Dihexa for Cognitive Enhancement - Quick Reference Sheet
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Dihexa for Cognitive Enhancement

Created on 09/22/2026 – Quick Reference based on Evidence Review created using AI4L / Opus 5 – Audit

Dihexa is a laboratory-made compound, sold as a research chemical, used to sharpen thinking by strengthening a natural growth signal that helps nerve cells build new connections. In rodents it restored memory damaged by drugs, ageing, or injury. No person has ever taken dihexa in a registered study, so its dose, side effects, and long-term safety are unknown. Three founding papers were withdrawn after images were found altered. (Full Review)

Protocol

The community approach
5 to 20 mg/day
Powder dissolved in dimethyl sulfoxide and applied topically, or taken orally in capsules, in cycles of 4 to 8 weeks. The range brackets the roughly 20 mg/day that body-surface-area scaling of the 2 mg/kg rodent dose gives for a 70 kg adult. No regulator, trial, or medical body has established a dose.
Single versus split dosing
Single daily dose
A terminal half-life measured in days makes split dosing pharmacologically pointless, since plasma concentration is governed by accumulation rather than by peaks. Less-than-daily administration is defensible on the same reasoning.
Best time of day
Morning
Morning administration is the consistent convention, based on reports of delayed sleep onset with later dosing. If the mechanism is genuinely structural rather than stimulant, timing should matter only for tolerability.
Time to effect
Time to effect
Unknown in humans
In rodent studies behavioural improvement emerged over days to weeks of daily dosing rather than acutely. Any perceived effect within hours of a first dose is more likely to be expectation than pharmacology.
Fair assessment period
At least 6 to 8 weeks
The long accumulation phase sets the floor. Absence of a measurable, reproducible change on a repeatable objective cognitive battery after 12 weeks is a result, not a reason to increase the dose.
Time to steady state
6 to 9 weeks
A terminal half-life of roughly 12 to 13 days in rats implies this long to steady state and a comparable washout, so early tolerability says little about steady-state exposure. These figures come from the developing parties and have never been independently verified.

Benefits

Contraindications
  • MET-directed kinase inhibitors (capmatinib, tepotinib, crizotinib, cabozantinib)
  • Hepatocyte growth factor and MET-targeting antibodies used in oncology trials
  • Active malignancy, or any malignancy treated within the past five years
  • Monitored precancerous lesion (Barrett's oesophagus, cervical intraepithelial neoplasia, colonic adenomas on surveillance, monoclonal gammopathy of undetermined significance, dysplastic naevi)
  • Hereditary cancer syndrome (hereditary papillary renal cell carcinoma, Lynch syndrome, Li-Fraumeni syndrome)
  • Hepatic impairment of Child-Pugh Class B or C, or renal impairment with an estimated glomerular filtration rate below 60 mL/min/1.73 m²
  • Pregnancy, attempting to conceive, or breastfeeding
  • Under 18 years of age
  • Established seizure disorder or history of unprovoked seizure
  • Proliferative diabetic retinopathy or another active proliferative vascular condition
    •
Key Interactions
  • Other tyrosine kinase inhibitors and antiangiogenic agents (sunitinib, sorafenib, bevacizumab)
  • Angiotensin-converting enzyme inhibitors (lisinopril, enalapril, ramipril) and angiotensin receptor blockers (losartan, valsartan, telmisartan)
  • Cholinesterase inhibitors (donepezil, rivastigmine, galantamine)
  • Anticholinergic medications available over the counter (diphenhydramine, dimenhydrinate, doxylamine)
  • Over-the-counter non-steroidal anti-inflammatory drugs (ibuprofen, naproxen)
  • Growth-signalling supplements with additive effects (alpha-glycerylphosphorylcholine, citicoline, huperzine A, Hericium erinaceus, semax, selank, cerebrolysin)
  • BPC-157 and other angiogenic peptides
  • Growth hormone secretagogues and insulin-like growth factor 1 raising agents (ipamorelin, CJC-1295, tesamorelin)
  • Rapamycin, metformin, and other growth-pathway suppressors
    •

Risk & Side Effects

  • High: Wholly uncharacterised human safety profile; failure of the intended effect because the mechanistic basis was retracted
  • Medium: Contaminated, mislabelled, or misdosed gray-market product
  • Low: Tumour promotion through sustained MET pathway activation; tissue accumulation from a very long terminal half-life; proliferative and angiogenic effects in non-neural tissue
  • Speculative: Lowered seizure threshold from excessive synaptic remodelling; maladaptive rewiring and loss of existing circuit precision; overstimulation, irritability, and disrupted sleep onset

Monitoring

Marker Target Why
Complete blood count with differential White cells 4.5–7.0 K/μL; platelets 175–250 K/μL; haemoglobin mid-reference for sex Detects marrow, immune, or occult proliferative change
Comprehensive metabolic panel: alanine and aspartate aminotransferase Alanine aminotransferase 10–26 U/L (men), 10–19 U/L (women); aspartate aminotransferase 10–26 U/L Liver is a MET-rich organ and a clearance route for the compound
Estimated glomerular filtration rate and creatinine Estimated glomerular filtration rate above 90 mL/min/1.73 m² Renal clearance contributes to elimination; impairment prolongs an already long half-life
Lactate dehydrogenase 140–180 U/L Non-specific marker of cell turnover and tissue proliferation; a rising trend warrants investigation
High-sensitivity C-reactive protein Below 0.9 mg/L Establishes whether the internal environment is inflammatory and growth-permissive before starting
Insulin-like growth factor 1 Mid-reference for age, roughly 120–160 ng/mL at ages 40–60 Indicates systemic growth signalling tone that dihexa's pathway would add to
Fasting insulin and haemoglobin A1c Insulin 2–5 μIU/mL; haemoglobin A1c 4.9–5.3% Insulin resistance both blunts neurotrophic signalling and raises proliferative risk
Plasma phosphorylated tau 217 Below the assay-specific cut-off for Alzheimer's-type change Indicates whether there is active neurodegeneration for the mechanism to address
Neurofilament light chain Below 10 pg/mL under age 50; below 20 pg/mL over age 60 Marker of ongoing nerve fibre damage; a rising value on treatment would be a stop signal
Prostate-specific antigen (men over 45) Below 1.0 ng/mL at ages 40–50; below 2.5 ng/mL thereafter The most accessible marker of a common hormone-responsive proliferative process

Cadence: Full panel at baseline, at 4 weeks, at 12 weeks, and every 3 months for as long as use continues, drawn fasting and in the morning; age-appropriate cancer screening maintained annually; a final panel 8 weeks after stopping.

Qualitative Assessment

  • Word-finding fluency and the frequency of tip-of-the-tongue episodes in ordinary conversation
  • Working memory in practice: holding a multi-step instruction, keeping track of several threads in a discussion
  • Sustained attention during a demanding task, and how long it holds before it degrades
  • Sleep onset latency and subjective sleep quality, given the reported evening-dosing effect
  • Mood stability and irritability, the two effects most commonly self-reported
  • A repeatable objective cognitive battery administered at the same time of day at baseline, 4 weeks, and 12 weeks
  • New physical findings: palpable masses, changing skin lesions, unexplained weight loss, persistent headache
Not medical advice. Educational distillation of a single evidence review. Confirm any decision with a qualified clinician, especially in the presence of prescription drugs or chronic conditions.