verapamil (Verelan Chrono / Veralan / Veratensin)

✓ Approved

Takeda · CACNA1C · 小分子

什么是 verapamil？

verapamil 是一种小分子，由Takeda研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名	Verelan Chrono, Veralan, Veratensin
公司	Takeda
药物类别	小分子
分子靶点	CACNA1C
给药途径	Oral (PO)
状态	Approved

来源： ClinicalTrials.gov, Takeda

作用机制

分子靶点

verapamil 作用于 1 个分子靶点：

CACNA1C

calcium voltage-gated channel subunit alpha1 C (CACNL1A1, CACNA1C-IT2)

需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

verapamil 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域	疾病/病症	分期
Vascular disorders	Hypertension	✓ Approved

相关研究文献

PubMedJournal of Asian natural products research2026-06-12

Suaeglaucin C: a new coumaronochromone isolated from Suaeda glauca.

Jia Jia J, Ding Xian-Rui XR, Zang Xiao-Han XH, Fang Ying-Jun YJ et al.

A new coumaronochromone (1), and 12 known compounds (2-13) were isolated from the ethyl acetate part of an aqueous EtOH extract of Suaeda glauca. Compounds 5-8 and 12 effectively ameliorated pericardial edema and venous congestion in zebrafish embryos induced by verapamil hydrochloride at 50 μM. Among these, 8 exhibited superior efficacy in reducing pericardial edema compared to the positive control, Digoxin. In contrast, 1-3 displayed significant lethality in zebrafish embryos, with LC50 values of 9.41, 39.59, and 24.47 μM, respectively. Furthermore, these three compounds showed potential cytotoxic effects on HCT116 cells at 30 and 50 μM.

PMID 42283297

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PubMedNeuroscience2026-06-12

Downregulation of Nrf2 and upregulation of TXNIP/NLRP3 signaling Induce postoperative cognitive dysfunction via oxidative stress and pyroptosis in the hippocampus.

Sun Jialong J, Cao Jie J, Yang Chun C, Gao Lizhi L et al.

Postoperative Cognitive Dysfunction (POCD) is a neurocognitive complication after anaesthesia and surgery, with oxidative stress as a key pathological driver. Nuclear factor erythroid-related factor 2 (Nrf2) and Thioredoxin-Interacting Protein (TXNIP) are critical regulators of oxidative stress and inflammation, and TXNIP directly facilitates NLRP3 inflammasome activation. Using an 18-month-old mouse model of POCD established by tibial fracture surgery, we investigated the changes in the expression of TXNIP and the regulatory mechanism of the Nrf2/TXNIP/NLRP3 signaling pathway. Cognitive function was assessed by the Morris water maze test, and hippocampal samples were analyzed for protein levels(Nrf2, TXNIP, and NLRP3 inflammasome-related protein), pro-inflammatory factors (IL-1β and IL-18), Reactive Oxygen Species (ROS), and neuronal apoptosis. Anesthesia/surgery significantly upregulated TXNIP expression. Inhibiting TXNIP with verapamil attenuated oxidative stress, neuronal injury, and NLRP3 inflammasome activation, thereby ameliorating cognitive impairment. Similarly, sulforaphane (SFN)-mediated upregulation of Nrf2 suppressed TXNIP expression, decreased NLRP3 inflammasome-related proteins and pro-inflammatory factors, and alleviated cognitive deficits. These findings demonstrate thatthe Nrf2/TXNIP/NLRP3 axis mediates hippocampal oxidative stress and pyroptosis in POCD pathogenesis, highlighting this pathway as a potential therapeutic target.

PMID 42276292

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PubMedbioRxiv : the preprint server for biology2026-06-12

A hERG Blocker Facilitates K + Channel Current by Agonizing Pore Opening while Blocking.

Docken Steffen S SS, Marquis Matthew J MJ, Ngo Khoa K, Wada Yuumu Y et al.

Many drugs that block voltage-gated K + channels encoded by the human Ether-à-go-go-Related Gene (hERG) can cause long QT syndrome and life-threatening cardiac arrhythmias, yet the molecular mechanisms that determine this risk remain unclear. A process that may counteract arrhythmogenic hERG block, termed facilitation, is common to many clinically-approved hERG blockers including nifekalant, amiodarone, promethazine, imipramine, nortriptyline, haloperidol, verapamil, carvedilol, metoprolol, propranolol, quinidine, fluoxetine, and chlorpheniramine. Facilitation is an increase in hERG current, under certain conditions, due to these blockers. Here, we propose that an agonism-while-blocking mechanism undergirds facilitation. We focus on nifekalant, a Class III antiarrhythmic drug and exemplar hERG blocker that induces facilitation. We tested the hypothesis that nifekalant opens hERG channel gates while blocking, and that unblock of these open-yet-blocked channels results in supranormal hERG current. We develop rate-theory kinetic models to identify features of agonism-while-blocking that produce facilitation. We generate atomistic models that predict that nifekalant blocks the hERG conduction path while modulating the intracellular conduction gate. Voltage-clamp measurements reveal that agonism-while-blocking undergirds nifekalant block and facilitation. We speculate that this agonism-while-blocking mechanism contributes to the relative safety of hERG blockers that induce facilitation.

PMID 42282827

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PubMedDiagnostics (Basel, Switzerland)2026-06-12

The Impact of Intravenous Versus Intra-Arterial Heparin Administration on Radial Artery Spasm During Transradial Coronary Angiography.

Tusun Eyyup E, Mercan Mehmet Han MH, Karakaş Müslüm M, Korucuk Necmettin N et al.

Background/Objectives: Radial artery spasm (RAS) is an important complication during transradial coronary angiography that may negatively affect procedural success and reduce patient comfort. The aim of this study was to comparatively evaluate the effects of intravenous (IV) and intra-arterial (IA) heparin administration on the development of RAS. Methods: This prospective, observational parallel-group cohort study included a total of 223 patients undergoing transradial coronary angiography. Patients were divided into two groups, receiving either IV heparin (n = 77) or IA heparin (n = 146). All patients received a standard dose of unfractionated heparin (5000 IU) and an IA spasmolytic cocktail consisting of 2.5 mg verapamil and 100 mcg nitroglycerin. RAS was defined as pain during the procedure, resistance during catheter manipulation, or the need for crossover. Logistic regression analysis and receiver operating characteristic (ROC) curve analyses were performed. Results: RAS developed in 40 of 223 patients (17.9%). The incidence of RAS was significantly higher in the IA heparin group than in the IV heparin group (23.3% [34/146] vs. 7.8% [6/77]; p = 0.004). Crossover to femoral access due to severe spasm was observed only in the IA group (6.2% [9/146] vs. 0% [0/77]; p = 0.026). Patients who developed RAS were younger, required a greater number of catheters, had longer angiography duration, and were exposed to a higher total radiation dose (p < 0.05 for all). In ROC analysis, the number of catheters used and angiography duration showed comparable performance in predicting RAS. In multivariable logistic regression analysis, IA heparin administration and the number of catheters used were identified as independent predictors of RAS. Conclusions: During transradial coronary angiography, intravenous heparin administration is associated with a significantly lower frequency of RAS and a reduced need for femoral crossover compared with intra-arterial administration. IV heparin may represent an easily applicable strategy for RAS prevention, although causality cannot be established from this observational study.

PMID 42279524

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PubMedJournal of advanced research2026-06-01

Ca2+ signaling in chronic rhinosinusitis with nasal polyps: Deciphering mechanistic insights and future therapeutic targets.

Kalaji Zaina Z, Hamadi Iyad Said IS, Al-Waa Ahmad Munzer AM, Hamoudi Rifat R et al.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a prevalent yet inadequately understood condition characterized by benign lesions originating from inflamed nasal sinuses. It impacts patients by inducing nasal obstruction, inflammation, and recurrent symptoms. The pathophysiological mechanisms underlying nasal polyposis are not fully elucidated, which constrains the efficacy of current therapeutic interventions such as intranasal corticosteroids (INCSs), functional endoscopic sinus surgery (FESS), and biologics, particularly in severe, treatment-resistant, or recurrent cases. Recent research indicates that calcium (Ca2+) channels, notably with the use of blockers like Verapamil, may provide therapeutic benefits by addressing these challenges, demonstrating promising outcomes without significant adverse effects. Nonetheless, the molecular mechanisms involving Ca2+-dependent signaling pathways in CRSwNP remain insufficiently characterized, with a paucity of studies examining their dysregulation and contribution to disease pathology. Consequently, identifying critical components involved in disruptions of Ca2+ signaling is of paramount importance. We aim to encourage further research into the role of Ca2+ signaling in nasal polyposis and to identify potential pathways and novel targets for innovative treatments. This review consolidates current knowledge concerning Ca2+ signaling in CRSwNP, highlighting the roles of various Ca2+ channels and their downstream signaling cascades in modulating key pathological and clinical outcomes that are uniquely characteristic of the disease. Furthermore, we provide novel in silico insights into the potential pathogenic role of KCa3.1 through its interactions with genes such as TRPM6, EGF, HRH1, BCL2A1, and CD209 in CRSwNP, an area that has not been previously examined. This implicates new components and explores potential targets for future therapeutic strategies.

PMID 42219029

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PubMedJournal of medicinal chemistry2026-05-30

From Scaffold Optimization to a Promising Lead: Discovery of a Novel Roemerine Analogue, a Multichannel Antiarrhythmic with Low hERG Liability and Functional Restoration Capacity.

Wu Zhanpan Z, Wang Wenping W, Yang Chunyan C, Peng Lin L et al.

This study identified 6-24, a novel antiarrhythmic lead derived from the roemerine scaffold, which exhibited a distinctive multichannel blockade profile targeting Nav1.5 and Cav1.2, while demonstrating only weak inhibition of hERG. This gentle multitarget profile avoided excessive single-channel blockade associated with proarrhythmic drugs, conferring low QT prolongation risk, a key advantage over agents like verapamil. Patch-clamp and iPSC-cardiomyocyte MEA confirmed prolonged action potentials and reduced conduction velocity. Multielectrode mapping in isolated hearts further revealed that the compound dose-dependently prolonged ventricular activation time and reduced conduction velocity, accompanied by a decrease in the heart rate, without significantly altering the QTc interval. Pharmacokinetic analysis further established that this active concentration could be achieved clinically. Beyond electrophysiological modulation, 6-24 uniquely restored cardiac function in vivo, normalizing ventricular dimensions and hemodynamics. With integrated efficacy, safety, and functional restoration, 6-24 represented a promising multitarget candidate for ventricular arrhythmia therapy.

PMID 42215017

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verapamil (Verelan Chrono / Veralan / Veratensin)

什么是 verapamil？

药物档案

作用机制

分子靶点

治疗适应症

相关研究文献

Suaeglaucin C: a new coumaronochromone isolated from Suaeda glauca.

Downregulation of Nrf2 and upregulation of TXNIP/NLRP3 signaling Induce postoperative cognitive dysfunction via oxidative stress and pyroptosis in the hippocampus.

A hERG Blocker Facilitates K + Channel Current by Agonizing Pore Opening while Blocking.

The Impact of Intravenous Versus Intra-Arterial Heparin Administration on Radial Artery Spasm During Transradial Coronary Angiography.

Ca2+ signaling in chronic rhinosinusitis with nasal polyps: Deciphering mechanistic insights and future therapeutic targets.

From Scaffold Optimization to a Promising Lead: Discovery of a Novel Roemerine Analogue, a Multichannel Antiarrhythmic with Low hERG Liability and Functional Restoration Capacity.

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