Drug Database
DI

diltiazem (diltiazam, Aptalis / diltiazem, SURECAPS)

✓ Approved

Adare Pharma Solutions · CACNA1C · Small Molecule

What is diltiazem?

diltiazem is a small molecule developed by Adare Pharma Solutions. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand Namesdiltiazam, Aptalis, diltiazem, SURECAPS
CompanyAdare Pharma Solutions
Drug ClassSmall Molecule
Molecular TargetCACNA1C
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Adare Pharma Solutions

Mechanism of Action

Molecular Targets

diltiazem 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

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

Therapeutic AreaConditionPhase
Cardiac disordersAngina pectoris✓ Approved

Related Research Articles

PubMedJournal of molecular medicine (Berlin, Germany)2026-10-07

The calcium channel blocker diltiazem ameliorates parthanatos in juvenile neuronal ceroid lipofuscinosis.

Kim Hyungkuen H, Hwang Eunmi E, Kim Sung-Jo SJ

Accumulation of pre-mutagenic 8-oxoguanine and impaired DNA repair can lead to poly(ADP-ribose) (PAR) accumulation and parthanatos in Alzheimer's disease, the leading cause of age-dependent dementia. However, the occurrence of parthanatos has not been well established in other types of dementia, including juvenile neuronal ceroid lipofuscinosis (JNCL), a major form of juvenile dementia. In this study, we investigated parthanatos-associated pathology in JNCL using patient-derived lymphoblasts (PDLs). Quantitative immunofluorescence microscopy revealed increased accumulation of 8-oxoguanine and PAR in JNCL-PDLs. JNCL is known to exhibit elevated intracellular calcium, which activates PAR polymerase - 1 (PARP1). The L-type calcium channel blocker diltiazem effectively suppressed PAR accumulation in JNCL-PDLs, even under co-treatment with a calcium ionophore. Diltiazem also reduced 8-oxoG accumulation in JNCL-PDLs, although this effect was largely calcium independent. Subcellular fractionation followed by immunoblotting showed that diltiazem enhanced nuclear recruitment of OGG1 and its partner proteins. These protective effects were abolished by OGG1 knockdown, suggesting a dual role of diltiazem in regulating both calcium signaling and OGG1 activity. Collectively, our data identify that parthanatos as novel therapeutic target for JNCL and propose diltiazem as a potential therapeutic agent. KEY MESSAGES: Increased poly(ADP-ribose) accumulation represents a novel therapeutic target in juvenile neuronal ceroid lipofuscinosis caused by CLN3 mutations. Increased PARP1 expression and decreased PARP1 cleavage lead to elevated poly(ADP-ribose) accumulation in juvenile neuronal ceroid lipofuscinosis. Diltiazem ameliorates poly(ADP-ribose) accumulation in patient-derived cell models of juvenile neuronal ceroid lipofuscinosis by suppressing PARP1 expression and 8-oxoguanine accumulation.

PMID 42841989
Read full article →
PubMedEMBO molecular medicine2026-10-07

Small molecules rescue pathogenic POLGA aggregation and restore its functions in a mouse model of PEO.

Mohammed Aftab A, Kaur Tavleen T, Panwar Priyanka P, Ghosh Samanwita S et al.

POLGA, the catalytic subunit of the mitochondrial DNA polymerase, is essential for mitochondrial DNA (mtDNA) replication and maintenance. Mutations in POLGA cause progressive external ophthalmoplegia (PEO), but the underlying pathogenic mechanisms remain unclear. Here, we show that the mitochondrial E3 ligase MITOL hyperubiquitylates PEO-associated POLGA mutants at lysine 1060, triggering conformational changes and formation of insoluble aggregates that impair their mitochondrial import and consequently compromise mtDNA replication and mitochondrial homeostasis. To identify compounds that disrupt POLGA aggregates and restore mutant POLGA function, we screened an FDA/EMA/PMDA-approved drug library using a split-GFP system. We identified two clinically approved compounds, diltiazem hydrochloride (C1) and sulbactam (C4), that disrupted POLGA aggregates, prevented aberrant MITOL recognition, restored mitochondrial import, and rescued mtDNA replication and mitochondrial function. Importantly, treatment with either compound significantly improved motor performance in a knock-in mouse model carrying the disease-relevant A467T-equivalent POLGA mutation. These findings establish pathogenic aggregation as a previously underrecognized disease mechanism and demonstrate that disrupting POLGA aggregates with repurposed drugs can restore mitochondrial function in vivo, providing a potential therapeutic strategy for POLGA-associated mitochondrial disease.

PMID 42839124
Read full article →
PubMedPLoS pathogens2026-10-06

Targeting the Cav1.2-KCa1.1 axis prevents rabies virus internalization and protects against lethal infection.

Sun Ziruo Z, Wang Jinqiu J, Wen Zhiyuan Z, Shuai Lei L et al.

Rabies is an almost always fatal disease caused by rabies virus (RABV). Once RABV enters the central nervous system, the mortality rate is almost 100%. Therefore, preventing RABV from entering the nervous system is crucial for the development of anti-RABV therapeutics. Here, we found that the L-type calcium channel Cav1.2 pore-forming subunit (Cav1.2) and potassium calcium-activated channel subfamily M alpha 1 (KCa1.1) are involved in the internalization of RABV using an siRNA approach. RABV glycoprotein interacts with Cav1.2, a process that is required for the subsequent activation of the channel. The activated Cav1.2 then interacts with and activates KCa1.1 to regulate the endocytosis of RABV by promoting the F-actin polymerization. Importantly, diltiazem, a blocker of Cav1.2 and an FDA-approved drug, has been shown to substantially reduce mortality in mice infected with RABV. Approximately 70% of mice survived following treatment with diltiazem at 50 mg/kg, whereas the 25 mg/kg dose resulted in 26% survival. Our findings suggest that Cav1.2 is a promising target for the development of antiviral drugs against rabies and enhances our comprehension of the RABV entry mechanism.

PMID 42837418
Read full article →
PubMedFrontiers in pharmacology2026-10-06

Calcium channel blocker-associated pulmonary toxicity: epidemiology, mechanisms, and clinical management.

Jiang Qiu Q, Cui Wen-Hui WH, He Jia-Yi JY, Xie Zhi-Qi ZQ et al.

Calcium channel blockers are first-line medications for the treatment of hypertension, angina pectoris, and arrhythmias, and are generally well-tolerated. However, in recent years, there have been reports indicating that CCBs may cause severe pulmonary toxicity, such as non-cardiogenic pulmonary edema and acute respiratory distress syndrome. This article employs a comprehensive review methodology to systematically summarize the clinical types, incidence, risk factors, mechanisms of injury, and management strategies for CCB-related pulmonary toxicity. Current evidence indicates that pulmonary toxicity is extremely rare at standard therapeutic doses; however, the incidence increases significantly in cases of acute overdose and among specific populations (pregnant women, patients with underlying cardiopulmonary diseases). Pharmacovigilance studies have identified significant signals suggesting an association between nifedipine, diltiazem, and verapamil to pulmonary edema, with amlodipine having the highest number of related clinical reports. Major risk factors include drug overdose, pregnancy, underlying cardiopulmonary disease, and differences among CCB subclasses. Toxicity associated with dihydropyridine CCBs is primarily characterized by vasodilatory shock, whereas non-dihydropyridine CCBs exhibit a combination of cardiac depressant and vasodilatory effects. Mechanisms involve hemodynamic changes, increased capillary permeability, inflammatory activation, and alveolar epithelial dysfunction. Early recognition, drug discontinuation, selection of vasoactive agents based on the type of shock, and life support are key to improving prognosis.

PMID 42835333
Read full article →
PubMedInjury2026-10-06

Evaluation of the wound healing effects of a hydrogel containing hydroalcoholic extract of Chelidonium majus in a rat model.

Farabi Mostafa Mojtahedzadeh MM, Valiallahi Jalal J, Rezanejad-Gatabi Zahra Z, Livani Zohreh Z et al.

This study aimed to develop an innovative wound dressing by loading Chelidonium majus L. extract into an alginate hydrogel matrix and to assess its efficacy in wound healing. The extract of C. majus, famous for its anti-inflammatory and antioxidant features, was obtained from plant material collected in Mazandaran Province, Iran, and incorporated into sodium alginate hydrogels at concentrations of 2% and 5% w/w. The hydrogel formulations were characterized in terms of their morphological, thermal, and swelling properties, demonstrating interconnected porous structures, altered thermal behavior indicating increased amorphous content, and high moisture absorption capacity. To evaluate biological activity, the antioxidant and flavonoid content of the extract were measured, showing notable free radical scavenging ability and high levels of flavonoids. An in vivo wound healing model using adult male Wistar rats compared the effectiveness of control, bare hydrogel, C. majus-loaded hydrogels (2% and 5%), and diltiazem treatments. Wounds treated with the 5% C. majus hydrogel showed accelerated closure rates and improved tissue regeneration, as confirmed by histological examination and enhanced expression of proliferative and regenerative genes (TGF-β) alongside decreased inflammatory markers (TNF-α and IL-1β), in comparison with the control group. These results indicate that C. majus-loaded alginate hydrogel, especially at a 5% concentration, promotes wound healing through offering a wet environment, supporting cell proliferation, and modulating inflammation. This hydrogel may represent a promising topical therapeutic option for treating skin wounds.

PMID 42837756
Read full article →
PubMedBiomedical engineering letters2026-09-27

Medication-specific risk of atrial fibrillation in patients with coronary artery disease.

Kim Taehyun T, Ryu Gayeon G, Choi Ye Eun YE, Shin Hangsik H

Cardiovascular medications used in coronary artery disease (CAD) can potentially modulate the risk of incident atrial fibrillation (AF). However, comprehensive data regarding medication-specific AF risk in the CAD population remain limited. This study aimed to identify prevalent medications prescribed to patients with CAD and evaluate their independent associations with AF risk. In this retrospective cohort study of 157,750 patients with CAD and related comorbidities, CAD-predominant medications were identified based on a frequency analysis of prescriptions in the overall cohort. Among 99,370 patients who received at least one such medication, associations with incident AF were evaluated using extended Cox proportional hazards models with time-varying covariates. Overall, 30 CAD-predominant medications were identified across nine pharmacological classes. In multivariable Cox proportional hazards models, six medications were significantly associated with AF risk, of which one was associated with a lower risk and five with a higher risk. Ezetimibe/rosuvastatin was associated with reduced AF risk, whereas diltiazem HCl, torasemide, heparin sodium, bisoprolol fumarate, and norepinephrine were associated with increased risk. Torasemide showed the strongest positive association. AF risk demonstrated heterogeneity across different CAD medications. Antilipidemic agents were associated with a lower AF risk, whereas certain diuretics, antianginal agents, antihypertensive, and vasoactive agents were associated with a higher risk. These results may have implications for individualized pharmacotherapy and AF prevention in patients with CAD. The online version contains supplementary material available at https://doi.org/10.1007/s13534-026-00589-6.

PMID 42801026
Read full article →

+9157 more articles available with a free account

Sign up free to view all articles →

Ask about diltiazem