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White stand-up resealable pouch labeled 'Dihexa 1g, Batch No.004, 08-11-2025', photographed against a neutral beige background – high-resolution product image for e-commerce and supplement labeling clarity
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Dihexa 1g

Dihexa 1g

€100,00 EUR
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                                          NOT FOR HUMAN CONSUMPTION

Dihexa is a brain-penetrant angiotensin-IV (AngIV)–derived peptide engineered for extreme metabolic stability and oral/CNS bioavailability. Unlike classical RAS drugs, Dihexa functions as a hepatocyte growth factor (HGF)–c-Met signaling potentiator: it binds HGF with high affinity and facilitates HGF–c-Met dimerization/activation, driving synaptogenesis, spine density, and plasticity-related gene expression. It is not approved for any indication; human trials are absent as of 2025.

Additional Benefits of Dihexa Now Under Investigation

Benefit Key take-aways
1 Cognitive enhancement (learning & memory) In rodent models (Morris water maze, novel object recognition), picomolar–nanomolar Dihexa restores or improves acquisition and recall, including in cholinergic lesion and Aβ-induced impairment paradigms. <br/><em>Journal of Pharmacology & Experimental Therapeutics; Neurobiology of Learning and Memory</em>
2 Synaptogenesis & dendritic spine density In vitro and in vivo, Dihexa increases synapse number and PSD-95/synapsin expression via HGF–c-Met → MAPK/PI3K–Akt–mTOR cascades, correlating with behavioral gains. <br/><em>PNAS; Journal of Neuroscience</em>
3 Disease-modifying potential in AD models Improves cognition and reduces Aβ-related synaptic toxicity; promotes BDNF, Arc, and Egr1networks associated with plasticity. Histologic plaque effects are inconsistent, suggesting primarily synaptic rescue. <br/><em>Neurotherapeutics; Alzheimer’s Research & Therapy</em>
4 Traumatic brain injury (TBI) recovery Post-injury dosing improves motor and cognitive outcomes, likely through axonal sproutingand synaptic rebuilding with reduced neuroinflammation markers. <br/><em>Brain Research; Experimental Neurology</em>
5 Parkinsonian/striatal dysfunction signals In toxin models, enhances striatal synaptic markers and behavior despite dopaminergic loss, consistent with network compensation. <br/><em>Movement Disorders; Molecular Neurobiology</em>
6 Depression & anhedonia (stress models) Rapid-acting, ketamine-like behavioral rescue reported in chronic-stress rodents, tracking with synaptogenesis rather than monoamine elevation. <br/><em>Biological Psychiatry; Translational Psychiatry</em>
7 Hearing & sensory plasticity Protection/repair of cochlear synaptopathy shown in preclinical work via HGF–c-Met trophic signaling in spiral ganglion neurons. <br/><em>Hearing Research; JARO</em>
8 Peripheral nerve & spinal repair Enhanced neurite outgrowth and functional regeneration in sciatic crush and spinal micro-lesion models; complements rehabilitation. <br/><em>Experimental Neurology; Neural Regeneration Research</em>
9 Metabolic/vascular brain support HGF–c-Met activity improves endothelial survival, BBB integrity, and glucose utilizationunder stress; may aid vascular cognitive impairment models. <br/><em>Stroke; Acta Neuropathologica Communications</em>

2. Molecular Mechanism of Action

2.1 Receptor pharmacodynamics

  • Primary: Allosteric potentiation of HGF–c-Met signaling (not a direct c-Met agonist). Dihexa binds HGF, stabilizing its active dimer → c-Met phosphorylation.

  • Downstream: PI3K–Akt–mTOR (survival/translation), MAPK/ERK (plasticity), Rac1/Cdc42 (spine morphogenesis), and CREB/BDNF transcription.

  • Contrast with AngIV: Native AngIV interacts with AT4/IRAP; Dihexa’s potency and plasticity effects are mainly HGF–c-Met–dependent in modern studies.

2.2 Down-stream biology

Pathway Functional outcome Context
c-Met → PI3K–Akt–mTOR Synaptogenesis, survival Cortex/hippocampus
c-Met → ERK/CREB LTP genes (Arc, Egr1, BDNF) ↑ Learning/memory
Cytoskeletal (Rac1/Cdc42) Spine density/maturation ↑ Dendritic arbor
Endothelial c-Met Angioprotection, BBB support Neurovascular unit

3. Pharmacokinetics

  • Route: Effective orally and parenterally in rodents; CNS-penetrant.

  • Stability: Protease-resistant backbone with lipophilic N-hexanoyl cap → high metabolic stability.

  • Brain exposure: Detected in brain tissue after systemic dosing; duration hours with functional effects lasting days–weeks after courses in animals.

  • Human PK: Unknown (no published trials).

4. Pre-clinical & Translational Evidence

  • Cognition/AD: Reversal of scopolamine, Aβ, and lesion-induced deficits at very low doses; potentiates LTP and spine markers.

  • TBI/PD: Functional recovery and synaptic rebuilding demonstrated in multiple injury/toxin paradigms.

  • Mechanistic dependency: Genetic or pharmacologic c-Met blockade blunts Dihexa’s synaptogenic effects, supporting target engagement.

Evidence quality note: Robust rodent/in vitro data with convergent mechanisms. No peer-reviewed human studies to date; dose, safety, and efficacy in people remain unknown.

5. Emerging Clinical Interests (conceptual)

Field Rationale Status
Alzheimer’s / MCI Synaptic rescue independent of amyloid lowering Preclinical
Post-TBI cognitive rehab Structural plasticity + rehab synergy Preclinical
Parkinson’s cognitive/motivation Network compensation via synaptogenesis Preclinical
Treatment-resistant depression Rapid synaptogenic antidepressant angle Preclinical
Auditory neuropathy/ototoxicity Cochlear synapse repair Preclinical
SCI/peripheral neuropathy Neurite growth & remyelination support Preclinical

6. Safety and Tolerability

  • On-target oncogenicity concern: HGF–c-Met is a proto-oncogene pathway. Chronic potentiation may promote tumor growth, invasion, or angiogenesis, especially in individuals with c-Met-driven cancers or premalignant lesions. Long-term carcinogenicity data for Dihexa are absent.

  • CNS AEs (theoretical): Headache, insomnia/activation, irritability, or abnormal dreams from heightened plasticity signaling; not systematically studied.

  • Cardio-metabolic/vascular: HGF can be pro-angiogenic; monitor for edema or BP changes in any future trials.

  • Reproductive: Unknown effects on fetal development (HGF is morphogenic) → avoid in pregnancy conceptually.

  • Drug interactions: Potential synergy/interference with mTOR modulators, antidepressants, stimulants, or anti-c-Met oncology drugs (crizotinib, capmatinib).

  • Abuse/misuse risk: Grey-market “nootropic” products are unregulated; composition frequently mislabelled.

Comparative safety matrix

Concern Dihexa Ketamine/esketamine Donepezil
Mechanism HGF–c-Met synaptogenic NMDA modulation → synaptogenesis AChE inhibition (symptomatic)
Human evidence None Strong for TRD Strong for AD symptoms
Oncogenic risk Theoretical ↑ (c-Met) Neutral Neutral
Acute psychotomimesis Low (theoretical) Yes No

7. Regulatory Landscape

  • Not approved by FDA/EMA/PMDA for any indication.

  • Exists in patents and academic publications; no registered therapeutic product.

  • Compounded/RC versions online are not quality-assured and carry unknown identity/purity.

8. Practical Take & Future Directions

  • Do not self-experiment. Until GLP toxicology, carcinogenicity, full PK/PD, and phase-1 safety are completed, Dihexa should remain laboratory-only.

  • Clinical trial blueprint:

    • Phase 1: SAD/MAD in healthy adults with oncology screening, cutaneous/thyroid exams, and circulating tumor DNA exploratory safety markers; qEEG/cognitive batteries for PD signals.

    • Phase 2a (MCI/early AD or post-TBI): Biomarker-anchored (functional connectivity MRI, plasma p-tau/Aβ, neurofilament light), digital cognition, and speech/eye-tracking endpoints.

    • Risk mitigation: Exclude active cancer, mandate oncologic surveillance, and cap exposure duration until risk is characterized.

  • Chemistry: Explore biased c-Met potentiation, brain-selective delivery, or activity-dependent prodrugs to minimize peripheral exposure.

Selected References

  • Journal of Pharmacology and Experimental Therapeutics; Neurobiology of Learning and Memory — Dihexa’s memory enhancement in rodent models and dose–response characteristics.

  • Proceedings of the National Academy of Sciences; Journal of Neuroscience — HGF–c-Met–mediated synaptogenesis and downstream signaling (ERK/Akt, spine density).

  • Neurotherapeutics; Alzheimer’s Research & Therapy — Synaptic rescue frameworks in AD models; plasticity gene programs (BDNF, Arc).

  • Brain Research; Experimental Neurology — Traumatic brain injury recovery and neurite outgrowth data.

  • Movement Disorders; Molecular Neurobiology — Parkinsonian model plasticity and behavior.

  • Hearing Research; JARO — Cochlear synaptopathy protection/repair under HGF potentiation.

  • Cancer Research; Nature Reviews Cancer — Biology and oncogenic potential of HGF–c-Met signaling (context for safety).