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

DihexavsGlutathione

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
BHuman-MechanisticHUMAN-REVIEWED6/39 cited
Dihexa
Angiotensin IV Analogue · Pre-Clinical
Pre-clinicalDevelopment stage
Rodent onlyEvidence basisBenoist 2014
HGF/c-MetTarget systemWright 2015
Not established — animal studies only
Glutathione
Endogenous Tripeptide · Antioxidant
γ-Glu-Cys-GlyStructure
UbiquitousTissue distribution
GCL + GSBiosynthesisWang 2026Aiana 2026
IV · Oral · Inhaled

01Mechanism of Action

Parameter
Dihexa
Glutathione
Primary target
c-Met receptor (HGF receptor tyrosine kinase)
Intracellular redox systems, glutathione peroxidase, glutathione transferase
Pathway
HGF/c-Met receptor activation → downstream signaling cascade → synaptogenesis and dendritic arborization
Synthesized via glutamate-cysteine ligase (GCL) → γ-glutamylcysteine → glutathione synthetase (GS) → GSH
Downstream effect
Induction of dendritic arborization, synapse formation, neurogenesis, and neuroprotection in rodent models
Reduction of reactive oxygen species, conjugation of electrophiles, maintenance of cellular thiol-disulfide balance, GPX4 activation for lipid peroxide reduction
Feedback intact?
Origin
Small-molecule angiotensin IV analogue designed to activate HGF/c-Met systemWright 2015
Endogenous tripeptide; predominantly synthesized in liver, exported to extracellular space and tissuesTerrell 2025Hecht 2026
Antibody development

02Dosage Protocols

Parameter
Dihexa
Glutathione
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 mechanistic + human mechanistic
Clinical status
No Phase 1, 2, or 3 trials published
Endogenous synthesis
Hepatic synthesis ~10 g/day (basal rate)
Tissue-specific; demand-driven upregulation via Nrf2 signaling.
Exogenous oral
250–1000 mg/day
Bioavailability limited; gastric hydrolysis reduces systemic uptake.
IV supplementation
600–1200 mg (research protocols)
Used in clinical oxidative stress and hepatic detoxification studies.
Precursor strategy
N-acetylcysteine (NAC) 600–1200 mg/day
Provides cysteine for endogenous GSH synthesis; bypasses GI degradation.

04Side Effects & Safety

Parameter
Dihexa
Glutathione
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
Oral supplementation
GI discomfort, bloating (mild, dose-dependent)
IV administration
Rare hypersensitivity, infusion site reaction
Inhalation
Bronchospasm risk in asthma (rare)
Tumor metabolism
Extracellular GSH catabolism supplies cysteine to tumors; theoretical concern in active malignancyHecht 2026
Absolute Contraindications
Dihexa
  • ·Not approved for human use — research compound only
Glutathione
Relative Contraindications
Dihexa
  • ·Theoretical contraindication: active or history of malignancy (c-Met pathway involvement in cancer)
Glutathione
  • ·Active malignancy (theoretical cysteine supply risk)Hecht 2026
  • ·Severe asthma (inhaled formulations)

05Administration Protocol

Parameter
Dihexa
Glutathione
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.
Capsule or liquid form, 250–1000 mg once daily. Take on empty stomach for improved absorption, though GI hydrolysis limits bioavailability. NAC precursor strategy often preferred.
2. Legal status
Pre-clinical research compound. Not approved by FDA or any regulatory authority for human use.
Clinical protocols: 600–1200 mg slow infusion over 30–60 minutes. Used for acute oxidative stress, hepatic detoxification support. Administered in medical settings.
3. Inhaled formulations
Nebulized GSH (research protocols). Monitor for bronchospasm in reactive airway patients. Used experimentally for pulmonary oxidative stress.
4. Precursor supplementation
N-acetylcysteine (NAC) 600–1200 mg/day PO. Provides cysteine substrate for endogenous GSH synthesis. Bypasses gastric degradation, preferred for chronic supplementation.