Delving into the Latest Updates on Bulleyaconitine A with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms-

Target

VGSCs

Action

blockers

Mechanism

Voltage-gated sodium channels blockers

Therapeutic Areas

Nervous System DiseasesOther Diseases

Active Indication-

Inactive Indication

Pain

Originator Organization

KPC Pharmaceuticals, Inc.

Active Organization-

Inactive Organization

KPC Pharmaceuticals, Inc.

License Organization-

Drug Highest PhasePendingPreclinical

First Approval Date-

Regulation-

Structure/Sequence

Molecular FormulaC35H49NO10

InChIKeyGAZDXIGXYWVWQX-MIOGPJTISA-N

CAS Registry79592-91-9

Trigeminal neuralgia (TN), characterized by severe facial pain triggered by mild stimuli, is challenging to treat effectively and non-invasively. Traditional treatments, including microvascular decompression and medications like carbamazepine, have limitations. This study investigates the potential of Bulleyaconitine A (BAA), an alkaloid that selectively inhibits specific sodium channels, for managing TN in a rat model via intranasal administration.

METHOD:

Adult male Sprague-Dawley rats were subjected to a Chronic Constriction Injury (CCI) of the distal infraorbital nerve to model trigeminal neuralgia (TN). BAA was administered intranasally, and pain thresholds were assessed using the von Frey filament stimulation technique. Comparative analyses involved transnasal carbamazepine administration, with a focus on optimizing BAA dosage and delivery methods, including nasal drops, gavage, and subcutaneous injection.

RESULT:

Intranasal BAA significantly increased pain thresholds in TN rats, demonstrating superior performance compared to the control group and achieving efficacy comparable to carbamazepine over a two-week period. Among various administration routes evaluated, nasal delivery was identified as the most effective.

DISCUSSION:

The study shows BAA's superior efficacy compared to carbamazepine, highlighting its potential as a TTX-selective sodium channel blocker for TN. Intranasal BAA administration offers a novel, non-invasive therapeutic option. Further research on dosage forms for clinical use, such as drug-encapsulating nanoparticles or vesicles for targeted delivery in neurological disorders, is warranted.

12 Sep 2025·MEDICINE

Efficacy and safety of bulleyaconitine A in the treatment of osteoarthritis: A systematic review and meta-analysis

Review

Author: Ma, Fang-lan ; Xiao, Min ; Huang, Xia-han

Background::

This study evaluated the efficacy and safety of bulleyaconitine A in the treatment of osteoarthritis compared to non–bulleyaconitine A interventions.

Methods::

We searched PubMed, Embase, Web of Science, Cochrane Library, CBM, CNKI, VIP data, Wan Fang Data, ClinicalTrials.gov, the WHO International Clinical Trial Registry Platform (WHO ICTRP), and the Chinese Clinical Trial Registry (ChiCTR) from their inception to March 1, 2024, and selected relevant records based on inclusion criteria. Two independent reviewers screened the literature, extracted data, and assessed the risk of bias of the included studies. The meta-analysis was conducted using RevMan 5.3 software.

Results::

The study included 5 randomized controlled trials with a total of 424 participants, which revealed that the efficacy rate and Visual Analog Scale score of bulleyaconitine A for treating osteoarthritis were comparable to those of conventional therapy. However, the knee joint function improvement in the experimental group exceeded that of the control group, and there was a reduced incidence of adverse events.

Conclusion::

Bulleyaconitine A is effective in the treatment of osteoarthritis and has few adverse events.

01 May 2024·BULLETIN OF EXPERIMENTAL BIOLOGY AND MEDICINE

Effects of Bulleyaconitine A on Extracellular Matrix Secretion and Expression of Related Proteins in Acetaldehyde-Activated Hepatic Stellate Cells

Article

Author: Tang, X N ; Zhan, X D ; Yuan, Y P ; Sun, Q S ; Song, Q W ; Jiang, Y X

Activated hepatic stellate cells differentiate into myofibroblasts, which synthesize and secrete extracellular matrix (ECM) leading to liver fibrosis. It was previously demonstrated that bulleyaconitine A (BLA), an alkaloid from Aconitum bulleyanum, inhibits proliferation and promotes apoptosis of human hepatic Lieming Xu-2 (LX-2) cells. In this study, we analyzed the effect of BLA on the production of ECM and related proteins by LX-2 cells activated with acetaldehyde (AA). The cells were randomized into the control group, AA group (cells activated with 400 μM AA), and BLA+AA group (cells cultured in the presence of 400 μM AA and 18.75 μg/ml BLA). In the BLA+AA group, the contents of collagens I and III and the expression of α-smooth muscle actin and transforming growth factor-β1 (TGF-β1) were statistically significantly higher than in the control, but lower than in the AA group. Expression of MMP-1 in the BLA+AA group was also significantly higher than in the AA group, but lower than in the control. Expression of TIMP-1 in the BLA+AA group was significantly higher than in the control, but lower than in the AA group. Thus, BLA suppressed activation and proliferation of LX-2 cells by inhibiting TGF-β1 signaling pathway and decreasing the content of collagens I and III by reducing the MMP-1/TIMP-1 ratio.

100 Deals associated with Bulleyaconitine A

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