Lemairamin

Overview

Lemairamin is a non-peptide small-molecule cinnamamide alkaloid (N-phenethyl cinnamide) natural product, not approved for human use in any jurisdiction. All available data are preclinical (rodent, zebrafish, C. elegans, in vitro, and computational). It is sold exclusively as an unregulated 'research chemical' explicitly labeled 'not for human consumption'; quality, purity, and identity are not independently verified by any regulatory body. No human clinical trials, pharmacokinetic studies, or safety data exist.

Mechanism of Action

Reported in preclinical (rodent, cell-culture, in-silico) work as an agonist/activator of the alpha7 nicotinic acetylcholine receptor (α7 nAChR). Proposed threads include: (1) α7 nAChR activation driving JAK2/STAT3 and PI3K/AKT signaling to suppress pro-inflammatory cytokine release from microglia; (2) spinal α7 nAChR activation linked to IL-10 and beta-endorphin release from microglia, producing antinociceptive effects in rodent pain models; (3) direct biophysical interaction with amyloid-beta oligomers/protofibrils in vitro, disassembling preformed Aβ42 aggregates and inhibiting Aβ-induced neuronal apoptosis and calcium dysregulation in transgenic AD mouse models. These are distinct, only partially connected preclinical threads; no unified human pharmacology has been established.

Research Summary

No human data exist. No completed or registered human clinical trials were located on ClinicalTrials.gov, and no PubMed-indexed human pharmacokinetic, safety, or efficacy studies exist. All available data are preclinical: In transgenic Alzheimer's mice, gx-50 disassembled Aβ oligomers, decreased cortical Aβ accumulation, inhibited Aβ-induced neuronal apoptosis and calcium toxicity, improved Morris water maze performance, and was reported to cross the blood-brain barrier (Tang et al. 2013). In mouse and rat pain models (formalin tonic, neuropathic, bone-cancer pain), subcutaneous and intrathecal lemairamin dose-dependently reduced pain hypersensitivity/mechanical allodynia without evident tolerance, linked to spinal α7 nAChR activation and downstream IL-10/β-endorphin release (Wang et al. 2020). Murine microglial cell cultures showed gx-50 activation of α7 nAChR engaged JAK2/STAT3 and PI3K/AKT signaling to suppress pro-inflammatory cytokine secretion (Shi et al. 2016). Zebrafish DSS-induced colitis models showed lemairamin attenuated intestinal inflammation via Akt signaling (2024). C. elegans studies reported WGX-50 promoted markers of healthy ageing (daf-16/skn-1 longevity genes, 2025).

Reported Side Effects

• No human safety data exist
• Unregulated research chemical; purity and identity not verified
• Mechanistic data span multiple unrelated preclinical endpoints from small number of labs
• Quality and composition of gray-market product unknown
• No toxicology or formal safety pharmacology data in animals

Compare Lemairamin with Others

Research References

• A novel drug candidate for Alzheimer's disease treatment: gx-50 derived from Zanthoxylum bungeanum. 2013. PMID 23186988.
• Lemairamin, isolated from the Zanthoxylum plants, alleviates pain hypersensitivity via spinal alpha7 nicotinic acetylcholine receptors. 2020. PMID 32184015.
• Gx-50 Inhibits Neuroinflammation via alpha7 nAChR Activation of the JAK2/STAT3 and PI3K/AKT Pathways. 2016.
• Destabilization of Alzheimer's Abeta42 Protofibrils with wgx-50 by Molecular Dynamics Simulations. 2015. PMID 25996452.

Frequently asked questions

Has Lemairamin been independently lab-tested?

Disclosed Labs has collected 2 Certificates of Analysis (COA) for Lemairamin from 2 independent testing labs. 1 vendor has submitted material for testing. Products average 99.8% tested purity across the corpus. Full testing data is available at https://www.disclosedlabs.com/peptides/lemairamin/testing.

How does Lemairamin work?

Reported in preclinical (rodent, cell-culture, in-silico) work as an agonist/activator of the alpha7 nicotinic acetylcholine receptor (α7 nAChR). Proposed threads include: (1) α7 nAChR activation driving JAK2/STAT3 and PI3K/AKT signaling to suppress pro-inflammatory cytokine release from microglia; (2) spinal α7 nAChR activation linked to IL-10 and beta-endorphin release from microglia, producing antinociceptive effects in rodent pain models; (3) direct biophysical interaction with amyloid-beta oligomers/protofibrils in vitro, disassembling preformed Aβ42 aggregates and inhibiting Aβ-induced neuronal apoptosis and calcium dysregulation in transgenic AD mouse models. These are distinct, only partially connected preclinical threads; no unified human pharmacology has been established.

What does the research say about Lemairamin?

No human data exist. No completed or registered human clinical trials were located on ClinicalTrials.gov, and no PubMed-indexed human pharmacokinetic, safety, or efficacy studies exist. All available data are preclinical: In transgenic Alzheimer's mice, gx-50 disassembled Aβ oligomers, decreased cortical Aβ accumulation, inhibited Aβ-induced neuronal apoptosis and calcium toxicity, improved Morris water maze performance, and was reported to cross the blood-brain barrier (Tang et al. 2013). In mouse and rat pain models (formalin tonic, neuropathic, bone-cancer pain), subcutaneous and intrathecal lemairamin dose-dependently reduced pain hypersensitivity/mechanical allodynia without evident tolerance, linked to spinal α7 nAChR activation and downstream IL-10/β-endorphin release (Wang et al. 2020). Murine microglial cell cultures showed gx-50 activation of α7 nAChR engaged JAK2/STAT3 and PI3K/AKT signaling to suppress pro-inflammatory cytokine secretion (Shi et al. 2016). Zebrafish DSS-induced colitis models showed lemairamin attenuated intestinal inflammation via Akt signaling (2024). C. elegans studies reported WGX-50 promoted markers of healthy ageing (daf-16/skn-1 longevity genes, 2025).