Rankings / Cognitive

ACD-856 (NeuroRestore)

Cognitive · Pan-Trk positive allosteric modulator

Tier C+

Reviewed by Read Off Label · Last reviewed · How we grade

trk-pambdnfneurotrophinalzheimerdepressioninvestigationalfrontier
5.3 / 10
Tier C+
Ev 2 Bn 5 Sf 9

Bottom line

Read Off Label grades ACD-856 (NeuroRestore) as C+ (5.3/10) based on preclinical evidence, unclear benefit magnitude, and a low-risk safety profile.

AlzeCure Pharma (Sweden) lead clinical asset.

Studied, labeled, or reported-use context: 10-90 mg/day PO range tested in Phase 1 MAD; Phase 2a dose TBD — Investigational (Phase 2a planning); no off-label or compounding pathway; not individualized guidance.

What the evidence says

AlzeCure Pharma (Sweden) lead clinical asset. Novel mechanism — small-molecule pan-Trk allosteric kinase potentiator. Mechanistically distinct from anti-amyloid mAbs and cholinesterase inhibitors — directly relevant given the Cochrane 2026 finding that the entire anti-amyloid class produces only trivial cognitive benefit (see Anti-amyloid mAbs row). Phase 1 SAD safety/PK (Hagberg 2024 Eur J Clin Pharmacol) and Phase 1 MAD with QEEG biomarker (JPAD 2023) were the key clinical anchors; trial NCT05077501. €2.5M EU European Innovation Council grant awarded 2025 for the planned Phase 2a in AD patients. Other indications in preclinical/IND-enabling: depressive disorders, sleep disorders, TBI, Parkinson's-related cognitive impairment. As of May 2026 Phase 2 efficacy had not been reported; the compound was not commercially available and had no authorized compounding or off-label access pathway. Included because biohacker readers tracking the AD pipeline will encounter it, and Trk-PAM is a novel-enough mechanism to merit a watchlist row. Next decision-relevant event: Phase 2a efficacy readout (likely 2027-2028). Practical note: "ACD-856" sometimes appears in research-chemical channels — no authorized human-use access pathway exists outside registered trials.

Mechanism

Small-molecule triazinetrione that allosterically potentiates the intracellular kinase domain of all three neurotrophin receptors (pan-Trk: TrkA EC50=382 nM; TrkB=295 nM; TrkC=33 nM); amplifies endogenous BDNF/NGF signaling rather than mimicking it; downstream effects on neurite outgrowth; synaptic plasticity; BDNF expression; and anti-inflammatory pathways; orally bioavailable with CNS penetration; proposed disease-modifying via neurotrophin restoration — distinct from cholinesterase inhibitors and anti-amyloid antibodies

Studied, labeled, or reported dose & route

10-90 mg/day PO range tested in Phase 1 MAD; Phase 2a dose TBD

This records doses and routes described in studies, approved labeling, clinical practice, or documented use. It is not individualized guidance and does not establish safety; context changes with indication, formulation, health history, monitoring, and other medicines.

Citations

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Common questions

What does the evidence show about ACD-856 (NeuroRestore)'s effects?
Read Off Label rates the evidence for ACD-856 (NeuroRestore) as Preclinical and the benefit magnitude as unclear, producing an overall grade of C+ (5.3/10). AlzeCure Pharma (Sweden) lead clinical asset.
What safety findings are reported for ACD-856 (NeuroRestore)?
ACD-856 (NeuroRestore) has a low risk profile in the database. Low (Phase 1 MAD up to 90 mg/day x 7 days well-tolerated; no SAEs; favorable cardiac conduction profile) Legal status: Investigational (Phase 2a planning); no off-label or compounding pathway.
What doses or routes are reported for ACD-856 (NeuroRestore)?
10-90 mg/day PO range tested in Phase 1 MAD; Phase 2a dose TBD This is context from studies, approved labeling, clinical practice, or documented use; it is not individualized guidance and does not establish safety.
How does ACD-856 (NeuroRestore) work?
Small-molecule triazinetrione that allosterically potentiates the intracellular kinase domain of all three neurotrophin receptors (pan-Trk: TrkA EC50=382 nM; TrkB=295 nM; TrkC=33 nM); amplifies endogenous BDNF/NGF signaling rather than mimicking it; downstream effects on neurite outgrowth; synaptic plasticity; BDNF expression; and anti-inflammatory pathways; orally bioavailable with CNS penetration; proposed disease-modifying via neurotrophin restoration — distinct from cholinesterase inhibitors and anti-amyloid antibodies

This is an independent synthesis of published research by a non-clinician. Scores are opinions supported by citations, not prescriptions. See the full disclaimer and methodology for how this score was produced and what it does and doesn't mean.