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

AHK-CuvsARA 290

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

AAnimal-MechanisticHUMAN-REVIEWED14/43 cited
BPhase 2HUMAN-REVIEWED17/59 cited
AHK-Cu
Tripeptide-Copper Complex · Cosmetic
10⁻¹² – 10⁻⁹ MActive range (in vitro)Pyo 2007
Dermal papilla cellsPrimary targetPyo 2007
TopicalRoute
Topical · Scalp / Skin
ARA 290
EPO-Derived Peptide · Innate Repair Receptor Agonist
28 daysPhase 2 durationCulver 2017
Non-erythropoieticSafety profileBrines 2015Liu 2014

01Mechanism of Action

Parameter
AHK-Cu
ARA 290
Primary target
Dermal papilla cells (DPCs) — specialized fibroblasts in hair follicle morphogenesisPyo 2007
Innate repair receptor (EPO receptor / CD131 heterodimer)
Pathway
AHK-Cu → DPC proliferation → VEGF elevation, TGF-β1 suppression → Angiogenesis, follicle elongationPyo 2007
EPO/CD131 → JAK2 activation → PI3K/AKT, MAPK signaling → anti-inflammatory, anti-apoptotic cascades
Downstream effect
Stimulates hair follicle elongation ex vivo, reduces dermal papilla cell apoptosis, elevates Bcl-2/Bax ratio, reduces cleaved caspase-3 and PARPPyo 2007
Tissue protection, nerve fiber regeneration, suppression of inflammatory macrophage activation, altered T-cell differentiation (↑Treg, ↑Th2, ↓Th1)Liu 2014Culver 2017
Feedback intact?
N/A — does not interact with hematopoietic EPO receptorLiu 2014
Origin
Synthetic tripeptide with Cu²⁺ chelation — alanine substitution variant of GHK-Cu
11-amino-acid sequence from EPO helix B, engineered to eliminate hematopoietic activity while retaining tissue-protective properties
Antibody development
Not reported in clinical trials

02Dosage Protocols

Parameter
AHK-Cu
ARA 290
Effective concentration (in vitro)
10⁻¹² – 10⁻⁹ MPyo 2007
Stimulated human hair follicle elongation ex vivo and DPC proliferation in vitro.
Topical formulation
0.001–0.01% (estimated cosmetic range)
No standardized human protocol published — extrapolated from in vitro data.
Frequency
Once or twice daily (topical application)
Once daily
Self-administered subcutaneously.
Route
Topical — scalp or dermal application
SubcutaneousBrines 2015
Evidence basis
Ex vivo hair follicle / in vitro DPC studiesPyo 2007
Phase 2 RCTsCulver 2017Brines 2015
64-subject sarcoidosis trial, type 2 diabetes trial.
Duration
Not established — cosmetic protocols typically 8–12 weeks
28 days (Phase 2)Culver 2017
Corneal nerve improvements observed by day 28.
Standard dose (Phase 2)
4 mg / dayBrines 2015Culver 2017
Sarcoidosis SFN and diabetic neuropathy trials.
Timing
Any time of day
No circadian dependence reported.

03Metabolic / Fat Loss Evidence

Parameter
AHK-Cu
ARA 290
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.

04Side Effects & Safety

Parameter
AHK-Cu
ARA 290
Local irritation
Mild erythema, pruritus at application site (copper peptide class effect)
Copper sensitivity
Rare hypersensitivity reaction in copper-sensitive individuals
Systemic absorption
Minimal via topical route — systemic copper toxicity unlikely at cosmetic doses
Data limitations
No published human safety trials — cosmetic use presumed safe per class precedent (GHK-Cu)
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 2017Brines 2015
Absolute Contraindications
AHK-Cu
  • ·Known copper allergy or Wilson's disease
ARA 290
  • ·Hypersensitivity to ARA 290
Relative Contraindications
AHK-Cu
  • ·Broken or inflamed skin (increased absorption risk)
  • ·Concurrent use of other copper-containing formulations
ARA 290
  • ·Active malignancy (theoretical EPO-axis concern; not observed in trials)

05Administration Protocol

Parameter
AHK-Cu
ARA 290
1. Topical application
Apply to clean, dry scalp or target dermal area. Typical cosmetic formulations: 0.001–0.01% AHK-Cu in serum or cream base.
Reconstitute lyophilised powder per manufacturer instructions. Use sterile technique.
2. Frequency
Once or twice daily. Evening application preferred for overnight contact time.
Subcutaneous — abdomen, thigh, or upper arm. Rotate sites to avoid lipohypertrophy.
3. Scalp preparation
For hair growth: apply directly to scalp, massage gently. No need to rinse. Allow absorption for minimum 2–4 hours.
Once daily, any time of day. Self-administered in Phase 2 trials.Brines 2015
4. Storage
Room temperature, protected from light. Copper complexes may degrade in UV exposure.
4 mg daily for 28 days (Phase 2 protocol). Duration for chronic use not established.Culver 2017
5. Duration
Minimum 8–12 weeks to assess efficacy in hair growth applications, per typical cosmetic peptide protocols.
Lyophilised: store at controlled room temperature. Reconstituted: refrigerate, use within specified timeframe.

06Stack Synergy

AHK-Cu
+ GHK-Cu
Moderate
View GHK-Cu

Both tripeptide-copper complexes share overlapping angiogenic and wound-healing mechanisms (VEGF elevation, TGF-β modulation, fibroblast proliferation). AHK-Cu's alanine substitution may offer distinct receptor affinity or pharmacokinetics. Co-formulation could provide complementary dermal signaling, though no direct synergy studies exist. Often used interchangeably or in alternating protocols.

AHK-Cu
0.001–0.01% topical · AM
GHK-Cu
0.001–0.01% topical · PM
Frequency
Daily alternation or combined formulation
Primary benefit
Comprehensive dermal regeneration, angiogenesis, hair follicle support
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