Drug Database
VE

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

PubMedPesticide biochemistry and physiology2026-09-04

Functional characterization of ABC transporters in chlorpyrifos resistance in Nilaparvata lugens.

Xiao Tianxiang T, Deng Mengqing M, Wang Wenxiu W, Lu Kai K

ATP-binding cassette (ABC) transporters play important roles in insecticide resistance, but their functional contributions and structural basis of substrate recognition remain poorly understood. Here, we demonstrate that ABCG9 is an important determinant of chlorpyrifos resistance in Nilaparvata lugens, a destructive rice pest throughout Asia. Verapamil synergism suggested the involvement of active efflux, and expression profiling identified ABCB7, ABCC5, and ABCG9 as constitutively upregulated in the resistant strain and inducible by chlorpyrifos. However, only RNAi-mediated knockdown of ABCG9 significantly increased chlorpyrifos susceptibility, suggesting that this transporter plays a critical role in chlorpyrifos resistance in N. lugens. Structural analysis revealed that ABCG9 adopts a canonical ABCG half-transporter architecture with a conserved N-terminal nucleotide-binding domain (NBD) and a C-terminal transmembrane domain (TMD) containing six helices. Molecular docking and dynamics simulations showed that chlorpyrifos binds within a hydrophobic pocket at the TMD cavity entrance, stabilized primarily by van der Waals interactions (ΔGvdW = -39.04 kcal/mol), with a total binding free energy of -33.46 kcal/mol. Notably, the predicted hydrogen bond was transient, whereas hydrophobic contacts persisted throughout the 100 ns simulation, highlighting the importance of dynamic approaches over static docking alone. These findings identify ABCG9 as a phase III efflux transporter completing the chlorpyrifos detoxification cascade and provide structural insights into substrate recognition by insect ABCG transporters.

PMID 42697681
Read full article →
PubMedFrontiers in physiology2026-09-03

Characterization of calcium sources and downstream signaling pathways following electrical field stimulation of rodent longitudinal esophageal muscle.

Gräfe Michelle M, Kriese Julius-Neven JN, Kirschstein Timo T, Köhling Rüdiger R et al.

To explore the mechanisms involved in esophageal body longitudinal muscle contraction induced by electrical field stimulation. Isometric contractions of esophageal segments from wistar rats in an organ bath were induced by electrical field stimulation (duration 1 s, frequency 1-100 Hz, intensity 30-90 V) before and after application of pharmacological probes to test involvement of muscarinic receptors, Rho kinase, Ca2+ release, protein kinase C, calmodulin and L-type Ca2+ channels. Electrical field stimulation (EFS) induced contractions showed a frequency and intensity-dependent behavior. Based on the effect size, expressed by the Cohen's d, they were insensitive to the muscarinic receptor blocker atropine (1 µM), the Rho kinase inhibitor Y-27632 (10 µM) as well as the inhibitors of Ca2+ release 2-aminoethoxydiphenylborane (2-APB, 100µM) and 1,1'-diheptyl-4,4'-bipyridinium (DHBP, 100 µM). In contrast, contractions were reduced by the protein kinase C inhibitor chelerythrine (10µM) and by the calmodulin antagonist N-[6-aminohexyl]-5-chloro-1-naphthalenesulfonamide hydrochloride (W-7, 100 µM). Verapamil (100 µM) abolished EFS-induced contractions. Based on our findings with 2-APB, DHBP, and verapamil, extracellular Ca²+ appears to be the source of the increase in intracellular Ca²+ underlying EFS-induced EB contractions. Furthermore, the effects observed with chelerythrine and W-7 may suggest that this increase in intracellular Ca²+ may subsequently activate PKC- and calmodulin-dependent signaling pathways.

PMID 42688097
Read full article →
PubMedBioorganic & medicinal chemistry2026-09-03

Design, synthesis, and biological evaluation of novel phenylindole derivatives as P-gp inhibitors to overcome multidrug resistance in MCF-7/ADR cells.

Yang Zhikun Z, Ding Yingjia Y, Xu Keren K, Han Jiajia J et al.

Overcoming multidrug resistance (MDR) remains a formidable obstacle in cancer chemotherapy, largely attributable to drug efflux mediated by the P-glycoprotein (P-gp) pump. To address this challenge, we designed and synthesized 27 novel phenylindole derivatives and systematically assessed their MDR-reversal activity in MCF-7/ADR cells. Among these compounds, Ina4 demonstrated potent reversal activity (RF = 229.4), exceeding that of the reference P-gp inhibitors verapamil (RF = 51.0) and cyclosporine A (RF = 103.3), while exhibiting low intrinsic cytotoxicity. Mechanistic investigations, including western blot and Rhodamine 123 (Rh123) accumulation assays, revealed that Ina4 effectively inhibits the efflux function of P-gp without altering its protein expression levels. Furthermore, molecular docking analysis indicated that Ina4 may bind to the active pocket of P-gp, primarily via π-π stacking interactions. Notably, in a 3D tumor spheroid model, co-administration of Ina4 with doxorubicin (DOX) resulted in significant suppression of spheroid growth. Collectively, these findings indicate that Ina4 is a promising P-gp inhibitor.

PMID 42685504
Read full article →
PubMedJournal of ethnopharmacology2026-09-03

Fengshi Gutong Capsules alleviate aconitums-induced nephrotoxicity via PXR-mediated efflux of aconitum alkaloid.

Liu Jiahui J, Liu Feifei F, Hong Lili L, Hou Meirong M et al.

Fengshi Gutong Capsules (FSGT) is widely used for the treatment of rheumatoid arthritis (RA). However, its clinical application is limited because it contains Aconiti Radix Cocta and Aconiti Kusnezoffii Radix Cocta (AA), and the mechanism of compatibility and detoxification remains unclear. This study was to provide pharmacokinetic and mechanistic insights into the attenuation of AA-induced nephrotoxicity by FSGT compatibility. Collagen-induced arthritis (CIA) rats were treated with FSGT, its modified formulations (AA or FSGT-AA), or methotrexate, and renal injury was evaluated via biochemical indicators (BUN, CRE, UA) and histopathology. Aconite alkaloids (AC, HA, MA, BAC, BHA, BMA) were quantified in plasma, kidney, and urine by UPLC-MS/MS, while the FBXO44/PXR/P-gp signaling was investigated using Western blotting, immunofluorescence, ubiquitination assays, molecular docking, molecular dynamics simulations, and microscale thermophoresis (MST). FSGT maintained superior anti-RA efficacy while markedly mitigating AA-induced nephrotoxicity. Pharmacokinetically, FSGT accelerated the clearance and urinary excretion of toxic diester diterpenoid alkaloids, reducing their renal accumulation. Mechanistically, FSGT suppressed E3 ubiquitin ligase FBXO44 expression, inhibited FBXO44-mediated PXR ubiquitination/degradation, promoted PXR expression, and upregulated P-gp efflux transporter expression. Verapamil abolished this protective effect. 18α-glycyrrhetinic acid and kaempferol were confirmed as key active components directly binding FBXO44. FSGT reduces nephrotoxicity via FBXO44/PXR/P-gp signaling to accelerate toxic aconite alkaloids excretion, providing a scientific basis for "detoxification by compatibility" and preclinical mechanistic support for the safety profile of FSGT.

PMID 42685941
Read full article →
PubMedLasers in medical science2026-09-03

Energy-based devices for enhanced transdermal drug delivery in pathological scars: A review.

Zhao Yinhua Y, Ma Jiaxing J, Li Bo B, Lin Huang H

Although laser-assisted drug delivery (LADD) technology is well established, its clinical application has now expanded to include a broader range of energy-based devices (EBDs). This review aims to evaluate the use of energy-based device-assisted drug delivery (EADD) in the treatment of hypertrophic scars (HTS) and keloids. Following a comprehensive search of English and Chinese databases, 30 relevant studies were included. These studies evaluated the combined application of various EBDs-including ablative and non-ablative fractional lasers, micro-plasma radiofrequency (MPR), ultrasound, and thermomechanical fractional injury-with pharmacological agents such as corticosteroids, 5-fluorouracil (5-FU), verapamil, botulinum toxin type A (BTXA), and photosensitizers (5-aminolevulinic acid). The results indicate that for corticosteroids, EADD achieves efficacy comparable to that of intralesional injection while significantly reducing pain and lowering the risk of skin atrophy and telangiectasia, offering particular benefits for pediatric patients. The combination of EADD with 5-FU effectively improves scar thickness, whereas CO2 AFL-assisted photosensitizers delivery shows an exceptionally low recurrence rate in the treatment of acne-induced HTS. In contrast, for keloids, intralesional BTXA injections remain superior to CO2 AFL-assisted BTXA delivery. Furthermore, emerging strategies such as the triple-modality "light-light-sound" therapy, which combines intense pulsed light, CO₂ ablative fractional laser, and ultrasound, provide promising prospects for recalcitrant cases. In summary, EBDs enhance drug delivery through micropore formation or acoustic effects, establishing it as a key therapeutic strategy that balances efficacy with improved safety and patient compliance compared to monotherapy. However, standardized treatment protocols still require further validation through future research.

PMID 42684515
Read full article →
PubMedACS sensors2026-09-01

Strain Sensor-Integrated Tri-Layer Cantilever with Enhanced Sensitivity and Stability for Quantitative Cardiotoxicity Screening.

Liu Ke K, Shanmugasundaram Arunkumar A, Sun Haolan H, Li Longlong L et al.

Cantilever-based biosensors provide a powerful approach for monitoring cardiomyocyte contractility, but conventional designs often exhibit baseline bending that compromises sensitivity and limits predictive accuracy in drug screening. Here, we present a tri-layer polymer cantilever biosensing platform integrated with a full-bridge piezoresistive strain sensor for the quantitative measurement of cardiomyocyte contractility. The hybrid KMSF-SU-8-KMSF structure minimizes residual stress and reduces baseline deformation by more than 85% compared to SU-8-only cantilevers. This architecture improves strain transfer to the embedded sensors and achieves a limit of detection of approximately 1.2 kPa, which is lower than that of previously reported cantilever systems. The top KMSF layer functions as both an encapsulation barrier and a tissue-guiding interface, promoting alignment, enhancing sarcomere organization, and increasing connexin-43 expression to support cardiomyocyte maturation. Drug screening further confirms the platform's predictive accuracy, as the device successfully detects the expected pharmacological effects: verapamil decreases contractile force, isoproterenol increases both force and beat rate, blebbistatin suppresses myofilament activity, and astemizole induces arrhythmic beating consistent with hERG channel blockade. By providing stable, label-free, and high-sensitivity electronic readouts of cardiomyocyte contractility, this platform establishes a robust and scalable solution for preclinical cardiotoxicity testing, disease modeling, and personalized medicine.

PMID 42676015
Read full article →

+9996 more articles available with a free account

Sign up free to view all articles →

Ask about verapamil