Side-by-side · Research reference

DihexavsIGF-1 LR3

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

AAnimal-StrongHUMAN-REVIEWED7/28 cited

BAnimal-StrongHUMAN-REVIEWED10/58 cited

Dihexa

Angiotensin IV Analogue · Pre-Clinical

Pre-clinicalDevelopment stage

Rodent onlyEvidence basisBenoist 2014

HGF/c-MetTarget systemWright 2015

Not established — animal studies only

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

Dihexa

IGF-1 LR3

Primary target

c-Met receptor (HGF receptor tyrosine kinase)

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

Pathway

HGF/c-Met receptor activation → downstream signaling cascade → synaptogenesis and dendritic arborization

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

Downstream effect

Induction of dendritic arborization, synapse formation, neurogenesis, and neuroprotection in rodent models

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

Feedback intact?

—

No — exogenous IGF analogue bypasses GH-mediated regulation

Origin

Small-molecule angiotensin IV analogue designed to activate HGF/c-Met systemWright 2015

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

Antibody development

—

02Dosage Protocols

Parameter

Dihexa

IGF-1 LR3

Human dosing

Not established — no human trials

—

Animal studies

Mouse/rat models only — dosing not translatable to humans

—

Evidence basis

Pre-clinical / Rodent models

Animal / in vitro only

Clinical status

No Phase 1, 2, or 3 trials published

—

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

Dihexa

IGF-1 LR3

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

Dihexa

IGF-1 LR3

Human safety data

None available — no human clinical trials

—

Theoretical c-Met risks

c-Met receptor activation has been implicated in tumorigenesis; unknown cancer risk profile

—

Pre-clinical tolerability

Not systematically reported in available studies

—

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

Dihexa

·Not approved for human use — research compound only

IGF-1 LR3

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

Relative Contraindications

Dihexa

·Theoretical contraindication: active or history of malignancy (c-Met pathway involvement in cancer)

IGF-1 LR3

·Diabetes or glucose intolerance
·Family history of cancer

05Administration Protocol

Parameter

Dihexa

IGF-1 LR3

1. Human administration

No established protocol. Dihexa has not been tested in human subjects. Animal studies used various routes (typically subcutaneous or intraperitoneal in rodents) not translatable to clinical use.

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

2. Legal status

Pre-clinical research compound. Not approved by FDA or any regulatory authority for human use.

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

3. Reconstitution (research)

—

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

4. Stability

—

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

06Stack Synergy

Dihexa

— 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)