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nifedipine (Darbelan 10)

✓ Approved

Teva Pharmaceutical Industries Ltd. · CACNA1C · Small Molecule

What is nifedipine?

nifedipine is a small molecule developed by Teva Pharmaceutical Industries Ltd.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesDarbelan 10
CompanyTeva Pharmaceutical Industries Ltd.
Drug ClassSmall Molecule
Molecular TargetCACNA1C
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Teva Pharmaceutical Industries Ltd.

Mechanism of Action

Molecular Targets

nifedipine 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

nifedipine is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Cardiac disordersAngina pectoris✓ Approved
Vascular disordersHypertension✓ Approved

Related Research Articles

PubMedThe journal of obstetrics and gynaecology research2026-11-10

Hemodynamic Effects of Controlled-Release Nifedipine for Tocolysis in Normotensive Pregnant Women.

Ushida Takafumi T, Fujito Sumire S, Shiraishi Yoshitaka Y, Nozaki Yuki Y et al.

Nifedipine is widely used as a tocolytic agent for threatened preterm labor. However, its hemodynamic effects in normotensive pregnant women, particularly when administered as a controlled-release formulation, remain unclear. We evaluated changes in maternal hemodynamics and adverse effects after controlled-release nifedipine administration in normotensive pregnant women with threatened preterm labor. This retrospective observational study included normotensive women with singleton pregnancies who received controlled-release nifedipine as maintenance therapy for threatened preterm labor between 2018 and 2025. Maternal blood pressure, heart rate, respiratory rate, hypotension (systolic blood pressure < 90 mmHg or diastolic blood pressure < 60 mmHg), tachycardia (≥ 120 beats/min), and adverse maternal and fetal effects were evaluated before and after nifedipine administration. Overall, 38 women were included in the final analyses. Systolic blood pressure significantly decreased from 110.2 ± 9.1 mmHg to 107.5 ± 10.2 mmHg after administration (mean change, -2.7 mmHg; 95% confidence interval, -4.5 to -0.8; p < 0.01). Diastolic blood pressure did not change significantly (-0.7 mmHg; -2.2 to 0.8 mmHg; p = 0.35). Heart rate significantly decreased from 95.3 ± 14.5 to 90.9 ± 12.4 beats/min. The incidence of hypotension and tachycardia did not differ significantly after nifedipine administration. No emergency deliveries were attributed to maternal hypotension. Headache was the most commonly reported adverse effect (28.9%). Controlled-release nifedipine was associated with a small decrease in systolic blood pressure without serious maternal or fetal adverse events. With appropriate monitoring, controlled-release nifedipine may be a feasible option for maintenance or adjunctive tocolytic therapy in normotensive pregnant women.

PMID 43006657
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PubMedFrontiers in pharmacology2026-11-08

Engineered hyalurosomal gel co-delivering citicoline sodium and nifedipine for potential glaucoma management: formulation and pharmacodynamic evaluation.

Hegazy Doaa D, Ibrahim Mennatullah M MM, El-Shiekh Riham A RA, Saher Osama O et al.

Glaucoma is a neurodegenerative ocular disorder that requires multi-targeted therapeutic strategies to counteract intraocular pressure (IOP) elevation and oxidative stress-mediated retinal ganglion cells (RGCs) loss. This study developed an innovative hyalurosomal hydrogel platform co-delivering Nifedipine (NFD, a calcium channel blocker that promotes ocular vasodilation and IOP reduction) and Citicoline sodium (CTC, a potent neuroprotective and antioxidant agent) as a potential topical therapeutic approach for glaucoma. NFD-loaded hyalurosomes (NFD-HAs) were prepared using thin-film hydration and statistically optimized via a D-Optimal design. The optimized formulation (NFD-OF) was probe-sonicated, combined with CTC, and incorporated into an HPMC hydrogel. Sonicated NFD-OF displayed nanosized spherical vesicles (198.6 ± 23.1 nm), high entrapment efficiency (70.7 ± 1.8%), and stable zeta potential (-39.1 ± 1.3 mV). Transmission electron microscopy (TEM) analysis confirmed the distinct spherical morphology, non-aggregated state, and structural integrity of NFD-OF. The final CTC/NFD-OF gel exhibited pseudoplastic shear-thinning flow, an optimal ocular pH (6.9 ± 0.02), and sustained release over 24 h (65.5% for NFD and 99.5% for CTC). The dual gel demonstrated superior free radical scavenging capability (IC50 = 16.44±0.7 μg/mL) compared to free NFD (219.43 μg/mL) and CTC (234.62 μg/mL). Confocal microscopy confirmed a 2.2-fold enhancement in transcorneal penetration depth (110 μm) compared with the control solution (50 μm). In vivo pharmacodynamic evaluation revealed a significantly higher maximum IOP decrease (51.85 ± 8.2%), extended mean residence time (8.9 ± 2.7 h), and increased relative exposure (AUC0-∞ = 494.1 ± 191.9) compared to commercial Xola™ eye drops (36.4 ± 5.9% max IOP decrease, AUC0-∞ = 182.8 ± 33.7). Terminal gamma sterilization preserved physicochemical characteristics and release profiles. Draize and histopathological assays confirmed excellent ocular tolerability. Overall, the CTC/NFD-OF gel demonstrated promising ocular hypotensive activity and safety, supporting its potential as a multifunctional topical therapeutic approach for glaucoma.

PMID 42996362
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PubMedRSC advances2026-11-04

Drug-drug adsorption-based miniaturized solid phase extraction of amlodipine from biological samples before HPLC-PDA analysis.

Mohammadmehri Sina S, Farajzadeh Mir Ali MA, Khoubnasabjafari Maryam M, Shahedi Hojghan Ali A et al.

A nifedipine-assisted miniaturized solid phase extraction coupled with high-performance liquid chromatography-photodiode array method was developed for the extraction and quantification of amlodipine in biological samples. The extraction process was optimized by evaluating the influence of key parameters, including nifedipine amount, agitation mode and time, aqueous phase pH, salt addition, and desorption solvent conditions. Optimal performance was obtained using 7 mg of nifedipine, vortex agitation for 3 min, pH 9, without salt addition, and using ethanol (175 µL) as the desorption solvent. Under these conditions, the method showed good analytical sensitivity, with limits of detection and quantification of 0.54 and 1.7 µg L-1 in deionized water; 2.2 and 6.8 µg L-1 in plasma; and 1.9 and 6.3 µg L-1 in urine, respectively. A linear response was observed over the concentration range of 6.8-200 µg L-1 in plasma, with a correlation coefficient 0.998. The method demonstrated acceptable precision, with relative standard deviation values below 8%, and an extraction recovery of 68 ± 4%. The applicability of the developed method was confirmed through analysis of spiked plasma and urine samples at the concentration levels of 10, 25, and 50 µg L-1. The relative recovery values ranged between 88% and 96% and indicated negligible matrix effects, which confirms the suitability of the method for reliable determination of amlodipine in biological matrices.

PMID 42979374
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PubMedCPT: pharmacometrics & systems pharmacology2026-11-04

Drug-Drug Interactions of Cenobamate With Medications: Dose-Dependent Induction/Inhibition and Clinical Implications.

Ichida Hiroyuki H, Nakao Takaharu T, Mori Takanori T, Makino Reina R et al.

Cenobamate causes dose-dependent cytochrome P450 (CYP)2B6 and CYP3A4 induction and CYP2C19 inhibition, raising concern over multi-pathway drug-drug interactions (DDIs) in patients with epilepsy treated with cardiovascular co-medications. We developed a physiologically based pharmacokinetic (PBPK) model for cenobamate and verified it using reported DDIs for cenobamate 200 mg using three probe substrates: bupropion (CYP2B6), midazolam (CYP3A4), and omeprazole (CYP2C19). The verified model predicted exposure changes (area under the curve ratio [AUCR] and maximum concentration [Cmax] ratio with/without cenobamate) for eight drugs, including anticoagulants and antiplatelets (apixaban, cilostazol, clopidogrel, and rivaroxaban), and antihypertensives (amlodipine, bisoprolol, carvedilol, and nifedipine). Regarding anticoagulants and antiplatelets, for apixaban, AUCR/Cmax ratios were 0.78/0.92 (100 mg), 0.71/0.87 (200 mg), and 0.63/0.83 (400 mg), respectively. For cilostazol, parent exposure decreased (0.67/0.85, 0.55/0.77, 0.45/0.70), while the active metabolite OPC-13015 was predicted to increase in Cmax. For clopidogrel, parent exposure was unchanged, but formation of 2-oxo-clopidogrel and clopidogrel-H4 were decreased and increased, respectively. For rivaroxaban, the AUCR/Cmax ratios were 0.78/0.90, 0.69/0.85, and 0.61/0.80. Among antihypertensives, amlodipine showed decreased AUCR/Cmax ratios (0.57/0.66, 0.45/0.55, 0.37/0.47). The exposure changes of bisoprolol were minor (AUCR 0.84-0.92, Cmax ratio 0.95-0.98); AUCR/Cmax ratios of carvedilol fell to 0.73/0.80, 0.63/0.71, and 0.55/0.64; and nifedipine decreased markedly (0.41/0.54, 0.29/0.41, 0.21/0.32). In conclusion, cenobamate induced CYP2B6 weakly and CYP3A4 moderately, and it inhibited CYP2C19 moderately to drive dose-dependent decreases in exposure for seven of eight drugs with minimal change for bisoprolol. The verified PBPK framework enables risk assessment in scenarios not yet clinically tested.

PMID 42982766
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PubMedPrehospital emergency care2026-10-30

Prevalence of Persistent Severe Hypertension and Rates of Treatment Among Pregnant Patients in the Prehospital Setting.

Maffetone Nicholas N, Livingston Caroline A CA, Wilcox Kevin M KM, Wingate Austin H AH et al.

Hypertensive disorders of pregnancy (HDP) contribute to maternal and fetal morbidity and mortality and require time-sensitive intervention. In April 2025, the American College of Obstetricians and Gynecologists (ACOG), in collaboration with the National Association of EMS Physicians (NAEMSP) and the National Association of EMTs (NAEMT), published new guidelines on the prehospital management of elevated blood pressure in pregnancy. The objective of this study was to determine the prevalence of persistent severe hypertension among pregnant patients encountered by prehospital clinicians, characterize baseline frequency of pre-guideline treatment, and establish a benchmark to inform implementation of these guidelines. We conducted a retrospective observational cohort study using the 2024 ESO Data Collaborative public release research dataset (January 1 to December 31, 2024). We identified all 9-1-1 ground EMS scene responses for patients documented as pregnant beyond 20 weeks of gestation. We excluded injury-related encounters and patients outside the World Health Organization-defined childbearing age range (15 to 49 years). Consistent with the new guidelines, we defined persistent severe hypertension as at least two documented blood pressure measurements with systolic blood pressure ≥ 160 mmHg or diastolic blood pressure ≥ 110 mmHg. We defined guideline-adherent treatment as administration of both magnesium sulfate (MgSO4) and an antihypertensive medication (labetalol, hydralazine, or nifedipine). We identified 39,546 eligible 9-1-1 ground EMS scene responses for patients beyond 20 weeks of gestation. The prevalence of persistent severe hypertension was 3.1% (n = 1,234/39,546). Among these patients, 77 (6.2%) received magnesium sulfate only, 19 (1.5%) received an antihypertensive medication only, and 10 (0.8%) received guideline-adherent treatment with both magnesium sulfate and an antihypertensive medication. Approximately 1 in 32 pregnant patients beyond 20 weeks of gestation encountered by prehospital clinicians had persistent severe hypertension. In the year prior to dissemination of the 2025 ACOG, NAEMSP, and NAEMT-supported guidelines, fewer than 1% received guideline-adherent treatment with both magnesium sulfate and an antihypertensive medication. These findings establish a national benchmark and identify opportunities to improve prehospital care through protocol development, medication availability, clinician education, and implementation of updated guidelines.

PMID 42961073
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PubMedMicrobiology spectrum2026-10-29

Slowly burning down the house: the role of calcium in spotted fever rickettsiosis pathogenesis.

Farner Jennifer M JM, Nguyen Trung T, Londoño Andrés F AF, Kim Yuri Y et al.

Spotted fever group rickettsiae (SFGR) infect microvascular endothelial cells, increasing vascular permeability, a major pathophysiological effect with unclear underlying factors. To accurately model this disease feature, we used a microvascular barrier model that continuously monitors transendothelial electrical resistivity in brain microvascular endothelial cell barriers. Using this model, we previously showed that Rickettsia parkeri-infected microvascular endothelial cells treated with voltage-gated L-, T-, and N-type calcium channel blocker (VGCCb) benidipine delayed in vitro vascular permeability. This study aimed to investigate whether host calcium signaling modulation and metabolic stress with SFGR infection are primary drivers of rickettsial fitness and the subsequent loss of vascular integrity. We hypothesize that SFGR infections, while consuming host cell energy resources such as ATP, lead to modulation of microvascular endothelial cell calcium transport that enhances bacterial fitness, prefacing collateral barrier dysfunction. We confirmed that benidipine, the L-type VGCCb nifedipine, and the membrane-active divalent ion chelator DP-b99 have dose-dependent effects on vascular permeability, as measured by electric cell-substrate impedance sensing, which result in delayed rickettsial growth, as measured by qPCR, without direct bactericidal activity. During R. parkeri infection, intracellular calcium concentrations increased and ATP concentrations decreased simultaneously; these effects were mitigated by benidipine. VGCCb and DP-b99 treatment sustained VE-cadherin junctions, seen with immunofluorescence microscopy, similar to uninfected microvascular endothelial cells, corresponding to barrier integrity preservation. In addition to delayed rickettsial growth, VGCCbs and DP-b99 inhibited rickettsial actin tail formation, reduced cell-to-cell spread, and increased bacterial length by impacting FtsZ-ring localization, evaluated by immunofluorescence microscopy and plaque assay. Furthermore, bacterial protein synthesis is required, as replicating but not heat-killed R. parkeri caused microvascular endothelial cell barrier dysfunction, and a subinhibitory doxycycline dose delayed R. parkeri-induced microvascular endothelial cell dysfunction without impacting R. parkeri growth. Limiting calcium access disrupts R. parkeri growth by interrupting bacterial elongation and division, actin tail formation, and cell-to-cell spread, mitigating R. parkeri-induced microvascular endothelial cell barrier permeability in vitro. This suggests that rickettsial interference with host cell metabolism triggers calcium entry and accessibility, key in rickettsial fitness, and pathogenicity.IMPORTANCEThis work investigated pathogen- and host-associated factors contributing to SFGR disease pathogenesis, as measured by vascular permeability. Our findings demonstrate that SFGR disrupts endothelial cell homeostasis by causing intracellular calcium influx, a process that is critical for rickettsial fitness and pathogenesis. Rickettsial growth and cell-to-cell spread are dependent on host cell calcium, underscoring the essential role of Ca²+ access and linking bacterial fitness to calcium-dependent host processes. Although blocking calcium channels suppresses immune cell activation in vitro and increases mortality in an SFGR murine model in vivo, these findings warrant further investigation into whether selectively targeting endothelial cell-specific calcium signaling could reduce SFGR-associated vascular permeability without compromising innate immune responses. Such an approach may improve SFGR-related morbidity and mortality. Elucidating the role of calcium signaling in the obligate intracellular lifestyle of rickettsiae provides deeper insight into fundamental rickettsial biology and the mechanisms driving severe disease.

PMID 42954458
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