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

AOD-9604vsIGF-DES

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

APhase 2HUMAN-REVIEWED10/47 cited
BAnimal-StrongHUMAN-REVIEWED8/60 cited
AOD-9604
HGH 176-191 · β3-AR Lipolytic
250–300 mcgDaily doseHeffernan 2001
Phase 2Evidence levelHeffernan 2001Ng 2000
~30 minHalf-life
SQ · Abdomen · Daily fasted
IGF-DES
IGF-1 Analogue · Truncated N-Terminal
~10×Potency vs IGF-1
ReducedIGFBP binding
ResearchStatus
Injection (local or systemic) · Research protocols onlyBredehöft 2008

01Mechanism of Action

Parameter
AOD-9604
IGF-DES
Primary target
β3-adrenergic receptor (proposed)Ng 2000
IGF-1 receptor (IGF1R)Shields 2007
Pathway
β3-AR activation → cAMP → hormone-sensitive lipase activation → triglyceride breakdown to FFA + glycerolNg 2000
IGF1R activation → PI3K/Akt & MAPK signaling → protein synthesis, proliferation
Downstream effect
Lipolysis of adipose tissue triglycerides; FFA release for oxidation; minimal IGF-1 / insulin impactHeffernan 2001
Enhanced muscle protein synthesis, myoblast differentiation, reduced apoptosis, cell proliferation
Feedback intact?
No GH-axis or IGF-1 feedback
Unknown — no human endocrine feedback data
Origin
Synthetic modified C-terminal hexadecapeptide fragment of human GH (176-191) with N-terminal Tyr substitutionNg 2000
Synthetic truncation of native IGF-1 — removal of N-terminal Gly-Pro-Glu tripeptideBredehöft 2008
Antibody development

02Dosage Protocols

Parameter
AOD-9604
IGF-DES
Standard dose
250–300 mcg / dayHeffernan 2001
Anecdotal SQ range. Phase 2 trial dose 1 mg/day oral.
Frequency
Once daily, fasted
Variable — daily to multiple times daily in research
Lower / starter dose
150 mcg / day
Evidence basis
Phase 2 trials + animal-strongHeffernan 2001Ng 2000
Animal models + in vitro only
Duration
8–12 weeks per cycle
Reconstitution
Bacteriostatic water, 1 mL per 2 mg vial → 2 mg/mL
Timing
Morning fasted preferred (pre-cardio)
Aligns with circadian lipolysis.
Half-life
~30 min plasma
Shorter than IGF-1 due to reduced IGFBP binding
Rapid tissue uptake, limited systemic circulation.
Research dose range
10–100 ng/mL (in vitro); μg doses (animal models)
Highly context-dependent; no standardized human protocol.
Route
Subcutaneous or intramuscular (local injection favored)
Local delivery maximizes tissue-specific uptake.
Human data
None — no clinical trials

03Metabolic / Fat Loss Evidence

Parameter
AOD-9604
IGF-DES
Primary mechanism
Indirect via muscle hypertrophy → metabolic rate elevation
Direct lipolysis
Minimal evidence — IGF-1 axis primarily anabolic, not lipolytic
Prostate model
Inhibited BPH cell proliferation when combined with vitamin D3 analogueCrescioli 2002
Context-specific anti-proliferative effect, not fat loss.

04Side Effects & Safety

Parameter
AOD-9604
IGF-DES
Injection site reaction
Mild erythema
Expected — erythema, irritation, local swelling
GI symptoms
Rare mild nausea
Cardiovascular
Possible mild HR increase via β3-AR (theoretical β1 cross-reactivity)
IGF-1 elevation
None — designed to lack GH-axis activityHeffernan 2001
Insulin sensitivity
Neutral — no glucose impairmentHeffernan 2001
Cancer risk
No GH/IGF-1 axis activity → lower theoretical risk vs HGH
Pregnancy / OB
Avoid
Hypoglycemia risk
Theoretical — IGF-1 axis enhances glucose uptake
Mitogenic risk
Chronic IGF-1 receptor activation may promote cell proliferation, potential tumor growthCrescioli 2002
Edema / Fluid retention
Possible via sodium retention (IGF-1 axis effect)
Human safety data
Absent — no human trials, all effects theoretical or extrapolated
Unknown long-term effects
No chronic dosing studies in humans; endocrine, metabolic consequences unknown
Absolute Contraindications
AOD-9604
  • ·Pregnancy / breastfeeding
  • ·Severe cardiovascular disease (caution with β-receptor agonists)
IGF-DES
  • ·Active malignancy or history of cancer (mitogenic risk)
  • ·Pregnancy / lactation (no safety data)
  • ·Hypoglycemia disorders
Relative Contraindications
AOD-9604
  • ·Concurrent β-blocker therapy (theoretical antagonism)
  • ·Pheochromocytoma
IGF-DES
  • ·Diabetes mellitus (unpredictable glucose effects)
  • ·Renal or hepatic impairment (clearance unknown)
  • ·Edema-prone conditions (heart failure, nephrotic syndrome)

05Administration Protocol

Parameter
AOD-9604
IGF-DES
1. Reconstitution
Add 1 mL bacteriostatic water to 2 mg vial → 2 mg/mL = 200 mcg per 0.1 mL.
Des(1-3)IGF-1 has no approved human protocol. All administration details are derived from animal or in vitro research and should not be construed as medical guidance.
2. Injection site
SQ — abdomen preferred. Rotate sites.
Sterile water or bacteriostatic water per research protocol. Gently swirl; do not shake. Store reconstituted peptide at 2–8 °C.
3. Timing
Morning, fasted, ideally pre-cardio for amplified fat oxidation.
Subcutaneous (abdomen, thigh) or intramuscular (deltoid, vastus lateralis). Local injection to target tissue (e.g., muscle group) may enhance regional uptake.
4. Storage
Lyophilised: room temp, light-protected. Reconstituted: refrigerate, ≤30 days.
Frequency and timing vary by research design. Post-exercise or fasted state may theoretically enhance muscle uptake.
5. Needle
29–31G, 4–8 mm insulin syringe.
27–31G insulin syringe for subcutaneous; 25–27G for intramuscular.
6. Monitoring
Glucose monitoring essential (hypoglycemia risk). No established IGF-1 or safety labs for human use.

06Stack Synergy

AOD-9604
+ MOTS-c
Moderate
View MOTS-c

AOD-9604 mobilises FFAs from adipose via β3-AR; MOTS-c upregulates AMPK / PGC-1α / FAO machinery so that mobilised FFAs are efficiently oxidised. The pathways are sequential — supply (AOD) plus demand (MOTS-c) — and produce more durable lipolytic effects than either alone in anecdotal protocols.

AOD-9604
250–300 mcg SQ · morning fasted (daily)
MOTS-c
5 mg SQ · 2–3× per week (pre-workout)
Primary benefit
Fat mobilisation + mitochondrial oxidation, no IGF-1 concern
IGF-DES
+ BPC-157
Moderate
View BPC-157

Des(1-3)IGF-1 promotes myoblast differentiation and protein synthesis, while BPC-157 enhances tissue repair, angiogenesis, and collagen synthesis. Both act on distinct pathways (IGF1R vs gastric pentadecapeptide mechanisms) to support muscle recovery and connective tissue integrity. Synergy is mechanistic but lacks direct co-administration studies.

Des(1-3)IGF-1
Research dose post-workout (local IM)
BPC-157
250–500 mcg SQ, daily or twice daily
Frequency
Daily or per research protocol
Primary benefit
Accelerated muscle repair, enhanced hypertrophy, connective tissue support
+ TB-500
Moderate
View TB-500

TB-500 (Thymosin Beta-4 fragment) promotes cell migration, angiogenesis, and wound healing via actin regulation. Des(1-3)IGF-1 drives protein synthesis and myoblast proliferation. Combined, these peptides may synergistically enhance muscle recovery, repair, and hypertrophy through complementary anabolic and regenerative pathways. No direct human co-administration data.

Des(1-3)IGF-1
Research dose post-workout (local IM)
TB-500
2–5 mg SQ, 2× weekly
Frequency
Per research cycle
Primary benefit
Muscle hypertrophy, injury recovery, vascular support