spec sheet8 rows
CF3CN is a laboratory code for an optimised replacement for 7,8-dihydroxyflavone, redesigned to resist the metabolism that destroys the parent compound and to reach the brain better. Its catechol ring is swapped for a fused imidazole carrying a trifluoromethyl group, and a nitrile replaces the electron-donating group on the other ring. ⚠️ It is the one compound in this family with a real binding measurement. Surface plasmon resonance gave a dissociation constant of 80.2 nanomolar against the TrkB extracellular domain, measured alongside 7,8-dihydroxyflavone at 184.5 nanomolar in the same experiment. ⚠️ It also has no public registry identity at all: no CAS number, no PubChem record, no ChEMBL entry.
- The only compound in this family with a genuine binding measurement rather than a signalling readout
- Measured against the parent compound as an internal control in the same experiment
- Binding site mapped to specific receptor domains rather than asserted
- Deliberately engineered to fix the metabolism and brain exposure problems of its parent
- No safety data, toxicology or human exposure
- No public reference structure, so nothing sold under this name can be verified
Mechanism
The design is deliberate and worth understanding, because it explains what the molecule is for. The parent compound, 7,8-dihydroxyflavone, carries a catechol that gets conjugated and cleared very quickly and keeps oral low. Here that catechol is replaced by a fused imidazole ring bearing a trifluoromethyl group, chosen to be hydrophobic and electron-withdrawing so more of the molecule reaches the brain, and the other ring's electron-donating group is replaced with a nitrile to reduce breakdown by liver enzymes [1].
⚠️ The binding evidence is better than anything else in this family. Surface plasmon resonance against the immobilised extracellular domain gave a dissociation constant of 80.2 nanomolar, with 7,8-dihydroxyflavone measured at 184.5 nanomolar in the same run as an internal control. Mapping with truncated receptor constructs put the interaction on the leucine-rich motif most strongly and then a cysteine-rich region, with no binding to either immunoglobulin domain, and this compound displaced the parent from that site in a dose-dependent way.
⚠️ Two caveats belong with that. It has not been reproduced by any laboratory outside the group that reported it. And a binding constant against an isolated extracellular domain on a chip is a different thing from demonstrating receptor activation in a cell, which is the specific step independent groups could not reproduce for the earlier compounds in this series.
⚠️ 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 [3][4], and a later review reached the same conclusion [5]. Downstream biological effects are often reproducible; the step in dispute is whether they happen by binding the receptor.
receptor fingerprint
(NTRK2) extracellular domainBinds (surface plasmon resonance)
leucine-rich motif (residues 37 to 111)Binding site by domain mapping
Evidencehow good the literature is
Essentially one paper [1], reporting the design, the binding measurement and effects in Alzheimer's model mice on pathology and cognition.
The chemical characterisation in it is partial. Mass spectrometry, purity above 98 percent and proton NMR are reported; no molecular formula, no elemental analysis and no systematic chemical name are printed.
⚠️ No independent laboratory has worked on this compound, no trial exists, and there is no human pharmacokinetic, safety or efficacy data.
⚠️ A typesetting note that causes real confusion: some journal renderings strip the subscript and print the name as CFCN or CF3-CN. They refer to the same molecule.
Dosingtypical ranges, not medical advice
interested in protocols and clinical dosages? make an account to see them! ^_^
Safetyrisks and cautions, not medical advice
No human exposure, no toxicology and no safety study of any kind.
⚠️ A specific practical warning applies here more than to most entries. This compound has no CAS number, no PubChem record and no ChEMBL entry, so there is no public reference structure. Anything sold under this name cannot be checked against anything.
History
The compound came out of a 2021 medicinal chemistry effort to fix the two things that make 7,8-dihydroxyflavone impractical, its rapid metabolism and its poor brain exposure, by replacing the metabolically vulnerable groups rather than masking them as the prodrug approach does. It remains a laboratory compound with no development programme, no sponsor and no registry identity.
Resources
This entry is here for reference.
Research
- 2010first citedA selective TrkB agonist with potent neurotrophic activities by 7,8-dihydroxyflavone
- 2021most recentDo Small Molecules Activate the TrkB Receptor in the Same Manner as BDNF? Limitations of Publis…
- 1.Optimized TrkB Agonist Ameliorates Alzheimer's Disease Pathologies and Improves Cognitive Functions via Inhibiting Delta-Secretase
- 2.A selective TrkB agonist with potent neurotrophic activities by 7,8-dihydroxyflavone
- 3.A monoclonal antibody TrkB receptor agonist as a potential therapeutic for Huntington's disease
- 4.Multiplex quantitative assays indicate a need for reevaluating reported small-molecule TrkB agonists
- 5.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.
5 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Does the 80.2 nM number settle the TrkB argument?
It is the right kind of evidence and it is not enough on its own. Surface plasmon resonance against the isolated receptor domain is exactly what critics of this class said was missing, and running the parent compound in the same experiment as a control is good practice. But it comes from the same laboratory whose earlier results others could not reproduce, nobody has repeated it, and binding to a domain on a chip is a different claim from activating the receptor in a living cell.
Limitations of the evidence
- The binding measurement has not been reproduced by any laboratory outside the originating group
- A Kd against an isolated domain on a chip is not the same as receptor activation in a cell, which is the disputed step
- No CAS number, no PubChem record and no ChEMBL entry
- Its paper prints no molecular formula, no elemental analysis and no systematic name
- One paper, no independent work, no trial and no human data
Adverse effects
- No safety data, toxicology or human exposure
- No public reference structure, so nothing sold under this name can be verified