Side-by-side · Research reference

ARA 290vsHGH Fragment 176-191

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

APhase 2HUMAN-REVIEWED17/59 cited

BAnimal-StrongHUMAN-REVIEWED28/59 cited

ARA 290

EPO-Derived Peptide · Innate Repair Receptor Agonist

4 mgDaily doseBrines 2015 Culver 2017

28 daysPhase 2 durationCulver 2017

Non-erythropoieticSafety profileBrines 2015 Liu 2014

SQ · DailyBrines 2015 Culver 2017

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)

01Mechanism of Action

Parameter

ARA 290

HGH Fragment 176-191

Primary target

Innate repair receptor (EPO receptor / CD131 heterodimer)

Beta-3 adrenergic receptors on adipocytesHeffernan 2001

Pathway

EPO/CD131 → JAK2 activation → PI3K/AKT, MAPK signaling → anti-inflammatory, anti-apoptotic cascades

Fragment → β3-AR upregulation → Enhanced lipolytic sensitivityHeffernan 2001

Downstream effect

Tissue protection, nerve fiber regeneration, suppression of inflammatory macrophage activation, altered T-cell differentiation (↑Treg, ↑Th2, ↓Th1)Liu 2014 Culver 2017

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

Feedback intact?

N/A — does not interact with hematopoietic EPO receptorLiu 2014

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

Origin

11-amino-acid sequence from EPO helix B, engineered to eliminate hematopoietic activity while retaining tissue-protective properties

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

Antibody development

Not reported in clinical trials

Not reported in available studies

02Dosage Protocols

Parameter

ARA 290

HGH Fragment 176-191

Standard dose (Phase 2)

4 mg / dayBrines 2015 Culver 2017

Sarcoidosis SFN and diabetic neuropathy trials.

—

Frequency

Once daily

Self-administered subcutaneously.

Once daily (animal models)

Duration

28 days (Phase 2)Culver 2017

Corneal nerve improvements observed by day 28.

—

Evidence basis

Phase 2 RCTsCulver 2017 Brines 2015

64-subject sarcoidosis trial, type 2 diabetes trial.

Animal studies only

Route

SubcutaneousBrines 2015

—

Timing

Any time of day

No circadian dependence reported.

—

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

Duration tested

—

14–19 daysHeffernan 2001 Ng 2000

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.

03Metabolic / Fat Loss Evidence

Parameter

ARA 290

HGH Fragment 176-191

Primary effect

Improved metabolic control (HbA1c, fasting glucose)Brines 2015

Secondary to neuropathy treatment; direct lipolytic effects not established.

—

HbA1c

Significant reduction vs placebo

Observed in type 2 diabetes + neuropathy trial.

—

Fasting glucose

Improved in ARA 290 group

—

Body composition

Not directly quantified

Fat loss not a primary endpoint; metabolic improvements may reflect insulin sensitivity.

—

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 2000 Heffernan 2001

Human evidence

—

None published — pre-clinical only

04Side Effects & Safety

Parameter

ARA 290

HGH Fragment 176-191

Injection site reaction

Mild, transient

—

Hematopoiesis

None — non-erythropoietic

Distinguishes ARA 290 from native EPO.

—

Cardiovascular

No thrombotic events or hypertension reported

—

Immunogenicity

No antibody formation reported

—

Tolerability

Well-tolerated in Phase 2 trialsCulver 2017 Brines 2015

—

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.

Absolute Contraindications

ARA 290

·Hypersensitivity to ARA 290

HGH Fragment 176-191

·Competitive athletes (WADA-banned)Cox 2015

Relative Contraindications

ARA 290

·Active malignancy (theoretical EPO-axis concern; not observed in trials)

HGH Fragment 176-191

·Absence of human safety data — experimental use only

05Administration Protocol

Parameter

ARA 290

HGH Fragment 176-191

1. Preparation

Reconstitute lyophilised powder per manufacturer instructions. Use sterile technique.

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

2. Injection site

Subcutaneous — abdomen, thigh, or upper arm. Rotate sites to avoid lipohypertrophy.

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

3. Timing

Once daily, any time of day. Self-administered in Phase 2 trials.Brines 2015

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

4. Dosing

4 mg daily for 28 days (Phase 2 protocol). Duration for chronic use not established.Culver 2017

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

5. Storage

Lyophilised: store at controlled room temperature. Reconstituted: refrigerate, use within specified timeframe.

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

06Stack Synergy

ARA 290

+ BPC-157

Moderate

View BPC-157 →

ARA 290 targets the innate repair receptor (EPO/CD131) for nerve regeneration and anti-inflammatory signaling, while BPC-157 promotes angiogenesis and tissue repair through distinct mechanisms (likely involving VEGF, growth hormone receptor pathways). Combined, they may address both neuroinflammation and structural tissue repair in neuropathy or injury models. No direct clinical data; mechanistic overlap in tissue protection.

ARA 290: 4 mg SQ · daily
BPC-157: 250–500 mcg SQ · daily
Frequency: Once daily, same or separate injections
Primary benefit: Nerve regeneration, pain reduction, tissue healing

HGH Fragment 176-191

— no documented stacks