ReviewInflammopharmacology2026
Pharmacological properties, safety, pharmacokinetic and clinical trials of kukoamine A and B.
Review in Inflammopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
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Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Kukoamine A (KuA) and kukoamine B (KuB) are spermine alkaloids characterized by polyamine backbones conjugated with phenolic moieties, primarily isolated from Lycium chinense root bark (Lycii Cortex). This review comprehensively analyses their pharmacological properties, mechanistic pathways, safety profiles, and clinical potential. KuA and KuB exhibit potent antioxidant activity by scavenging reactive oxygen species, enhancing superoxide dismutase and catalase activity, and chelating Fe2+. Their anti-inflammatory effects involve neutralizing pathogen-associated molecular patterns (e.g., LPS, CpG-DNA), suppressing TLR4/9-MyD88-NF-κB signaling, and reducing pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β). Both compounds demonstrate antimicrobial efficacy against sepsis triggers (e.g., E. coli) by inhibiting bacterial toxin-induced inflammation. Additionally, KuA and KuB significantly improve antidiabetic outcomes by activating the AKT/GSK-3β pathway, thereby enhancing insulin sensitivity, inhibiting DPP-4 and amyloid aggregation, and ameliorating metabolic disorders. Neuroprotective roles include mitigating oxidative stress, inhibiting neuronal apoptosis (via modulation of Bax/Bcl-2 and caspase-3), and attenuating the pathology of Parkinson’s and Alzheimer’s diseases by regulating α-synuclein and iron homeostasis. Additional benefits encompass anti-osteoporotic effects through osteoblast differentiation promotion and bone mineral density preservation. Moreover, pharmacokinetic studies indicate rapid plasma distribution and urinary excretion of KuB, with Phase I/II trials confirming tolerability in healthy and septic subjects (0.06–0.24 mg/kg doses). Safety assessments reveal mild adverse events (e.g., transient headaches). Despite promising preclinical data, clinical validation remains limited. Future research should prioritize mechanistic depth, large-scale trials, and therapeutic applications for neurodegenerative, metabolic, and inflammatory diseases.
Indexed as
Identifiers
41701421What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.