to 24 months (cell culture)Timofeeva 2005 Brodskiĭ 2001

Route

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Oral or subcutaneous

Resists peptidase hydrolysis, enabling oral bioavailability.Timofeeva 2005

Human data

—

None in provided literature

03Metabolic / Fat Loss Evidence

Parameter

HGH Fragment 176-191

Livagen

Primary fat target

Adipose tissue (general) — beta-3 AR mediated lipolysisHeffernan 2001

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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.

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Body fat reduction

Significant decrease in body weight and body fat in obese mice (14 days)Heffernan 2001

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Lipolytic activity

Increased adipose tissue lipolytic activityNg 2000

Direct measurement in treated animals.

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Beta-3 AR expression

Upregulated β3-AR mRNA in obese mice to lean-comparable levelsHeffernan 2001

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Insulin sensitivity

No adverse effect — euglycemic clamp confirmedNg 2000

Contrasts with intact hGH diabetogenic effects.

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IGF-1 impact

No elevation — fragment does not activate GH/IGF-1 axis

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Beta-3 AR dependency

Effect abolished in β3-AR knockout miceHeffernan 2001

Confirms β3-AR as primary mechanism.

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Route of administration

Efficacy demonstrated via oral and IP routesNg 2000 Heffernan 2001

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Human evidence

None published — pre-clinical only

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04Side Effects & Safety

Parameter

HGH Fragment 176-191

Livagen

Insulin sensitivity

No adverse effects observed in euglycemic clamp (animal)Ng 2000

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GH/IGF-1 axis

No activation — avoids diabetogenic effects of full GHNg 2000

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Human safety data

Not available — no published human trials

No human trials in provided literature

WADA status

Banned as performance-enhancing drugCox 2015

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Metabolic profile

Six metabolites identified; CRSVEGSCG most stableCox 2015

Detection window implications for doping control.

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Reported adverse effects

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None documented in animal studies

Peptide hydrolysis

—

Weakly hydrolyzed; minimal breakdown by intestinal enzymesTimofeeva 2005

Absolute Contraindications

HGH Fragment 176-191

·Competitive athletes (WADA-banned)Cox 2015

Livagen

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Relative Contraindications

HGH Fragment 176-191

·Absence of human safety data — experimental use only

Livagen

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05Administration Protocol

Parameter

HGH Fragment 176-191

Livagen

1. Route

Subcutaneous injection primary route in research context. Oral administration demonstrated efficacy in animal models at 500 mcg/kg.

Oral administration supported by peptidase resistance. Subcutaneous route used in organotypic culture experiments.Timofeeva 2005 Khavinson 2001

2. Frequency

Once daily dosing used in animal studies. Timing not specified; GH-independent mechanism suggests flexibility.

No specific timing documented. Two-week protocols used in animal models with daily administration.Timofeeva 2005

3. Duration

Animal protocols: 14–19 days. Human duration not established — no published trials.

Elderly individuals may exhibit different enzyme normalization patterns than younger cohorts, based on rat age-stratified findings.Timofeeva 2005

4. Storage

Lyophilized peptide storage per standard peptide protocols. Metabolite stability suggests refrigerated reconstituted solution viable.

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5. Detection

Detectable in urine via SPE-LC-MS at 50 pg/mL LOD. Extended detection window via stable metabolite CRSVEGSCG.Cox 2015

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