ACD-856, NeuroRestore ACD856, ACD856 (AlzeCure) · Evidence-based safety and harm-reduction overview.
| Also known as | ACD-856, NeuroRestore ACD856, ACD856 (AlzeCure) |
| Category | Research Chemical |
| Drug class | Triazinetrione; small-molecule positive allosteric modulator (PAM) of Trk receptors |
| Molecular target | TrkA / TrkB / TrkC (NGF and BDNF signaling); weaker activity at IGF1R and FGFR1 |
| Developer | AlzeCure Pharma AB (Sweden), NeuroRestore platform |
| Route | Oral |
| Human half-life | Approximately 19-20 hours; near-complete oral bioavailability |
| Trial stage | Phase 1 SAD and MAD plus Phase Ib completed; Phase 2 in Alzheimer's stated as planned (as of 2026) |
| US legal status | Investigational drug, not FDA-approved and not approved by any regulator anywhere. ACD856 is a proprietary new chemical entity owned by AlzeCure Pharma AB and is in clinical trials; it is not a marketed medicine, not a lawful dietary supplement, and not otherwise legal to sell for human consumption in the United States. There is no legitimate consumer or research-chemical supply chain for it, and any product marketed online under this name would be of unknown identity and purity and outside any regulatory framework. Informational only; Peptropix does not sell this compound. |
ACD856 is an orally active, first-in-class small molecule developed by the Swedish company AlzeCure Pharma as part of its NeuroRestore platform. It is described as a positive allosteric modulator (PAM) of the tropomyosin receptor kinase (Trk) family, meaning it is proposed to amplify signaling downstream of the neurotrophins nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) rather than acting as a direct receptor agonist. The lead target indication is cognitive dysfunction in Alzheimer's disease, with depression, sleep disorders and traumatic brain injury pursued as secondary, earlier-stage possibilities. As of 2026 it has completed Phase 1 single- and multiple-ascending-dose studies plus a Phase Ib study, and the developer has stated Phase 2 is being planned. Efficacy in any disease has not been demonstrated in patients. ACD856 should be understood as an experimental drug candidate, not a nootropic that can be obtained or used.
ACD856 is reported to bind the intracellular kinase domain of Trk receptors as a positive allosteric modulator, potentiating signaling that is triggered by the endogenous neurotrophins rather than activating the receptor on its own. Reported in vitro potencies are roughly EC50 ~382 nM at TrkA, ~295 nM at TrkB and in a similar range at TrkC, with weaker allosteric activity described at IGF1R and FGFR1. Because it amplifies NGF- and BDNF-driven signaling, downstream effects described in preclinical models include increased TrkB phosphorylation, ERK1/2 activation, greater neurite outgrowth, higher SNAP-25 and BDNF levels, and protection of cultured cortical neurons against amyloid-beta and energy-deprivation toxicity. This mechanism is the scientific rationale for the program; it has not been shown to translate into cognitive or antidepressant benefit in humans.
The chemical series originated from an unexpected observation that the veterinary antiparasitic triazinetriones toltrazuril and ponazuril possess Trk-potentiating activity, noted around 2013. AlzeCure screened on the order of 25,000 compounds and carried out structural optimization of that scaffold to improve drug-like properties for human use; ponazuril (referenced as ACD855) was considered to have too long an elimination half-life. ACD856 emerged as a lead of the NeuroRestore program. It advanced into first-in-human microdose and single-ascending-dose studies, followed by multiple-ascending-dose and Phase Ib work through the mid-2020s, with the company positioning it for Phase 2 in Alzheimer's disease and reporting European Innovation Council funding to support development.
Human data are early and confined to safety, tolerability, pharmacokinetics and exploratory pharmacodynamic (qEEG) readouts in healthy volunteers; no efficacy trials in Alzheimer's, depression or any patient population have been reported. A double-blind, placebo-controlled single-ascending-dose study in 56 healthy subjects (1-150 mg oral) reported the compound was well tolerated with no serious adverse events, near-complete bioavailability and an elimination half-life of roughly 19-20 hours. A multiple-ascending-dose / Phase Ib program (reported doses in the 10-90 mg/day range for 7 days) again reported good tolerability, measurable cerebrospinal-fluid exposure (evidence the drug crosses into the brain), and dose-dependent qEEG changes (increased relative theta power, decreased fast alpha/beta, increased theta/beta ratio) most pronounced at 90 mg. The authors themselves cautioned that these statistically significant qEEG shifts do not by themselves support conclusions about cognitive benefit. All claims about memory, neuroprotection or antidepressant action rest on in vitro and rodent work, not on human outcomes. There are, at present, no robust human efficacy trials.
Informational only, not a protocol and not a recommendation. Doses that appear in the published Phase 1 literature were chosen by investigators purely to characterize safety and pharmacokinetics in healthy volunteers, not to treat anyone: single oral doses ranged from about 1 mg up to 150 mg, and the multiple-dose / Phase Ib work used repeated daily oral doses reported in roughly the 10-90 mg/day range for 7 days. These figures describe what was studied under medical supervision in a trial; no therapeutic dose has been established for any condition, and there is no validated regimen for out-of-trial use. Nothing here should be read as guidance to take ACD856.
This is general research/context information, not medical advice or a recommended protocol.
There is no evidence base for combining ACD856 with anything, and doing so is not advisable. It is an investigational single agent under study in isolation; no combination has been tested for safety or benefit in humans. Layering an unproven Trk modulator with other nootropics, stimulants, or neuroactive supplements would compound unknown pharmacology with unknown interaction risk. For people genuinely interested in supporting BDNF-related brain health, the defensible levers are lifestyle ones (aerobic exercise, sleep, and where appropriate clinician-directed treatment of mood or cognitive disorders), not experimental stacks.
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Get tested with Ulta Lab Tests →No. It is an investigational drug in clinical trials, not approved by the FDA or any regulator, and not a legal supplement. It is not legitimately available to consumers, and anything sold under the name would be of unverifiable identity and purity.
That has not been shown. Human studies so far only assessed safety, pharmacokinetics and brain-activity (qEEG) signals in healthy volunteers. Claims about cognition and antidepressant effects come from cell and rodent studies, not from patient efficacy trials.
It is described as a positive allosteric modulator of Trk receptors, meaning it amplifies signaling driven by the neurotrophins NGF and BDNF rather than switching the receptor on directly. In preclinical models this raised markers of neuroplasticity and protected neurons, but that mechanism has not been shown to produce clinical benefit.
We do not give dosing guidance. Published trials used single oral doses from about 1 to 150 mg and repeated daily doses reported around 10-90 mg for 7 days, chosen to study safety and pharmacokinetics under medical supervision. No therapeutic dose exists, and anyone with a genuine clinical question should consult a physician.
Short-term Phase 1 exposure in healthy volunteers was reported as well tolerated, with mild headache the main possibly-related event and no serious adverse events up to 150 mg. But long-term safety, safety in patients, drug interactions, and reproductive safety are all uncharacterized, and unregulated material carries additional risk.
ACD856 was chemically optimized from the veterinary antiparasitic triazinetriones toltrazuril and ponazuril, which were found to have Trk-potentiating activity. Ponazuril (referenced as ACD855) was considered unsuitable for humans partly due to too long a half-life, motivating development of ACD856.
Medical & legal disclaimer. This site is for informational and harm-reduction purposes only. It is not medical advice and is not a substitute for a licensed healthcare professional. The compounds discussed are largely not approved by the FDA for human use and many are sold strictly as research chemicals 'not for human consumption.' Nothing here is an endorsement to purchase, possess, or use any substance. Laws vary by jurisdiction. Always consult a qualified physician and follow the law where you live.
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