ArticleFrontiers in pharmacology2026
The underlying mechanism of scorpion venom peptide BmK AS in reducing epilepsy seizures: mediated through dual modulation of Nav1.6 and the inflammasome pathway.
Article in Frontiers in pharmacology, 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Voltage-gated sodium channel (VGSC) dysregulation, particularly of the Nav1.6 subtype, is a core mechanism underlying epileptogenesis and its associated neuropsychiatric comorbidities. The scorpion venom peptide BmK AS has demonstrated anticonvulsant potential, but its efficacy in chronic epilepsy and the precise mechanisms of action remain undefined. Methods: Here, we show that BmK AS exerts robust anti-epileptic and neuroprotective effects through converging mechanisms. In a kainic acid-induced mouse model, BmK AS treatment reduced mortality and seizure parameters. Electrophysiological studies assessed BmK AS modulation of VGSC subtypes. The functional relevance of Nav1.6 targeting was confirmed by the loss of BmK AS's anti-seizure efficacy upon its pharmacological blockade in a PTZ-induced model. Furthermore, in both KA-induced chronic epilepsy models and native hippocampal neurons, BmK AS was evaluated for neuronal hyperexcitability and NLRP1 inflammasome-mediated pyroptosis. Results: BmK AS reduced mortality to 0% (vs. 40% in the model group) and significantly reduced seizure duration by 10.5% and the frequency of severe (stages 4 and 5) seizures by 68.8%. It also improved cognitive and psychiatric outcomes, significantly reversing epilepsy-associated spatial memory deficits and anxiety-/depression-like behaviors. Electrophysiological studies show that BmK AS nonlinearly inhibited multiple VGSC subtypes, with pronounced potency against Nav1.6, reducing the peak sodium current to 43% of control at 5 nM. BmK AS attenuated neuronal hyperexcitability and suppressed neuroinflammation by inhibiting the NLRP1 inflammasome pathway and the associated pyroptosis. Discussion: Our findings establish BmK AS as a promising multimechanistic therapeutic candidate, highlighting the strategic value of dual therapeutic actions, namely, Nav1.6 modulation and neuroinflammation inhibition, for epilepsy treatment.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.