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ENT-A011 is a synthetic derivative of DHEA reported to activate the TrkB receptor, the target of BDNF, without touching the related TrkA and TrkC receptors or the p75 receptor. It belongs to a Greek series of so-called microneurotrophins built from the same steroid backbone. ⚠️ It is a TrkB agonist, not a TrkA agonist, and that error is common enough to be worth flagging first. The same series contains ENT-A013, which is TrkA selective, and sources routinely confuse the two. Everything known about it comes from a single 2024 paper, entirely in cells, at one concentration.
- Activates TrkB without touching TrkA, TrkC or p75, which is the selectivity profile a BDNF mimetic would need
- Protected human stem-cell derived neurons from Alzheimer's donors against amyloid beta, comparably to BDNF itself
- No safety data of any kind exists; the compound has never been given to an animal
Mechanism
The compound is reported to phosphorylate , and specifically not TrkA or TrkC, while leaving the p75 neurotrophin receptor pathway alone [1]. That selectivity is the paper's central claim and is what distinguishes it from its siblings in the same chemical series.
Downstream, the effects described are the ones expected of activation: neuron survival under serum withdrawal, restored proliferation of neural stem cells exposed to amyloid beta, and reduced apoptosis in human induced-pluripotent-stem-cell neurons from both healthy and Alzheimer's donors, in each case comparable to itself.
⚠️ Where the compound binds is unknown. Molecular modelling suggested two possible sites at the interface between 's extracellular region and the neurotrophin, but that is docking, which proposes a site rather than measuring one. No binding assay has been run.
⚠️ The structure is not public. The paper states that the compound was made from DHEA in several steps with confirmed stereochemistry, and puts the structure in supplementary material only. There is no CAS number, no PubChem record and no ChEMBL entry, so the molecule cannot be looked up independently.
receptor fingerprint
TrkA and TrkCNo activation
(NTRK2), the receptorReported selective agonist
Evidencehow good the literature is
One paper, published in 2024, in cells only [1].
The work is reasonably done for what it is. It spans mouse embryonic neural stem cells, a TrkB-expressing fibroblast line, and human induced-pluripotent-stem-cell derived neural progenitors from three donors including people with Alzheimer's disease. Against amyloid beta, the compound restored proliferation and mitochondrial activity and cut the proportion of dying cells from about 23 percent to about 10 percent, closely matching BDNF's own effect.
⚠️ What is absent matters more than what is present. There is no in vivo experiment, no pharmacokinetics, no half-life, no bioavailability, no toxicology and no demonstration that the molecule crosses into a brain. Every number in the paper comes from a single concentration of 1 micromolar, so nothing about its potency can be stated. Searching the clinical trial registry returns nothing.
Dosingtypical ranges, not medical advice
interested in protocols and clinical dosages? make an account to see them! ^_^
Safetyrisks and cautions, not medical advice
No safety data exists. There has been no animal study, no toxicology and no human exposure.
The only relevant observation is that the compound was not toxic to cultured cells at concentrations up to 100 micromolar, which is a statement about a cell dish and nothing more.
History
The compound comes from a collaboration between the National Hellenic Research Foundation and the University of Crete that has been building small-molecule neurotrophin mimics from a DHEA scaffold for over a decade, an approach the group calls microneurotrophins. The earlier prototype in that lineage targeted TrkA and the p75 receptor; this one was designed for TrkB. No commercial sponsor is named in the paper.
Subjective profileweighing the evidence above
A clean piece of early cell biology and nothing more. The selectivity result is genuinely interesting, because activating TrkB without TrkA, TrkC or p75 is the profile a BDNF mimetic would need, and the work was done across mouse and human stem-cell derived neurons including cells from Alzheimer's donors. ⚠️ But there is no animal experiment of any kind, no measurement of what it binds, no structure in the public record, and no evidence it reaches a brain. Its entire dataset sits at 1 micromolar, roughly a million-fold weaker than BDNF's own affinity for the same receptor, and no potency has ever been fitted. Treat it as a laboratory tool at this stage rather than a candidate.
Resources
This entry is here for reference.
Research
- 1.Comprehensive characterization of the neurogenic and neuroprotective action of a novel TrkB agonist using mouse and human stem cell models of Alzheimer's disease
1 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Is ENT-A011 a TrkA agonist?
No, and this is the most common error about it. It activates TrkB, the BDNF receptor, and specifically does not phosphorylate TrkA or TrkC. The TrkA-selective compound from the same laboratory series is ENT-A013, a different molecule.
How does it compare to BDNF itself?
In the cell experiments the effects were similar in size. On potency there is no comparison to make: BDNF binds TrkB at picomolar concentrations, and every experiment with this compound was run at 1 micromolar with no potency fitted, so the gap could be very large.
Limitations of the evidence
- Everything known about it comes from one paper, entirely in cells
- No in vivo experiment, no pharmacokinetics and no evidence it reaches a brain
- The whole dataset sits at one concentration, so no potency can be stated
- No binding measurement; the proposed site comes from docking
- No structure, CAS number or public chemistry record, so it cannot be looked up independently
- Widely and wrongly described as a TrkA agonist, which is a different compound in the same series
Adverse effects
- No safety data of any kind exists; the compound has never been given to an animal