Side-by-side · Research reference

IGF-DESvsPE 22-28

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

AAnimal-StrongHUMAN-REVIEWED8/60 cited

BAnimal-StrongHUMAN-REVIEWED16/47 cited

IGF-DES

IGF-1 Analogue · Truncated N-Terminal

~10×Potency vs IGF-1

ReducedIGFBP binding

ResearchStatus

Injection (local or systemic) · Research protocols onlyBredehöft 2008

PE 22-28

TREK-1 Antagonist · Pre-Clinical

0.12 nMTREK-1 IC50Djillani 2017

7 AAPeptide lengthDjillani 2017

AnimalEvidence stage

IP · SQ · Once Daily (animal models)Djillani 2017 Pietri 2019

01Mechanism of Action

Parameter

IGF-DES

PE 22-28

Primary target

IGF-1 receptor (IGF1R)Shields 2007

TREK-1 two-pore-domain potassium channelDjillani 2017 Ma 2020

Pathway

IGF1R activation → PI3K/Akt & MAPK signaling → protein synthesis, proliferation

TREK-1 channel blockade → Neuronal membrane depolarisation → Enhanced hippocampal excitability → Increased neuroplasticity

Downstream effect

Enhanced muscle protein synthesis, myoblast differentiation, reduced apoptosis, cell proliferation

Antidepressant-like activity in forced swim test and tail suspension test; reduced A1-like reactive astrocyte activation; neuroprotection via NF-κB pathway modulationDjillani 2017 Cong 2023 Wu 2021

Feedback intact?

Unknown — no human endocrine feedback data

N/A — direct ion channel blockade; not receptor-mediated endocrine axis

Origin

Synthetic truncation of native IGF-1 — removal of N-terminal Gly-Pro-Glu tripeptideBredehöft 2008

Synthetic truncation of spadin (PE 12-28), itself derived from the sortilin propeptide C-terminus. Residues 22-28: Val-Val-Arg-Gly-Trp-Leu-Arg.Djillani 2017 Mazella 2018

Antibody development

—

Not reported in animal studies

02Dosage Protocols

Parameter

IGF-DES

PE 22-28

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.

—

Frequency

Variable — daily to multiple times daily in research

Once daily

Sustained antidepressant effect over 7+ days.

Evidence basis

Animal models + in vitro only

Multiple rodent RCTs; behavioral + electrophysiology endpointsDjillani 2017 Qi 2018 Wu 2021

Human data

None — no clinical trials

—

Half-life

Shorter than IGF-1 due to reduced IGFBP binding

Rapid tissue uptake, limited systemic circulation.

—

Animal dose (antidepressant)

—

0.3–3 µg/kg IP

Effective in forced swim test, tail suspension test, CUMS models.

Animal dose (neuroprotection)

—

0.03 µg/kg IPPietri 2019

Low-dose TREK-1 activation post-stroke for 7 days, then high-dose blockade.

Onset (animal)

—

Within hours (acute); full effect 4–7 days

Duration (animal)

—

7–28 days testedQi 2018 Pietri 2019

Comparison to fluoxetine

—

PE 22-28 outperforms fluoxetine in CUMS-sensitive rats by day 7

Chronic administration shows superior long-term efficacy.

Human equivalent (extrapolated)

—

Not established — no clinical trials

Allometric scaling from rodent data unavailable.

03Metabolic / Fat Loss Evidence

Parameter

IGF-DES

PE 22-28

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

IGF-DES

PE 22-28

Hypoglycemia risk

Theoretical — IGF-1 axis enhances glucose uptake

—

Mitogenic risk

Chronic IGF-1 receptor activation may promote cell proliferation, potential tumor growthCrescioli 2002

—

Injection site reaction

Expected — erythema, irritation, local swelling

—

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

—

Toxicity (animal)

—

No adverse effects reported at therapeutic doses

Cardiovascular (theoretical)

—

TREK-1 expressed in cardiac tissue; arrhythmia risk unclear

Weight change

—

Not reported in animal studies

Neurological

—

No seizures or behavioral abnormalities noted

Long-term safety

—

Unknown — longest animal study 28 days

Absolute Contraindications

IGF-DES

·Active malignancy or history of cancer (mitogenic risk)
·Pregnancy / lactation (no safety data)
·Hypoglycemia disorders

PE 22-28

·Human use — no clinical safety data available

Relative Contraindications

IGF-DES

·Diabetes mellitus (unpredictable glucose effects)
·Renal or hepatic impairment (clearance unknown)
·Edema-prone conditions (heart failure, nephrotic syndrome)

PE 22-28

·Cardiac arrhythmia or channelopathy (theoretical TREK-1 cardiac role)

05Administration Protocol

Parameter

IGF-DES

PE 22-28

1. Research context only

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.

Dissolved in sterile saline or vehicle. Intraperitoneal injection, 0.3–3 µg/kg body weight. Once daily administration in rodent behavioral studies.

2. Reconstitution (if lyophilized)

Sterile water or bacteriostatic water per research protocol. Gently swirl; do not shake. Store reconstituted peptide at 2–8 °C.

Shorter peptide length (7 AA) confers improved plasma stability vs 17-AA spadin. Exact storage conditions not detailed in published protocols.Djillani 2017

3. Injection site

Subcutaneous (abdomen, thigh) or intramuscular (deltoid, vastus lateralis). Local injection to target tissue (e.g., muscle group) may enhance regional uptake.

Enhanced CNS bioavailability vs full spadin, likely due to smaller size. Mechanism (passive diffusion vs active transport) not fully characterized.

4. Timing

Frequency and timing vary by research design. Post-exercise or fasted state may theoretically enhance muscle uptake.

Not established — peptide synthesis methods for research use only. No pharmaceutical-grade formulation available.

5. Needle gauge

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

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

PE 22-28

— no documented stacks