Side-by-side · Research reference

AdipotidevsIGF-1 LR3

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

AAnimal-StrongHUMAN-REVIEWED15/49 cited

BAnimal-StrongHUMAN-REVIEWED10/58 cited

Adipotide

Pro-apoptotic Vascular-Targeting Peptide · Preclinical Only

PreclinicalStatus

PHB1TargetHossen 2013

ApoptosisMechanismHossen 2013

IV · Systemic · Preclinical Protocols OnlyHossen 2013

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

Adipotide

IGF-1 LR3

Primary target

Prohibitin-1 (PHB1) on adipose vasculature endotheliumHossen 2013

IGF-1 receptor (IGF-1R)McTavish 2009

Pathway

CKGGRAKDC domain binds PHB1 → Peptide internalisation → D(KLAKLAK)₂ mitochondrial membrane disruption

IGF-1R → IRS-1 → PI3K/Akt → Cell proliferation, protein synthesis, anti-apoptosisMuhlbradt 2009

Downstream effect

Endothelial apoptosis → Adipose vascular collapse → Adipocyte involution → Weight loss

Enhanced cell proliferation, muscle anabolism, inhibition of apoptosis, increased telomerase activity

Feedback intact?

N/A — Direct apoptotic mechanism, non-hormonal

No — exogenous IGF analogue bypasses GH-mediated regulation

Origin

Synthetic bioconjugate: PHB1-targeting homing peptide + pro-apoptotic KLA sequence

Synthetic 83-AA analogue: 13-AA N-terminal extension + Arg substitution at position 3

Antibody development

—

02Dosage Protocols

Parameter

Adipotide

IGF-1 LR3

Animal dose (mouse)

Low dose (not specified in abstract)Hossen 2013

Systemic injection in diet-induced obesity (DIO) models.Hossen 2013

—

Route

Intravenous (systemic injection)

—

Frequency

Not specified in available data

—

Evidence basis

Preclinical animal models only

Animal / in vitro only

Human data

None — no clinical trials 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

Adipotide

IGF-1 LR3

Primary fat target

White adipose tissue (all depots)

—

Mechanism

Vascular apoptosis → adipose blood supply collapse → adipocyte deathHossen 2013

IGF-1R activation → lipolytic signaling; secondary to anabolic effects

Body weight reduction

Significant reduction in DIO miceHossen 2013

Absolute values not provided in abstract.

—

Leptin levels

Significant decrease

Parallel to adipose mass reduction.

—

Effect on adipocytes

Antiobesity effect on dysfunctional adipose cells (adipocytes + macrophages)Hossen 2013

—

Ectopic fat

Reduction in ectopic fat depositionHossen 2013

Marker of dysfunctional adipose tissue / metabolic syndrome.

—

Species tested

Obese rhesus monkeys, DIO mice

—

Human translation

Unknown — no clinical trials

—

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

Adipotide

IGF-1 LR3

Safety profile

Unknown — preclinical data only

—

Vascular selectivity

Targets adipose vasculature; off-target vascular effects unknown

—

Apoptotic mechanism risk

Pro-apoptotic payload may affect unintended tissues if selectivity incomplete

—

Kidney / liver toxicity

Not reported in available data

—

Immunogenicity

Not assessed in available data

—

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

Adipotide

·Human use — not approved, no clinical safety data

IGF-1 LR3

·Active malignancy or history of cancer
·Not approved for human use

Relative Contraindications

Adipotide

·Any condition requiring intact adipose-tissue vascularisation

IGF-1 LR3

·Diabetes or glucose intolerance
·Family history of cancer

05Administration Protocol

Parameter

Adipotide

IGF-1 LR3

1. Route

Intravenous injection (systemic) in preclinical models. No human protocols exist.

IGF-1 LR3 is not FDA-approved for human use. All administration data derives from animal or in vitro studies.

2. Formulation

Bioconjugate peptide. May also be encapsulated in nanoparticles (prohibitin-targeted nanoparticle formulation, KLA-PTNP, showed superior efficacy vs. free bioconjugate in mice).Hossen 2013

Subcutaneous or intraperitoneal injection in animal models. In vitro: added directly to culture medium at concentrations of 10–1000 ng/mL.Thomas 2007

3. Preclinical dosing

Low-dose systemic injection (exact dosing not specified in available abstract). Frequency and duration not detailed.Hossen 2013

Lyophilised powder reconstituted in sterile water or buffered saline per manufacturer protocol. Store at 2–8 °C after reconstitution.

4. Storage

Not specified — likely requires peptide-grade lyophilised storage and reconstitution.

Enhanced stability vs native IGF-1 due to reduced IGFBP binding; exact half-life in vivo not fully characterized in humans.

06Stack Synergy

Adipotide

— no documented stacks

IGF-1 LR3

+ GHRP-6

Multi-pathway

View GHRP-6 →

GHRP-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-pathway

View Ipamorelin →

Ipamorelin (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)