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verapamil (verapamil, Mylan / verapamil SR, Mylan / verapamil ER)

✓ Approved

Mylan · CACNA1C · Small Molecule

What is verapamil?

verapamil is a small molecule developed by Mylan. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand Namesverapamil, Mylan, verapamil SR, Mylan, verapamil ER
CompanyMylan
Drug ClassSmall Molecule
Molecular TargetCACNA1C
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Mylan

Mechanism of Action

Molecular Targets

verapamil acts on 1 molecular target:

CACNA1Ccalcium voltage-gated channel subunit alpha1 C (CACNL1A1, CACNA1C-IT2)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

verapamil is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved

Related Research Articles

PubMedBiomedical chromatography : BMC2026-07-15

Development and Validation of a Sensitive UHPLC-MS/MS Analytical Method for Fulzerasib in Rat Plasma and its Application to Pharmacokinetics Studies.

Liu Qiang Q, Zhao Jin-Zhu JZ, Wang Li L, Zhou Fu-Sheng FS et al.

Fulzerasib is a novel, potent, and irreversible covalent inhibitor targeting the KRAS G12C mutation, recently approved in China for advanced nonsmall cell lung cancer. This study aimed to develop and fully validate a rapid, specific and sensitive UHPLC-MS/MS method for the quantification of Fulzerasib in rat plasma. Sample preparation was streamlined using a simple protein precipitation technique with acetonitrile. Chromatographic separation was achieved within a 4.0-min run on a C18 column, with verapamil as the internal standard and detection via multiple reaction monitoring. The method was rigorously validated over a linear range of 5 to 5000 ng/mL (R2 > 0.9933), demonstrating excellent accuracy (102%-112.7%) and precision (≤ 10.3% for QCs). Stability was confirmed under various storage and processing conditions. The validated method was successfully applied in the first pharmacokinetic study of Fulzerasib in Sprague-Dawley rats following single intravenous (1 mg/kg) and oral (3 mg/kg) administration. Fulzerasib exhibited favorable pharmacokinetic properties, including low plasma clearance (5.02 mL/min/kg), moderate volume of distribution and notably high oral bioavailability of 38.6%. The established method is reliable, efficient and readily applicable, thereby providing a vital tool for accelerating the ongoing preclinical and translational research of Fulzerasib.

PMID 42448637
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PubMedSignal transduction and targeted therapy2026-07-14

RBM20 variants disrupt Ca2+ handling and metabolism in dilated and non-compaction cardiomyopathy stem cell models.

Rebs Sabine S, Sedaghat-Hamedani Farbod F, Kayvanpour Elham E, Eberl Hanna H et al.

Mutations in the splice-regulator RBM20 cause heart failure with reduced ejection fraction (HFrEF), typically manifesting as dilated cardiomyopathy (DCM). Mutations at position 634 in the RS-domain cause DCM with (R634L) or without (R634W) left ventricular non-compaction (LVNC). However, the mechanisms underlying phenotype variability and personalized therapy beyond HFrEF remain unclear. We generated induced pluripotent stem cell-derived cardiomyocytes (iPSC-CM), 3D-cardiospheres and engineered myocardial tissues from patients with RBM20 mutations R634L (LVNC) or R634W (DCM). Using CRISPR/Cas9, we created isogenic rescue and mutation-insertion lines, identifying RBM20 mis-localization, splicing errors in TTN and RYR2, and sarcomere irregularities in both. DCM-CM showed increased resting Ca2+ leak and reduced Ca2+ transient amplitude, typical of HFrEF, and spatial disorganization of sarcoplasmic reticulum and mitochondria. In contrast, LVNC-CM exhibited elevated Ca2+ transient amplitude with faster kinetics, driven by elevated cAMP and mis-spliced, hyperactive CAMK2D, leading to PLN-hyperphosphorylation and increased metabolic respiration. Further, LVNC showed desmosomal derangement potentially from mis-splicing of Junction plakoglobin and reduced 3D cardiosphere compaction. Despite distinct mechanisms, contractile force was reduced in both. Isogenic controls confirm mutation causality. Drug intervention with verapamil partially improved selected abnormal Ca2+ handling and contractile phenotypes in LVNC- and DCM-CM, whereas the CAMK2D inhibitor AIP improved systolic Ca2+ handling predominantly in LVNC-CM. In conclusion, different amino acid substitutions at the same RBM20-residue induce opposing Ca2+-handling and structural phenotypes. While DCM features impaired Ca2+ handling, LVNC shows defective cell-cell coupling and activated Ca2+ handling and metabolism, yet insufficient to compensate for organ-level dysfunction. This supports personalized pharmacological therapies in early HF, and potential CRISPR/Cas9 repair for RBM20 cardiomyopathy.

PMID 42443149
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PubMedPaediatric drugs2026-07-13

Safety and Effectiveness of Pain Medications for Migraine Management During Pregnancy and Lactation.

Smirnoff Liza L, Mancera Nicolas Garzon NG, Hyppolite Tayina T, Lozano Daniela D et al.

The management of migraine during pregnancy and lactation poses a major challenge owing to the paucity of safety data. While very little safety data are available for new targeted migraine therapies such as calcitonin gene receptor protein (CGRP) blocking medications, including the CGRP monoclonal antibodies and gepants, well-established migraine therapies such as topiramate, valproate, and dihydroergotamine have known risk for teratogenicity. Likewise, the safety evidence for commonly used therapies for migraine in pregnancy such as propranolol and verapamil is of low quality, and the level of evidence for efficacy of verapamil is limited. Meanwhile women experience migraine at the highest rates during their reproductive years necessitating an effective and balanced approach that considers maternal and fetal risk as well as optimal benefit to the patient to ensure adequate and appropriate treatment during pregnancy and lactation. The purpose of this review is to provide an overview of the available data on the safety of available and efficacious medications in the management of migraine during pregnancy and lactation. Based on more recent studies, there is increased evidence for use of more specific and efficacious medications for migraine, such as onabotulinumtoxinA, local nerve blocks with lidocaine, and triptans during pregnancy and lactation.

PMID 42440212
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PubMedAmerican journal of ophthalmology2026-07-11

Epidemiology, Safety of Dilation, and Medication-Associated Risk of Acute Angle-Closure Crisis in the United States.

Shah Jainam J, Pathuri Sachin S, Adamovich-Zeitlin Richard R, Oseni Jessinta J et al.

To evaluate the epidemiology of acute angle-closure crisis (AACC), the safety of pharmacologic dilation, and medication-associated AACC risk in the United States. Retrospective clinical cohort study. Adults (≥18 years) in a multicenter federated electronic health record network. Using deidentified electronic medical record data from 2010 to 2025, AACC cases were identified using ICD-10-CM codes followed by definitive therapeutic intervention within 14 days. Incidence, prevalence, and diagnostic trends were evaluated with Mann-Kendall tests. Dilation-associated AACC risk was assessed among patients undergoing dilation-associated ophthalmic examinations, with incident AACC identified within 14 days (with 24-hour sensitivity analysis). Medication-associated AACC risk was evaluated using active-comparator cohorts with 1:1 propensity score matching and Cox proportional hazards models over a 30-day window. AACC incidence (per 100,000 dilation-associated examinations) and hazard ratios (HRs) with 95% confidence intervals (CIs) for medication-associated AACC risk. From 2010 to 2025, the cumulative incidence of AACC was 0.014%, and the prevalence of primary angle closure glaucoma (PACG) among patients with AACC was 16.7%. Both AACC incidence and the prevalence of PACG among patients with AACC increased over time (all P < 0.001). Gonioscopy utilization declined, whereas anterior segment imaging increased (all P < 0.001). Across 3,400,372 dilation-associated examinations among 2,444,570 patients, post-dilation AACC was rare (3.1 per 100,000; 95% CI: 2.3-3.4), with similar findings in a 24-hour sensitivity analysis; events concentrated among patients with anatomical risk factors. Increased AACC risk was observed for medications with established associations: pilocarpine (HR: 1.77), topiramate (2.07), hydrochlorothiazide (2.13), albuterol (1.57), enoxaparin (2.17), and trihexyphenidyl (2.12) (all P < 0.05). Commonly prescribed medications without established associations were also associated with increased risk: lactulose (1.67), metoclopramide (1.38), sumatriptan (1.64), prazosin (1.32), and terazosin (1.77) (all P < 0.05). Previously unreported associations were observed for calcitonin gene-related peptide (CGRP) antibodies (erenumab [HR: 1.33]), calcium channel blockers (verapamil [1.89], diltiazem [1.74]), and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors (alirocumab [1.54], evolocumab [1.46]) (all P < 0.05). AACC following pharmacologic dilation was rare and occurred predominantly among patients with anatomical risk factors, supporting the safety of dilation in routine clinical care. Medication-associated risk signals were observed across commonly prescribed drugs at the population level, including previously unreported associations, highlighting the importance of proactive ocular risk assessment and medication reconciliation in anatomically predisposed patients. Novel medication associations with calcium channel blockers, CGRP monoclonal antibodies, and PCSK9 inhibitors warrant further investigation.

PMID 42431436
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PubMedCardiovascular research2026-07-02

Metabolic crisis and TRPM4 activation cause QT prolongation in TANGO2 deficiency disorder.

Wang Lili L, Kim Kyungsoo K, Kannankeril Prince J PJ, Zheng Chen C et al.

TANGO2 deficiency disorder (TDD), caused by homozygous large deletions in TANGO2, is associated with impaired fatty acid oxidation and metabolic crises that frequently trigger QT prolongation and arrhythmias. The objective was to study the mechanisms responsible for QT prolongation and arrhythmogenesis in TDD. CRISPR/Cas9 were used to generate human induced pluripotent stem cell cardiomyocytes (hiPSC-CMs) carrying a TANGO2 exon 3-9 deletion (TANGO2-/-). Bioenergetic function (mitochondrial oxygen consumption rate, intracellular ATP/ADP ratio) and action potentials (APs) were studied under glucose- or palmitate-fueled conditions.This study reports a TDD clinical case of QT prolongation and arrhythmia that responded favorably to L-type calcium channel (LTCC) inhibition with verapamil or vitamin B-complex supplementation. The mechanisms underlying clinical presentations and therapeutic responses were investigated using TANGO2-/- hiPSC-CMs. In glucose-containing medium, the bioenergetic function was comparable between control and TANGO2-/- hiPSC-CMs. In contrast, using palmitate as energy substrate triggered a profound reduction in cellular ATP production rate and decreased ATP/ADP ratios in TANGO2-/- hiPSC-CMs, exacerbated by 24-hour fasting. This crisis was prevented by 2-week treatment with vitamins B5 and B9. During the crisis, TANGO2-/- hiPSC-CMs exhibited AP prolongation, prevented by intracellular delivery of Mg-ATP or creatine kinase. LTCC inhibition with verapamil prevented AP prolongation by normalizing ATP/ADP ratios and intracellular Ca mishandling. Importantly, the metabolic crisis upregulated TRPM4, an ATP- and Ca-regulated channel. TRPM4 siRNA knockdown or pharmacological block prevented AP prolongation without rescuing the energetic deficit of TANGO2-/- hiPSC-CMs. These findings suggest a mechanistic link between ATP deficiency, TRPM4 activation, and AP prolongation in TDD. Targeting TRPM4 therapeutically may help prevent QT prolongation and cardiac arrhythmias in TDD crisis.

PMID 42389941
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PubMedJACC. Case reports2026-07-02

Atrioventricular Block Induced by Right Coronary Artery Spasm in Vasospastic Angina.

Trimaille Antonin A, Faucher Loic L, Koenig Baudouin B, Schatz Alexandre A et al.

Vasospastic angina (VSA) is a reversible cause of myocardial ischemia due to transient coronary spasm and may rarely be associated with conduction disturbances. A 64-year-old man presented with nocturnal rest angina. The initial angiography results were normal. Holter monitoring during symptoms showed transient ST-segment elevation with Mobitz type I second-degree atrioventricular (AV) block progressing to 2:1 AV block, causing presyncope. He later experienced syncope. Repeat angiography revealed diffuse coronary vasospasm involving the right coronary artery, fully reversible with nitrates, confirming VSA. Verapamil therapy resulted in symptom resolution and no further conduction abnormalities during follow-up. Right coronary artery spasm may induce transient AV block due to ischemia of the AV node. VSA should be considered in unexplained AV block or syncope with ischemic electrocardiographic changes. Calcium-channel blockers are effective even in ischemia-induced conduction disorders.

PMID 42390417
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