Drug Database
IS

isosorbide dinitrate + hydralazine (hydralazine + ISDN / BiDil / ISDN + hydralazine)

✓ Approved

Arbor Pharmaceuticals, LLC · CACNA1C · Small Molecule

What is isosorbide dinitrate + hydralazine?

isosorbide dinitrate + hydralazine is a small molecule developed by Arbor Pharmaceuticals, LLC. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand Nameshydralazine + ISDN, BiDil, ISDN + hydralazine
CompanyArbor Pharmaceuticals, LLC
Drug ClassSmall Molecule
Molecular TargetCACNA1C
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Arbor Pharmaceuticals, LLC

Mechanism of Action

Molecular Targets

isosorbide dinitrate + hydralazine 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

isosorbide dinitrate + hydralazine is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Cardiac disordersCardiac failure✓ Approved

Related Research Articles

PubMedScientific reports2026-07-17

Higher insulin resistance is associated with gastrointestinal polyps in women and older adults.

Lin Ching-Huang CH, Chang Yu-Chen YC, Tsou Meng-Ting MT, Hwang Lee-Ching LC et al.

Type 2 diabetes mellitus increases the risk of developing certain cancers, particularly endocrine and gastrointestinal malignancies. However, the relationship between gastrointestinal polyps and insulin resistance has received relatively little attention. The current study explored associations between gastrointestinal polyps and insulin resistance using the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR). Specifically, we conducted a cross-sectional study at a Northern Taiwan health examination center with 4,139 enrollees who underwent a health checkup, had complete data regarding HOMA-IR, and manifested gastrointestinal polyps from 2008 to 2018. The prevalence of gastrointestinal polyps tended to increase across HOMA-IR quartiles (P-trend = 0.04). However, compared with participants in the lowest quartile of HOMA-IR, those with higher HOMA-IR levels were not significantly associated with gastrointestinal polyps. In subgroup analyses, women in the highest quartile had a higher prevalence of gastrointestinal polyps than those in the lowest quartile [odds ratio (OR) 1.39, 95% confidence interval (CI) 1.06-1.83]. Additionally, participants aged ≥ 60 years in the higher HOMA-IR quartiles had an increased odds of gastrointestinal polyps (OR 1.51, 95% CI 1.07-2.11 for Q2; OR 1.60, 95% CI 1.14-2.25 for Q3). Women and older individuals with higher HOMA-IR values were at a greater likelihood of gastrointestinal polyps. Primary care physicians should suggest endoscopic or abdominal sonography screening in high-risk populations.

PMID 42463746
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PubMedAdvanced materials (Deerfield Beach, Fla.)2026-07-17

Boosting Acidic Overall Water Splitting via Brønsted Acid Site-Induced Bridging-Oxygen-Assisted Deprotonation.

Chen Yuting Y, Liu Qing Q, Yan Yueying Y, Yang Yang Y et al.

Developing efficient and stable electrocatalysts for acidic overall water splitting is essential for proton exchange membrane water electrolysis (PEMWE), yet remains a significant challenge. In this work, Ir nanoparticles are anchored onto Fe-doped MoO2, yielding a novel material (Ir/Fe-MoO2) with high performance for both acidic oxygen evolution reaction (OER) and hydrogen evolution reaction (HER). Fe doping stabilizes the MoO2 lattice by forming Mo─O─Fe bonds and increases the Mo valence state, effectively suppressing over-oxidation and dissolution. The formed Ir─O─Fe interfacial structures enable bidirectional electron transfer, lowering the Ir oxidation state to prevent deactivation and activating bridging oxygen as Brønsted acid sites. These sites facilitate the deprotonation of oxygenated intermediates via a bridging-oxygen-assisted deprotonation mechanism, bypassing the rate-limiting steps of conventional adsorbate evolution pathways. As a result, Ir/Fe-MoO2 achieves ultralow OER and HER overpotential in 0.5 M H2SO4, and a PEMWE device employing Ir/Fe-MoO2 as both anode and cathode requires only 1.60 V to reach 500 mA cm-2 at 80°C and sustains this performance for 350 h. This work pioneers Brønsted acid sites in a Mo oxide-based matrix, offering a new design concept for cost-effective, highly active acidic OER and HER electrocatalysts.

PMID 42467168
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PubMedEnvironmental pollution (Barking, Essex : 1987)2026-07-17

Associations of Green Space and Air Pollution with Insulin Resistance: Analysis of Repeated-Measurements Health Examination Data.

Li Yishu Y, Ma Guoqiang G, Xu Jing J, Wu Yuefei Y et al.

Environmental green space and air pollution frequently coexist in urban settings and may have opposing associations with metabolic health. However, longitudinal evidence regarding their associations with insulin resistance (IR) and potential inflammatory pathways remains limited. We conducted a longitudinal study of 17,731 adults undergoing routine health examinations in Shijiazhuang, China, from 2021 to 2023, yielding 41,525 person-year observations. Green space exposure was assessed using the normalized difference vegetation index (NDVI) within a 500-m buffer around workplaces, and annual mean concentrations of PM2.5, PM10, NO2, SO2, and CO were obtained from the ChinaHighAirPollutants dataset. IR was primarily assessed using the metabolic score for insulin resistance (METS-IR), with triglyceride-glucose index (TyG), the triglyceride-glucose index combined with body mass index (TyG-BMI), and the ratio of triglycerides to high-density lipoprotein cholesterol (TG/HDL-C) included as supplementary indicators. Linear mixed-effects models were used to estimate associations and interaction effects, and exploratory mediation analyses evaluated the potential role of platelet-to-lymphocyte ratio (PLR). Higher NDVI was associated with lower METS-IR, whereas associations with TyG, TyG-BMI, and TG/HDL-C were not statistically significant. Each standard deviation increase in NDVI was associated with a decrease in METS-IR (β = -0.030; 95% CI: -0.039 to -0.021). Higher air pollutant concentrations generally showed positive associations with IR indices, with stronger and more frequently statistically significant associations observed for METS-IR. Interaction analyses suggested heterogeneous associations across levels of green space exposure. Exploratory mediation analyses indicated that PLR statistically accounted for a small proportion (approximately 1-10%) of associations involving several pollutants and IR indices. These findings suggest that workplace-based environmental exposures may be associated with insulin resistance, although patterns varied across surrogate indices. Further studies using refined exposure assessment and longitudinal mechanistic measurements are needed to clarify these associations.

PMID 42462950
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PubMedFrontiers in endocrinology2026-07-17

Insulin resistance as a predictor of long-term adverse cardiovascular event risk in patients with atrial fibrillation following radiofrequency catheter ablation.

Liu Hanxiong H, Pan Junli J, Luo Yan Y, Tang Yan Y et al.

Catheter ablation is the first-line therapy for atrial fibrillation (AF), yet a significant proportion of patients experience major adverse cardiovascular events (MACEs) post-ablation, highlighting a need for improved risk stratification. This study aimed to evaluate the association between four non-insulin-based insulin resistance (IR) indices and long-term MACEs in AF patients undergoing radiofrequency catheter ablation (RFCA), and to determine their incremental predictive value beyond established clinical risk factors. A retrospective observational study was conducted on 922 non-valvular AF patients who underwent index RFCA between March 2017 and July 2023. The primary endpoint was a composite of MACEs, defined as all-cause death, late AF recurrence, heart failure events, and stroke occurring after the 3-month blanking period. Associations between the four IR indices and MACEs were examined using multivariable Cox proportional hazards regression, restricted cubic spline analysis, and Kaplan-Meier survival estimation. The incremental predictive value of each index over a baseline clinical model was quantified using the C-statistic, net reclassification improvement (NRI), and integrated discrimination improvement (IDI). Over a median follow-up of 36 months, MACEs occurred in 242 patients (26.25%). After full multivariable adjustment, METS-IR and TyG-BMI were independently and significantly associated with elevated MACE risk across all models (both P < 0.001), while the TG/HDL-C ratio and TyG index did not reach statistical significance in fully adjusted models. METS-IR demonstrated an approximately linear dose-response relationship with MACEs on restricted cubic spline analysis. When added to the baseline clinical model (C-statistic: 0.702), METS-IR conferred the greatest incremental predictive gain, significantly improving the C-statistic to 0.717 (P < 0.001), alongside meaningful NRI (0.291, 95% CI: 0.126-0.426, P < 0.001) and IDI (0.015, 95% CI: 0.004-0.035, P = 0.004). Among the evaluated non-insulin-based IR indices, METS-IR demonstrated a statistically significant, albeit modest, incremental improvement in the prediction of composite MACE in AF patients following RFCA. These findings support the use of METS-IR in post-ablation risk assessment and may contribute to improved patient outcomes.

PMID 42466343
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PubMedPhysiological research2026-07-17

Hypothalamic Inflammation as a Critical Link Between Metabolic Dysfunction and Impaired Endometrial Receptivity in Obese Polycystic Ovary Syndrome.

Sun C C, Han Y Y, Pan Z Z, Li J J et al.

Obese polycystic ovary syndrome (PCOS) involves insulin resistance (IR) and impaired endometrial receptivity, potentially driven by hypothalamic inflammation. We investigated if inhibiting the hypothalamic Toll-like receptor 4 (TLR4)/IkappaB kinase beta (IKKbeta) pathway could ameliorate IR and improve endometrial receptivity in an obese PCOS rat model. An obese PCOS rat model was established using letrozole and high-fat diet. Rats were divided into control, PCOS, and three intervention groups: PCOS + intracerebroventricular (i.c.v.) TAK242 (central TLR4 inhibitor), PCOS + intraperitoneal (i.p.) TAK242 (systemic inhibitor), and PCOS + Metformin. We assessed hypothalamic inflammation (TLR4/IKKbeta pathway), metabolic parameters (body weight, OGTT, ITT, HOMA-IR), systemic inflammation, and reproductive phenotypes. Endometrial receptivity was evaluated at pregnancy day 6 by uterine morphology, histology, pinopode development (SEM), and receptivity markers (BMP2, VEGF, IGFBP-1). The obese PCOS model successfully induced hypothalamic inflammation (activated TLR4/IKKbeta pathway), systemic inflammation, profound IR, and impaired endometrial receptivity (poor decidualization, sparse pinopodes, suppressed receptivity markers). Central (i.c.v.) TAK242 administration was most effective, significantly suppressing the hypothalamic TLR4/IKKbeta pathway, attenuating weight gain, normalizing insulin sensitivity, and, critically, restoring endometrial receptivity. Metformin also improved IR and receptivity, but was less potent at inhibiting the hypothalamic TLR4/IKKbeta pathway. Systemic (i.p.) TAK242 showed the least efficacy, particularly on metabolic and endometrial outcomes. Hypothalamic inflammation (TLR4/IKKbeta pathway) appears to be a critical mechanism linking IR and impaired endometrial receptivity in obese PCOS. Targeted central inhibition was more effective than systemic inhibition, suggesting this pathway is a novel therapeutic target. Key words Polycystic ovary syndrome (PCOS) " Hypothalamic inflammation " Insulin resistance " Endometrial receptivity " TLR4/IKKbeta pathway.

PMID 42466701
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PubMedAmerican journal of cancer research2026-07-17

Erratum: lncRNA ASBEL and lncRNA Erbb4-IR reduce chemoresistance against gemcitabine and cisplatin in stage IV lung squamous cell carcinoma via the microRNA-21/LZTFL1 axis.

Liang Zong-Ying ZY, Zhang Zhi-Min ZM, Sun Guang-Rui GR, Zhao Bao-Shan BS et al.

[This corrects the article on p. 2732 in vol. 13, PMID: 37424811.].

PMID 42465013
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