Side-by-side · Research reference
ARA 290vsIGF-1 LR3
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-REVIEWED10/58 cited
IGF-1 LR3
IGF-1 Analogue · Research
3–10×Potency vs IGF-I
Low IGFBPBinding affinity
ResearchStatus
Research only · SQ typical in animal models
01Mechanism of Action
Parameter
ARA 290
IGF-1 LR3
Primary target
Innate repair receptor (EPO receptor / CD131 heterodimer)
IGF-1 receptor (IGF-1R)McTavish 2009
Pathway
EPO/CD131 → JAK2 activation → PI3K/AKT, MAPK signaling → anti-inflammatory, anti-apoptotic cascades
IGF-1R → IRS-1 → PI3K/Akt → Cell proliferation, protein synthesis, anti-apoptosisMuhlbradt 2009
Downstream effect
Tissue protection, nerve fiber regeneration, suppression of inflammatory macrophage activation, altered T-cell differentiation (↑Treg, ↑Th2, ↓Th1)Liu 2014Culver 2017
Enhanced cell proliferation, muscle anabolism, inhibition of apoptosis, increased telomerase activity
Feedback intact?
N/A — does not interact with hematopoietic EPO receptorLiu 2014
No — exogenous IGF analogue bypasses GH-mediated regulation
Origin
11-amino-acid sequence from EPO helix B, engineered to eliminate hematopoietic activity while retaining tissue-protective properties
Synthetic 83-AA analogue: 13-AA N-terminal extension + Arg substitution at position 3
Antibody development
Not reported in clinical trials
—
02Dosage Protocols
Parameter
ARA 290
IGF-1 LR3
Standard dose (Phase 2)
4 mg / dayBrines 2015Culver 2017
Sarcoidosis SFN and diabetic neuropathy trials.
—
Frequency
Once daily
Self-administered subcutaneously.
—
Evidence basis
Phase 2 RCTsCulver 2017Brines 2015
64-subject sarcoidosis trial, type 2 diabetes trial.
Animal / in vitro only
Timing
Any time of day
No circadian dependence reported.
—
Research dose (animal models)
—
Variable by protocol and species
In vivo murine atherosclerosis studies used sustained delivery.
In vitro typical concentration
—
10–1000 ng/mLThomas 2007
Dose-dependent effects on follicle growth and estradiol production.
Half-maximal stimulation
—
0.6 nM LR3 vs 1.5 nM native IGF-1Price 2004
2.5-fold greater potency in lung fibroblast proliferation.
Human use
—
Not FDA-approved; no published human trials
03Metabolic / Fat Loss Evidence
Parameter
ARA 290
IGF-1 LR3
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.
—
Mechanism
—
IGF-1R activation → lipolytic signaling; secondary to anabolic effects
Direct lipolytic evidence
—
Minimal — primarily anabolic/anti-apoptotic in literature
Atherosclerotic plaque effects
—
Reduced stenosis and core size in ApoE-KO micevon 2011
Plaque stabilization via vSMC phenotype modulation, not direct fat loss.
Human data
—
None published
04Side Effects & Safety
Parameter
ARA 290
IGF-1 LR3
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
—
Hypoglycemia risk
—
Theoretical — IGF-1 analogues can lower blood glucose
Excessive cell proliferation
—
Mitogenic signaling; theoretical tumor promotion risk
Telomerase activation
—
2–10-fold increase in prostate cancer cells (PC-3, DU-145, LAPC-4)Wetterau 2003
Critically involved in cancer cell immortalization.
Oocyte degeneration
—
Increased oocyte degeneration at high doses (≥1000 ng/mL) in bovine folliclesThomas 2007
Unregulated anabolism
—
Bypasses physiological GH/IGF-1 feedback; no pulsatility control
Unknown human safety profile
—
No published human trials; safety data absent
Absolute Contraindications
ARA 290
- ·Hypersensitivity to ARA 290
IGF-1 LR3
- ·Active malignancy or history of cancer
- ·Not approved for human use
Relative Contraindications
ARA 290
- ·Active malignancy (theoretical EPO-axis concern; not observed in trials)
IGF-1 LR3
- ·Diabetes or glucose intolerance
- ·Family history of cancer
05Administration Protocol
Parameter
ARA 290
IGF-1 LR3
1. Preparation
Reconstitute lyophilised powder per manufacturer instructions. Use sterile technique.
IGF-1 LR3 is not FDA-approved for human use. All administration data derives from animal or in vitro studies.
2. Injection site
Subcutaneous — abdomen, thigh, or upper arm. Rotate sites to avoid lipohypertrophy.
Subcutaneous or intraperitoneal injection in animal models. In vitro: added directly to culture medium at concentrations of 10–1000 ng/mL.Thomas 2007
3. Timing
Once daily, any time of day. Self-administered in Phase 2 trials.Brines 2015
Lyophilised powder reconstituted in sterile water or buffered saline per manufacturer protocol. Store at 2–8 °C after reconstitution.
4. Dosing
4 mg daily for 28 days (Phase 2 protocol). Duration for chronic use not established.Culver 2017
Enhanced stability vs native IGF-1 due to reduced IGFBP binding; exact half-life in vivo not fully characterized in humans.
5. Storage
Lyophilised: store at controlled room temperature. Reconstituted: refrigerate, use within specified timeframe.
—
06Stack Synergy
ARA 290
+ BPC-157
ModerateARA 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
IGF-1 LR3
+ GHRP-6
Multi-pathwayGHRP-6 stimulates endogenous GH release, which drives hepatic IGF-1 synthesis. IGF-1 LR3 provides exogenous, IGFBP-resistant IGF signaling. Combining upstream GH stimulation with downstream IGF receptor activation creates a dual-pathway anabolic effect. However, this bypasses natural feedback and carries compounded mitogenic risk.
- GHRP-6
- 100–200 mcg SQ · 2–3× daily
- IGF-1 LR3
- Research doses variable · post-workout typical in animal models
- Note
- Research context only — no human protocols exist
- Primary benefit
- Theoretical maximal anabolic signaling (GH + IGF axes)
+ Ipamorelin
Multi-pathwayIpamorelin (selective GHRP) stimulates pulsatile GH release without cortisol/prolactin elevation. IGF-1 LR3 directly activates IGF-1R independent of GH. This stack targets both upstream (GH secretion) and downstream (IGF receptor) nodes but eliminates physiological feedback, raising safety concerns around unchecked proliferation.
- Ipamorelin
- 200–300 mcg SQ · evening
- IGF-1 LR3
- Research doses only · timing variable
- Caution
- No human data; animal/in vitro only
- Primary benefit
- Dual-axis anabolic signaling (theoretical)