spec sheet8 rows
P7C3-S243 is a single-enantiomer member of the P7C3 series, purified to 99 percent excess rather than used as a mixture. It protects dopamine neurons in a Parkinson's model and protects rats in an Alzheimer's model from behavioural and neurodegenerative decline without touching amyloid deposits. ⚠️ It carries the only sub-micromolar protein affinity ever measured for any compound in this series, and it is an off-target: 350 nanomolar at TSPO. That number matters because the series is routinely described as clean and selective.
- Enantiopure rather than a mixture, which makes it the better-defined research tool
- Protected a rat Alzheimer's model from behavioural and neurodegenerative decline without altering amyloid
- Protected dopamine neurons in a Parkinson's model
- No human exposure, toxicology or pharmacokinetics
- Binds TSPO at 350 nanomolar, a mitochondrial protein involved in steroid synthesis and brain immune responses
Mechanism
The proposed mechanism is the series mechanism: support of NAD levels through the salvage enzyme NAMPT [4]. ⚠️ As with every member of this family, no binding or potency constant at that enzyme has ever been published.
⚠️ The one hard number in the series belongs to this compound and is an off-target. It binds TSPO, the translocator protein on the outer membrane, at about 350 nanomolar. Two things make that interesting rather than decisive. It is the only sub-micromolar protein affinity ever measured for anything in this series, so the frequent description of these compounds as clean and target-selective rests on nothing having been looked for. And it is not enantioselective, roughly 0.35 against 0.68 micromolar, while the biological effect is strictly enantioselective, which argues that TSPO is not the protein producing the protection.
⚠️ The -1 receptor pathway shown for the prototype P7C3 does not apply here; the source paper for that finding states this compound does not engage it [5].
The practical consequence of all this is worth stating plainly: after fifteen years, the protein through which the series works has not been identified.
receptor fingerprint
TSPO / translocator proteinBinds
Dopaminergic and hippocampal neuron survivalProtects
NAMPT / NAD salvageClaimed activator; no constant ever measured
-1 receptorNot engaged by this compound
Evidencehow good the literature is
Two well-designed animal studies and a chemistry paper.
In a rat Alzheimer's model the compound protected against neuropsychiatric deficits and neurodegeneration, and did so without changing amyloid deposition or reactive glia [2]. ⚠️ That dissociation is the most informative result in the entry: the benefit is not going through amyloid, which is both interesting and a reason to be careful about calling this an Alzheimer's mechanism.
In the 6-hydroxydopamine model of Parkinson's disease it protected dopamine neurons [3].
Its discovery paper reports the chemistry and the enantioselectivity of the effect [1], which is what makes the non-enantioselective TSPO binding informative as a negative.
⚠️ No clinical trial has ever been registered for this compound or any other in the series.
Dosingtypical ranges, not medical advice
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Safetyrisks and cautions, not medical advice
No human exposure, no toxicology and no pharmacokinetics have been published.
⚠️ The concentration-dependent neurotoxicity reported for its sibling in independent culture work [6] is a caution for the series rather than a finding about this compound specifically, since this one was not tested in that study.
TSPO binding at 350 nanomolar is worth noting on its own terms. That protein sits on mitochondria and is involved in steroid synthesis and in the response of immune cells in the brain, so meaningful occupancy is not obviously inert.
History
The compound came from a medicinal chemistry effort to improve on the original P7C3 scaffold, published in 2014, which produced a single enantiomer rather than the racemic mixtures used earlier. It has since been used mainly as a research tool in Parkinson's and Alzheimer's models, and like the rest of the series it has never entered clinical development.
Resources
This entry is here for reference.
Research
- 2011first citedDevelopment of proneurogenic, neuroprotective small molecules
- 2018most recent(-)-P7C3-S243 Protects a Rat Model of Alzheimer's Disease From Neuropsychiatric Deficits and Ne…
- 1.Discovery of a neuroprotective chemical, (S)-N-(3-(3,6-dibromo-9H-carbazol-9-yl)-2-fluoropropyl)-6-methoxypyridin-2-amine [(-)-P7C3-S243], with improved druglike properties.
- 2.(-)-P7C3-S243 Protects a Rat Model of Alzheimer's Disease From Neuropsychiatric Deficits and Neurodegeneration Without Altering Amyloid Deposition or Reactive Glia
- 3.Protective efficacy of P7C3-S243 in the 6-hydroxydopamine model of Parkinson's disease
- 4.P7C3 neuroprotective chemicals function by activating the rate-limiting enzyme in NAD salvage
- 5.GSK-3 inhibition through GLP-1R allosteric activation mediates the neurogenesis promoting effect of P7C3 after cerebral ischemic/reperfusional injury in mice
- 6.P7C3-A20 neuroprotection is independent of Wallerian degeneration in primary neuronal culture
- 7.Development of proneurogenic, neuroprotective small molecules
7 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
What does the TSPO number actually tell us?
Two things, and the second is more useful. It is the only sub-micromolar protein affinity ever measured for anything in this series, so calling these compounds selective mostly reflects that nobody has looked. And because it binds both mirror images almost equally while only one mirror image works biologically, TSPO is probably not the protein producing the effect. That leaves the real target unknown.
Is this better than P7C3-A20?
It is better defined. This one is a single purified enantiomer while A20 is a mixture, which matters because only one mirror image is active. On evidence they are comparable: both have animal results, neither has human data, and neither has a measured constant at the target they are said to share.
Limitations of the evidence
- The protein through which the series works has still not been identified after fifteen years
- Its only measured affinity is an off-target that its own enantioselectivity argues against as the mechanism
- No NAMPT binding or potency constant exists for it or any sibling
- No registered clinical trial for this compound or any other in the series
- Does not share the prototype P7C3's GLP-1 receptor mechanism
Adverse effects
- No human exposure, toxicology or pharmacokinetics
- Binds TSPO at 350 nanomolar, a mitochondrial protein involved in steroid synthesis and brain immune responses