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Deoxygedunin is a natural product from the Indian neem tree and from andiroba seed oil, a limonoid of the gedunin family. It is sold alongside the flavone TrkB compounds and is chemically unrelated to them; it appears in that group only because it came out of the same screen. ⚠️ Its literature is remarkably small. PubMed indexes six papers containing the word at all, one of which merely identifies it as a constituent of seed oil and has nothing to do with the nervous system. There is no second independent pharmacology programme anywhere.
- Animal results from several different groups and several different models
- Protected dopamine neurons, promoted nerve regeneration and prevented refractory neonatal seizures
- A natural product with a fully resolved chemical identity, unlike several compounds it is sold beside
- No human safety data, toxicology or pharmacokinetics
- Neem limonoids are broadly bioactive as a class and concentrated preparations have documented toxicity; nobody has placed this compound against that
Mechanism
The compound is a limonoid, a modified triterpene, carrying a furan ring, an acetate ester and a lactone. It is structurally unrelated to the flavones it is usually grouped with, and shares only the screen it emerged from.
It is described as a that mimics 's action and drives the downstream survival pathways [1].
⚠️ No binding constant for it at has been published. As with the flavones, the supporting evidence is phospho-protein readouts rather than a measured interaction.
⚠️ The whole class this belongs to rests on a contested claim. Nearly all the positive primary data for direct activation of by small molecules comes from one research group, and at least three independent teams have failed to reproduce receptor-level activation. Two of those were industrial drug-discovery groups using quantitative assays with a monoclonal antibody as a positive control [5][6], and a later review reached the same conclusion [7]. Downstream biological effects are often reproducible; the step in dispute is whether they happen by binding the receptor.
⚠️ A separate caution comes from its source. Neem limonoids are known for broad biological activity across many targets, including insecticidal and antiparasitic effects, which makes selectivity a real question for any member of the family and one nobody has addressed for this compound.
receptor fingerprint
Dopaminergic and peripheral neuron survivalProtects (downstream)
(NTRK2) receptorClaimed agonist; no affinity ever measured
Evidencehow good the literature is
Four relevant papers, from a total of six that mention the compound at all.
Reported results include protection of dopamine neurons in the 6-hydroxydopamine model of Parkinson's disease [2], promotion of axon regeneration in cut peripheral nerves [1], and prevention of refractory seizures after stroke in newborn mice [3]. A Chinese-language study examined Alzheimer-like changes in rats [4].
⚠️ That the effects come from several groups and several models is genuinely in its favour. What is missing is any independent programme aimed at the compound itself, any binding measurement, any pharmacokinetics and any human exposure. No trial has ever been registered.
Dosingtypical ranges, not medical advice
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Safetyrisks and cautions, not medical advice
No human safety data, no toxicology and no pharmacokinetic study.
Its parent plant is widely used and neem preparations are consumed traditionally, but that says nothing about a purified single limonoid given at pharmacological doses. Concentrated neem constituents have documented toxicity in infants, and no work has been done to establish where this compound sits.
History
The compound was pulled out of a phenotypic screen for molecules that behaved like BDNF, in the same programme that produced the flavone TrkB candidates, and has been used since as an occasional research tool. It never entered development, and its presence in supplement channels rests on that original designation rather than on anything that followed.
Resources
This entry is here for reference.
Research
- 2013first citedSmall-molecule trkB agonists promote axon regeneration in cut peripheral nerves
- 2021most recentDo Small Molecules Activate the TrkB Receptor in the Same Manner as BDNF? Limitations of Publis…
- 1.Small-molecule trkB agonists promote axon regeneration in cut peripheral nerves
- 2.Small molecule TrkB agonist deoxygedunin protects nigrostriatal dopaminergic neurons from 6-OHDA and MPTP induced neurotoxicity in rodents
- 3.TrkB agonists prevent postischemic emergence of refractory neonatal seizures in mice
- 4.[Effects of deoxygedunin on Alzheimer-like pathologic dysfunction induced by D-galactose combined with AlCl(3)].
- 5.A monoclonal antibody TrkB receptor agonist as a potential therapeutic for Huntington's disease
- 6.Multiplex quantitative assays indicate a need for reevaluating reported small-molecule TrkB agonists
- 7.Do Small Molecules Activate the TrkB Receptor in the Same Manner as BDNF? Limitations of Published TrkB Low Molecular Agonists and Screening for Novel TrkB Orthosteric Agonists.
7 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Is it related to the flavone TrkB compounds it is sold with?
Not chemically. It is a limonoid, a modified triterpene from the neem tree, while those are flavones. The only thing they share is the screen they came out of and the claim attached to them afterwards.
Limitations of the evidence
- Six PubMed papers mention it at all, and one of those is about seed oil chemistry
- No independent pharmacology programme has ever existed for it
- No binding constant at TrkB, and the class-level receptor claim failed independent replication
- Chemically unrelated to the flavones it is marketed alongside
- No pharmacokinetics in any species and no registered trial
Adverse effects
- No human safety data, toxicology or pharmacokinetics
- Neem limonoids are broadly bioactive as a class and concentrated preparations have documented toxicity; nobody has placed this compound against that