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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

PubMedFrontiers in cardiovascular medicine2026-07-25

Assessment of cardioprotective activity of a nitrate enriched food-based polyherbal formulation using experimental myocardial infarction in rats.

Ramagiri Sruthi S, Singh Hemraj H, Taliyan Rajeev R, Kumar Choudhary Yogendra Y et al.

Recently, Myocardial infarction (MI) became the foremost causes of mortality globally. Growing modern pharmacological evidences indicate that food based herbal formulations can offer promising therapeutic benefits in the management of cardiovascular diseases. In the current study, we investigated the therapeutic potential of a newly developed nitrate-enriched extract from Amaranthus leaves, Oxystorm, and its blend with bioactive food constituent, curcuminoids enriched turmeric extract (BCM-95) in an in vivo model of MI, induced by the ligation through left anterior descending coronary artery (LAD). The model caused significant alterations in cardiac function and structure. In both models, Wistar rats were randomly divided into different groups (three different control groups namely vehicle, sham, and LAD), a positive control group (verapamil), low-dose Oxystorm, and high-dose Oxystorm treatment groups, and a synergistic group administered with Oxystorm and turmeric extract. Following reperfusion, samples were collected to determine cardiac injury biomarkers; LDH, CK-MB, myoglobin, and troponin I. Moreover, inflammatory biomarkers (interleukin-6 and TNF-α) and endogenous oxidative stress markers were assessed. LAD-induced MI significantly increased LDH, CK-MB, oxidative stress, and cardiac inflammation. However, treatment with Oxystorm and its turmeric blend alleviated levels of lactate enzyme, CK-MB, troponin-I, interleukins, and malondialdehyde, which reduced infarct size, though enhanced antioxidant defense (GSH and SOD). The enriched dietary nitrate content in Oxystorm, when combined with polyphenol-rich turmeric extract (BCM-95), showed cardioprotective potential, which may be associated with nitrate/NO-related mechanisms, attenuation of oxidative stress, and suppression of inflammatory pathways. However, nitric oxide bioavailability and related signaling pathways were not directly assessed in the present study. Taken together, the pioneer observations, suggest that Oxystorm and its turmeric combination, may serve as adjuvants for the management of ischemia and related cardiac diseases.

PMID 42499795
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PubMedPakistan journal of pharmaceutical sciences2026-07-23

Calcium-channel blockade-mediated blood pressure-lowering and vasorelaxant effects of Brassica oleracea.

Haroon Mahwish M, Chaudhry Mueen Ahmad MA, Ambreen Munnaza M, Haider Muhammad Sajjad MS

Brassica oleracea L. (Brassicaceae), commonly known as cabbage, is usually used for dietary purposes and is also known for many medicinal uses, including blood pressure. The current research study aimed to authenticate the traditional claims of B. oleracea L. for hypertension on a scientific basis using in vivo and in vitro pharmacological techniques. Crude extract of B. oleracea L. was evaluated for its hypotensive and vasorelaxant effects in normotensive anesthetized wistar rats using an invasive blood pressure-measuring technique and isolated rat thoracic aorta, respectively. Normotensive anaesthetized rats used in experiments showed a gradual decrease in blood pressure parameters and heart rate when treated with Bo.Cr (0.1-100 mg/kg) comparable to verapamil (0.01-30 mg/kg). Whereas, in isolated aortic tissue, Bo.Cr (0.01-3 mg/ml) exhibited complete relaxation on high K+ [80 mM] and phenylephrine (1 µM)-mediated contractions. Crude extract at doses of 0.3 and 1 mg/ml also showed a reduction in response to Ca2+ concentration-response curves. Results indicate calcium channel-blocking activity, a possible cause of the blood pressure-lowering and vasodilator effects of B. oleracea.

PMID 42489302
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PubMedOncology letters2026-07-23

Molecular signatures of triple-negative breast cancer cells acquiring palbociclib resistance via continuous exposure.

Enomoto Daichi D, Iwasa Yumika Y, Irie Natsuho N, Ohata Haruki H et al.

Palbociclib, a cyclin-dependent kinase (CDK)-4/6 inhibitor, exhibits therapeutic potential for triple-negative breast cancer (TNBC), for which effective treatments remain limited. However, understanding the mechanisms underlying drug resistance is essential for its clinical application. Although the mechanisms underlying resistance to CDK4/6 inhibitors in hormone receptor-positive breast cancer have been investigated, the mechanisms by which continuous drug exposure induces resistance in TNBC cells remain unclear. Therefore, the present study aimed to establish palbociclib-resistant TNBC cells using a continuous drug exposure model and to elucidate their characteristics. MDA-MB-231 cells, a human TNBC cell type with wild-type retinoblastoma (Rb) protein, were continuously exposed to palbociclib at gradually increasing concentrations (0.01-1 µM) to establish resistant cells, which were named MB231/PalR cells. Drug sensitivity was subsequently evaluated using cell viability assays; gene and protein expression levels were analyzed by quantitative polymerase chain reaction and western blotting, respectively; and P-glycoprotein-mediated efflux capacity was evaluated using rhodamine 123 staining with a flow cytometer. Compared with parental cells, MB231/PalR cells exhibited reduced sensitivity to palbociclib and abemaciclib. Rb protein expression levels were decreased, without affecting RB1 mRNA expression, in MB231/PalR cells. The expression levels of CCNE1, CDK6, ATP-binding cassette (ABC)B1 mRNA and cyclin E1 protein were increased, whereas those of ABCG2 and CD274 mRNA were decreased in resistant cells. Furthermore, MB231/PalR cells exhibited reduced sensitivity to the CDK2 inhibitor CVT-313, and co-treatment with CVT-313 failed to restore palbociclib sensitivity. Although P-glycoprotein efflux capacity and ABCB1 mRNA expression were increased in resistant cells, verapamil treatment did not affect palbociclib sensitivity. In conclusion, continuous exposure of MDA-MB-231 cells to palbociclib induced alterations associated with CDK4/6 inhibitor action, resulting in drug resistance. These findings provide mechanistic insights into CDK4/6 inhibitor resistance in TNBC and may support the development of biomarkers and therapeutic strategies to overcome or prevent resistance.

PMID 42488713
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PubMedJournal of cardiovascular electrophysiology2026-07-19

Apparent Unmasking of Left Anterior Fascicular Ventricular Tachycardia After Prior Left Posterior Fascicular Ablation: Possible Alternative Exit From a Shared Septal Purkinje Substrate.

Abed Robert R, Yeung-Lai-Wah Paul P, Saedifard Farzane F, Petrovic Luka L et al.

Fascicular ventricular tachycardia (FVT) is a Purkinje-mediated ventricular tachycardia classically associated with verapamil sensitivity and reentry within the left ventricular conduction network. Although catheter ablation is usually effective, recurrent tachycardia with a different fascicular QRS axis after prior ablation raises important mechanistic questions. Contemporary models suggest that the septal fascicular network may provide a shared, interconnected substrate with multiple potential fascicular exits. We report a 39-year-old man with complete heart block, pacemaker dependence, and prior ablation for left posterior fascicular ventricular tachycardia (LPFVT), who presented with recurrent incessant ventricular tachycardia and severe left ventricular dysfunction (left ventricular ejection fraction, 15%). The presenting arrhythmia demonstrated right bundle branch block morphology with a right inferior axis, consistent with left anterior fascicular ventricular tachycardia (LAFVT). Electrophysiology study revealed a 1:1 relationship between conduction-system activation and ventricular activation, with the earliest Purkinje potential 60 ms pre-QRS near the proximal septum, approximately 1.5 cm below the His bundle. Radiofrequency ablation at this site resulted in transient acceleration, rapid tachycardia termination, and noninducibility. The patient had complete arrhythmia suppression and recovery of left ventricular function to 50%-55%. This case is best interpreted as apparent unmasking of an alternative fascicular exit from a shared septal Purkinje substrate after prior distal LPF ablation, rather than definitive proof of simple circuit transformation or rerouting. The septal fascicular network model provides a physiologically plausible framework for the emergence of a new fascicular VT morphology after ablation. However, alternative mechanisms remain plausible, including focal Purkinje automaticity, bundle branch/interfascicular reentry, and scar-related Purkinje VT. Recurrent FVT after prior distal fascicular ablation may reflect dynamic expression of a shared septal Purkinje network with alternative exits. Careful proximal septal and fascicular mapping is important, while mechanistic conclusions should remain appropriately cautious when definitive circuit evidence is lacking.

PMID 42472351
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PubMedKidney & blood pressure research2026-07-17

Verapamil reduces collagen synthesis to alleviate ureteral scar formation by inhibiting KDM1A-mediated epigenetic silencing of SESN2.

He Junhuan J, Li Jun J, Wu Xuecheng X, Zhu Zhiwei Z et al.

Ureteral scar formation is a fibrotic process linked with collagen synthesis. Although autophagy prevents collagen synthesis, its role in ureteral scarring remains unclear. Therefore, this study investigated the modulation of SESN2-mediated autophagy by verapamil during ureteral scar formation. An in vitro fibrosis model was constructed using TGF-β1-stimulated primary fibroblasts. We established a rat model of ureteral stricture (US), and KN-93 was used to inhibit the phosphorylation of CaMK II. Histopathological alterations and collagen accumulation in rat ureteral tissues were examined using hematoxylin-eosin and Masson staining. The levels of Vimentin, α-SMA, and LC3 were determined using immunofluorescence. Autophagic flux was assessed using an mCherry-GFP-LC3 assay. mRNA and protein levels were assessed by RT-qPCR and Western blot, respectively. Additionally, CoIP and GST pull-down assays were used to detect the binding relationship between CaMK II and KDM1A. The interaction of H3K4me2 and KDM1A with the SESN2 promoter in fibroblasts was verified using ChIP. Verapamil increased autophagy in TGF-β1-stimulated fibroblasts and alleviated ureteral fibrosis in US rats by inhibiting CaMK II phosphorylation (p-CaMK II) to reduce collagen synthesis. Moreover, p-CaMK II promoted the nuclear translocation of KDM1A by phosphorylating KDM1A. Additionally, the effects of KDM1A knockdown on the autophagy and collagen synthesis in TGF-induced fibroblasts were reversed by SESN2 knockdown. Finally, KDM1A knockdown further enhanced the effect of verapamil in promoting SESN2-mediated fibroblast autophagy and suppressed collagen synthesis. Verapamil reduced collagen synthesis during ureteral scar formation by inhibiting the phosphorylation of KDM1A by p-CaMK II, thus, decreasing the demethylation of H3K4me2 on the SESN2 promoter to enhance SESN2-mediated autophagy.

PMID 42467600
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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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