spec sheet8 rows
R7 is a 7,8-dihydroxyflavone derivative that appears in research-chemical channels as a prodrug of that compound. ⚠️ It is a rejected candidate, and that is essentially the whole entry. R7 was one of twenty derivatives screened in a 2018 study, and it was eliminated before any animal work for a specific reason: it barely released 7,8-dihydroxyflavone in human liver preparations. A sibling from the same screen, R13, was the one that advanced. That single sentence is the entire published literature on R7. There is no structure, no formula, no measured affinity for anything, no animal study, no pharmacokinetics and no safety data.
- No safety data of any kind exists, in any species
- With no published structure, there is no way to verify what a given sample actually contains
Mechanism
There is no established mechanism, and the intended one is documented as failing.
R7 was designed on the same principle as its siblings: mask the hydroxyls of 7,8-dihydroxyflavone with an ester or carbamate so the molecule survives the gut, then let enzymes uncover it in the body. Six of the twenty derivatives made it past the stability screen; R7 was among them [1].
⚠️ It failed the next step. In human liver preparations R7 barely yielded free 7,8-dihydroxyflavone, and it was set aside along with two others for the same reason. Only R13 went on to animal work.
⚠️ Even if it did convert, the mechanism it would deliver is contested. Direct activation by 7,8-dihydroxyflavone has failed reproduction in independent laboratories using quantitative assays [2][3].
⚠️ Its structure has never been published. The source paper draws only R13's structure, and no chemistry database carries a record under this designation, so there is no formula, no molecular weight and no way to verify what any given sample is.
receptor fingerprint
7,8-dihydroxyflavone release ( conversion)Fails to convert
Evidencehow good the literature is
One sentence, in one paper.
R7 appears in a 2018 study that made twenty ester and carbamate derivatives of 7,8-dihydroxyflavone and screened them for stability and conversion [1]. It passed the stability step and failed the conversion step, and the paper's only statement about it is that it barely yielded free 7,8-dihydroxyflavone in human liver microsomes.
⚠️ Searches return nothing else. No paper pairs this designation with TrkB, with prodrug chemistry or with any cognitive or neuroprotective claim; no trial exists; no chemistry database holds a record.
⚠️ One circulating claim is worth naming as unsupported: that R7's exposure is 7.2 times the parent compound's. No pharmacokinetic data of any kind is reported for R7 in the source paper, and that figure could not be traced to any verifiable source.
Dosingtypical ranges, not medical advice
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Safetyrisks and cautions, not medical advice
No safety data of any kind exists. There has been no animal study, no toxicology and no human exposure in any published work.
⚠️ Absence of reported harm here means absence of looking, not absence of risk. With no published structure, a buyer also has no way to confirm that what they received is the compound named on the label.
History
R7 exists as a line in a screening table from a 2018 effort to make 7,8-dihydroxyflavone orally usable. It was made, tested, found not to release its payload in human liver preparations, and dropped. Its presence in research-chemical listings appears to come from the designation surviving in that table rather than from any result attached to it.
Resources
This entry is here for reference.
Research
- 2017first citedMultiplex quantitative assays indicate a need for reevaluating reported small-molecule TrkB ago…
- 2021most recentDo Small Molecules Activate the TrkB Receptor in the Same Manner as BDNF? Limitations of Publis…
- 1.The prodrug of 7,8-dihydroxyflavone development and therapeutic efficacy for treating Alzheimer's disease
- 2.Multiplex quantitative assays indicate a need for reevaluating reported small-molecule TrkB agonists
- 3.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.
3 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Why is there so little about R7?
Because it was rejected early. It was one of twenty derivatives in a 2018 screen, and it failed the test that mattered: it barely released 7,8-dihydroxyflavone in human liver preparations. The researchers dropped it and carried R13 forward. Nothing else has ever been published about it.
Is R7 a stronger version of 7,8-DHF?
There is no evidence for that and one piece of evidence against it. A prodrug is meant to release its payload, and the only measurement ever made on R7 found that it barely does so in human liver preparations. The claim that its exposure is 7.2 times the parent's does not appear in the source paper or anywhere traceable.
Limitations of the evidence
- Its entire published literature is one sentence, and that sentence is a negative result
- It failed to release 7,8-dihydroxyflavone in human liver preparations, which is the job a prodrug exists to do
- It was eliminated from development before any animal study; a sibling, R13, went forward instead
- No structure, formula, molecular weight or chemistry database record
- No target data, no pharmacokinetics, no animal work and no human exposure
- The circulating claim that its exposure is 7.2 times the parent's appears in no primary source
- The mechanism it is sold on also depends on TrkB activation that independent laboratories could not reproduce
Adverse effects
- No safety data of any kind exists, in any species
- With no published structure, there is no way to verify what a given sample actually contains