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CAD-31 is a preclinical Alzheimer's candidate from the Salk Institute, selected for its ability to make neural precursor cells divide and then tested in aged Alzheimer's model mice, where it reduced memory deficits and brain inflammation. ⚠️ It has no known molecular target. No binding or potency measurement against any protein has ever been published for it, and its stated mechanism of fatty acid metabolism and inflammation is a description of what changed downstream rather than of what the molecule does. ⚠️ It is frequently grouped with CMS121 as a fisetin derivative. It is not one. Its own paper traces it back through J147 to curcumin, which is different chemistry from a different programme in the same laboratory.
- Tested therapeutically in mice that were already old and symptomatic, which is a harder design than dosing from youth
- Reduced memory deficit and brain inflammation and raised synaptic protein in that model
- Protective in six separate nerve cell assays modelling old-brain damage
- Reported to be brain-penetrant
- No formal toxicology, no no-effect dose and no human exposure
- Described as likely safe on preliminary work with no supporting numbers
Mechanism
⚠️ No molecular target has ever been identified, and this is not an oversight to be filled in later; it is the compound's defining characteristic. No Ki, Kd, IC50 or EC50 against any protein has been published. The only quantitative values that exist are six cell-based protective concentrations from a single table in a single paper.
The compound was found by phenotype rather than by target: it was selected because it made human embryonic stem cell derived neural precursors divide, and because it worked in Alzheimer's model mice [1]. That approach is deliberate in this laboratory, which argues that starting from a single target has repeatedly failed in Alzheimer's disease, and it means a target was never the goal.
The mechanism in the paper's title, fatty acid metabolism and inflammation, comes from measuring which small molecules and which genes changed in brain and plasma after treatment. ⚠️ That is a correlate, not a mechanism: it describes the state the brain ended up in rather than what the molecule bound to get there. And the headline fatty-acid and ketone-body signature was significant mainly in normal mice rather than in the Alzheimer's model animals, which weakens it further.
Its chemical lineage runs curcumin to CNB-001 to CNB-023 to J147 to this compound. ⚠️ It is a trifluoroacetyl arylhydrazone; CMS121 is a quinoline from the separate fisetin programme [3]. The two are often listed together as sibling geroprotectors and they are not chemically related.
receptor fingerprint
Neural precursor proliferationStimulates
No molecular target identifiedNone known
Brain fatty acid metabolism and inflammationAlters (downstream correlate)
Evidencehow good the literature is
One paper, from 2017, and nothing since [1].
That paper is better designed than most in this area. It gave the compound to APP and PS1 mice starting at ten months, when the animals were already old and already symptomatic, and continued for three months. It reported reduced memory deficit, less brain inflammation and increased synaptic protein expression, plus protection in six separate nerve cell assays modelling the kinds of damage seen in an ageing brain.
⚠️ A later paper comparing several candidates from the same laboratory for geroprotective effects [2] provides some context, but no independent group has ever tested this compound.
⚠️ A citation trap is worth naming. Searching PubMed for this compound's name returns two records, and one of them is a false positive matching a street address in an author's affiliation. Any source listing two papers for this compound has confused an existence check for a subject check.
Dosingtypical ranges, not medical advice
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Safetyrisks and cautions, not medical advice
Only preliminary work exists. The source paper describes the compound as brain-penetrant and likely safe on the strength of preliminary toxicology, with no numbers given.
⚠️ There is no formal toxicology study, no no-effect dose, no repeat-dose work and no human exposure. Half-life, exposure, bioavailability and clearance have never been published in any species.
History
The compound came out of the Salk Institute's programme of selecting Alzheimer's candidates on old-brain phenotypes rather than on amyloid, and was announced in 2017 as a drug candidate being moved toward the clinic.
It did not move. Its chemical parent J147 was advanced instead and has completed a phase 1, while this compound has produced no publications, no trials and no regulatory activity since its introduction.
Resources
This entry is here for reference.
Research
- 2012first citedChemical modification of the multitarget neuroprotective compound fisetin
- 2021most recentGeroprotective effects of Alzheimer's disease drug candidates
- 1.A novel Alzheimer's disease drug candidate targeting inflammation and fatty acid metabolism
- 2.Geroprotective effects of Alzheimer's disease drug candidates
- 3.Chemical modification of the multitarget neuroprotective compound fisetin
3 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Is CAD-31 related to CMS121?
Only by laboratory, not by chemistry. CAD-31 is a trifluoroacetyl arylhydrazone whose lineage runs back through J147 to curcumin; CMS121 is a quinoline from a separate programme built on fisetin. They come from the same group and are often listed together, which is where the confusion starts.
What does CAD-31 actually bind?
Nobody knows, and nobody has published a measurement against any protein. It was found by testing what molecules did to cells and to mice rather than by aiming at a target, which is a deliberate strategy in the laboratory that made it. The fatty acid and inflammation mechanism in its paper title describes what changed after treatment, not what the molecule attaches to.
Limitations of the evidence
- No molecular target has ever been identified, and no affinity against any protein has been measured
- The stated mechanism is a downstream metabolic correlate rather than an action
- The headline fatty-acid signature was significant mainly in normal mice, not the disease model
- One paper, from 2017, with nothing published since and no independent replication
- No trials, no chemistry database record, no regulatory activity
- Not a fisetin derivative, despite being grouped with CMS121; its lineage runs through J147 to curcumin
Adverse effects
- No formal toxicology, no no-effect dose and no human exposure
- Described as likely safe on preliminary work with no supporting numbers