data + articles · 4 listed
newest 2023spec sheet11 rows
L-Clausenamide, or (-)-clausenamide, is a pyrrolidinone alkaloid isolated from the leaves of Clausena lansium (wampee) and studied in China as a nootropic and neuroprotective anti-dementia drug candidate [1]. It is the eutomer of the clausenamide enantiomers, improving learning and memory through multi-target actions including modulation of intracellular calcium, cholinergic support, enhancement of synaptic plasticity and long-term potentiation, and antioxidant protection [1]. In cellular and animal models it protects neurons against beta-amyloid, okadaic-acid and ischemic injury and inhibits ferroptosis in dopaminergic neurons [2][3][4].
- Improves learning and memory in preclinical models
- Broad neuroprotection against ischemic, amyloid and oxidative injury
- Enhances synaptic plasticity and long-term potentiation
- Inhibits ferroptosis in dopaminergic neurons
- Theoretical interactions with cholinergic or other neuroactive drugs are unstudied.
Overview
Clausenamide is a small chiral molecule (a gamma-lactam / pyrrolidinone) first obtained from Clausena lansium, a plant used in traditional Chinese medicine. Because the molecule has several chiral centers, many enantiomers exist; systematic synthesis and testing at the Institute of Materia Medica of the Chinese Academy of Medical Sciences established the (-)-enantiomer as the eutomer, or active form, for cognitive enhancement, with the (+)-enantiomer largely inactive [1].
Mechanistically, (-)-clausenamide is described as a genuinely multi-target nootropic: it mildly elevates intracellular calcium, modulates the cholinergic system, regulates synaptic plasticity and long-term potentiation, and switches on cellular signaling pathways tied to learning and memory [1]. It also carries a strong neuroprotective and antioxidant character. In primary cortical neurons it blunts oxygen-glucose-deprivation injury by inhibiting endoplasmic-reticulum stress and apoptosis [2]; it protects neurons against okadaic-acid and beta-amyloid toxicity while improving learning in ovariectomized rats [4]; and it prevents ferroptotic death of dopaminergic neurons by interacting with 5-lipoxygenase (ALOX5), improving behavior in a Parkinson's disease model [3].
The compound is supplied as a research powder. It is best understood as an extensively studied preclinical anti-dementia and neuroprotection candidate, not an approved drug.
- Clausenamide has multiple chiral centers, and Chinese chemists synthesized its full set of enantiomers, showing that the (-)-form is the active eutomer while the (+)-form is essentially inactive [1].
- The molecule protects dopaminergic neurons by physically blocking a specific phosphorylation site on the enzyme 5-lipoxygenase, halting a ferroptosis-driving lipid pathway [3].
Mechanism
The action of (-)-clausenamide is attributed to a convergence of several mechanisms rather than a single receptor. It produces a mild elevation of intracellular calcium, modulates cholinergic transmission, and enhances plasticity and hippocampal , all of which support the encoding of learning and memory [1]. In parallel it activates intracellular signaling cascades associated with neuronal survival and plasticity.
Its neuroprotection operates through complementary routes. Against ischemic (oxygen-glucose deprivation) injury it suppresses the GRP78/eIF2-alpha-ATF4-CHOP endoplasmic-reticulum stress pathway and the resulting caspase-mediated apoptosis, preserving neuronal viability [2]. It scavenges lipid peroxidation products and, in dopaminergic neurons, binds the PKC-alpha phosphorylation site (Ser663) of 5-lipoxygenase (ALOX5), preventing its nuclear translocation and the production of toxic 5-HETE lipids that drive ferroptosis [3]. Against Alzheimer-relevant insults it counters beta-amyloid- and okadaic-acid-induced calcium overload, tau hyperphosphorylation and apoptosis [1][4]. This breadth is the basis for its description as a multi-target anti-dementia candidate.
receptor fingerprint
Cholinergic systemModulates
/ plasticityEnhances
Endoplasmic-reticulum stress (GRP78/eIF2-alpha-ATF4-CHOP)Inhibits
5-Lipoxygenase (ALOX5)Inhibits
Dosingtypical ranges, not medical advice
interested in protocols and clinical dosages? make an account to see them! ^_^
Safetyrisks and cautions, not medical advice
Clausenamide comes from an edible plant and has been studied fairly extensively in Chinese preclinical work without major toxicity signals reported, but there are no published human clinical safety trials, so its side-effect and interaction profile in people is not established. As a compound that modulates calcium, cholinergic tone and lipoxygenase signaling, theoretical interactions with cholinergic drugs or other neuroactive agents cannot be ruled out. It should be regarded as a research chemical rather than a proven supplement; the encouraging preclinical safety picture does not substitute for human data.
History
Clausenamide was isolated from Clausena lansium (wampee), a fruit tree used in traditional Chinese medicine, and was developed as a nootropic lead principally at the Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College in Beijing, with Zhang Juntian and colleagues driving much of the enantioselective synthesis and pharmacology over several decades [1][4]. It stands as one of China's notable home-grown anti-dementia drug candidates.
Reputation
In the neuropharmacology literature (-)-clausenamide is well regarded as a thoroughly studied natural-product nootropic with a coherent multi-target mechanism and reproducible neuroprotective data across ischemia, Alzheimer and Parkinson models [1][2][3]. In the nootropic community it is relatively obscure and hard to source, and the honest caveat is that despite a strong preclinical dossier it has not been validated in human trials, so its real cognitive benefit in people remains unproven.
Subjective profileweighing the evidence above
The preclinical case is broader and more coherent than most nootropic candidates ever assemble, and not one human trial has been published. Worth watching if the development program moves; not worth buying as a research powder today.
Resources
This entry is here for reference.
Research
- 2007first cited[Protective effect of (-) clausenamide against neurotoxicity induced by okadaic acid and beta-a…
- 2023most recentALOX5 inhibition protects against dopaminergic neurons undergoing ferroptosis.
- 1.The anti-dementia drug candidate, (-)-clausenamide, improves memory impairment through its multi-target effect.
- 2.(-)-Clausenamide alleviated ER stress and apoptosis induced by OGD/R in primary neuron cultures.
- 3.ALOX5 inhibition protects against dopaminergic neurons undergoing ferroptosis.
- 4.[Protective effect of (-) clausenamide against neurotoxicity induced by okadaic acid and beta-amyloid peptide25-35].
4 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Where does clausenamide come from?
It is an alkaloid isolated from the leaves of Clausena lansium, the wampee, a fruit tree used in traditional Chinese medicine.
Why the L or (-) designation?
Clausenamide exists as several enantiomers, and the (-)-form is the eutomer, meaning it carries the cognitive-enhancing and neuroprotective activity while the (+)-form is largely inactive.
Has it been tested in humans?
No. The evidence is preclinical, spanning cell and rodent models of ischemia, Alzheimer's and Parkinson's disease, without published human trials.
What makes it a multi-target compound?
It simultaneously modulates calcium and cholinergic signaling, boosts synaptic plasticity, calms endoplasmic-reticulum stress and inhibits lipoxygenase-driven ferroptosis.
Limitations of the evidence
- No human clinical safety data exist despite extensive animal study.
Adverse effects
- Theoretical interactions with cholinergic or other neuroactive drugs are unstudied.
Notes and cautions
- Sourcing and purity vary since it is a niche research compound.
- Only the (-)-enantiomer is active, so racemic or mislabeled material may underperform.