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nitroglycerin

✓ Approved

Eisai Co., Ltd. · Small Molecule · Small Molecule

What is nitroglycerin?

nitroglycerin is a small molecule developed by Eisai Co., Ltd.. It is approved for therapeutic indications via transdermal.

Drug Profile

CompanyEisai Co., Ltd.
Drug ClassSmall Molecule
RouteTransdermal
StatusApproved

Therapeutic Indications

nitroglycerin is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Cardiac disordersAngina pectoris✓ Approved
Cardiac disordersCardiac failure✓ Approved

Related Research Articles

PubMedThe European journal of neuroscience2026-07-23

Cochlear Functional Changes and CGRP Modulation in a Chronic Nitroglycerin Migraine-Like Rat Model.

Koçdor Pelin P, Shomalizadeh Narges N, Salman Fatmanur Akpunar FA, Demirhan Feride F et al.

Auditory and vestibular symptoms in vestibular migraine, cochlear migraine, and Ménière's disease overlap, yet mechanisms linking migraine biology to inner ear dysfunction remain unclear. Calcitonin gene-related peptide (CGRP) is a key mediator of trigeminovascular activation and a major therapeutic target in migraine, but its contribution to cochlear dysfunction is not well defined. Using a repeated nitroglycerin (NTG) paradigm in male Wistar rats, we investigated whether a systemic migraine-like state affects cochlear function and whether these effects are dependent on CGRP. Rats received saline, NTG, or NTG followed by the CGRP receptor antagonist olcegepant (OLC). NTG increased plasma TNF-α and elevated trigeminal c-Fos; olcegepant partially normalized these markers, whereas behavioral changes in the open-field test were interpreted cautiously because baseline immobility differed across groups before treatment. NTG produced frequency-dependent changes in distortion-product otoacoustic emissions and auditory brain stem response thresholds. Electrocochleography showed limited changes, and scala media proportions did not differ significantly among groups, indicating no evidence of overt endolymphatic hydrops at the studied time point. Inner hair-cell synaptic markers showed no significant group differences for CtBP2, whereas GluR2 puncta differed between NTG and NTG + OLC (p = 0.012). Olcegepant attenuated NTG-associated cochlear functional changes and was associated with differences in postsynaptic GluR2 puncta, alongside region-specific changes in cochlear CGRP immunoreactivity. These findings support a mechanistic link between migraine-like trigeminovascular activation and early cochlear dysfunction and suggest that CGRP receptor blockade may benefit migraine patients with cochlear or vestibular symptoms. Future studies should assess females, estrous cycle tracking, hormones, and sex-specific auditory responses.

PubMedThe European journal of neuroscience2026-07-23

Rapid Assessment of Stroke Severity: Development of a Visual Infarct and Comprehensive Scoring System in Ischemic Rats With Middle Cerebral Artery Occlusion.

Mu Changqing C, Ding Yuchuan Y, Elmadhoun Omar O, Li Fengwu F et al.

Reliable assessment of infarct severity is essential in experimental stroke research, yet commonly used approaches such as 2,3,5-triphenyltetrazolium chloride (TTC) staining and magnetic resonance imaging require additional tissue processing, specialized equipment, or substantial time and cost. In this study, we developed and validated a rapid visual Infarct Score to determine infarct volume and evaluate neuroprotective efficacy in rat middle cerebral artery occlusion (MCAO) models. A retrospective analysis was performed using data from 315 male Sprague-Dawley rats, including TTC-derived infarct volume, visual Infarct Score, neurological deficit scores, and body weight changes. The Infarct Score demonstrated the strongest correlation with infarct volume among individual indicators in both nontreatment (Rho = 0.71) and treatment cohorts (Rho = 0.68). We further developed a Comprehensive Score by integrating the Infarct Score with the Longa 5-point score at 48 h, which showed the highest overall correlation with infarct volume (Rho = 0.75 in both cohorts) and strong discrimination of infarct severity (AUC = 0.90). Interrater reliability analysis demonstrated excellent agreement among independent raters (intraclass correlation coefficient = 0.89; Kendall's W = 0.83, both p < 0.001). Neuroprotective interventions, including therapeutic hypothermia, nitroglycerin, and remote ischemic conditioning combined with physical exercise, significantly reduced infarct volume, Infarct Score, Comprehensive Score, neurological deficits, and weight loss. These findings indicate that the Infarct Score offers a rapid, practical, and cost-effective method for infarct assessment, whereas the Comprehensive Score further improves the predictive accuracy and may serve as a useful tool for evaluating stroke severity and treatment outcomes in preclinical studies.

PubMedRespiratory medicine2026-07-18

Anxiety Sensitivity in Heart Failure with Preserved Ejection Fraction: Bias in Dyspnea Ratings and Respiratory Exercise Response.

Ritz Thomas T, Kelley Niya N, Balmain Bryce N BN, Tomlinson Andrew R AR et al.

Anxiety sensitivity, the fear of anxiety symptoms, is linked to elevated symptom reports in health and illness. Dyspnea on exertion, a dominant complaint in heart failure with preserved ejection fraction (HFpEF), could be affected by this personality characteristic. We examined whether patients with HFpEF and high anxiety sensitivity provide elevated dyspnea reports in global measures or in response to cardiopulmonary exercise testing under regular or pharmacological challenge conditions. Fifty-three patients (37 women, mean age 71.4 years) with HFpEF completed the Anxiety Sensitivity Index (ASI), Dyspnoea-12 questionnaire, and modified Medical Research Council dyspnea rating (mMRC), and pulmonary function testing. They also performed six-minute constant-load cycling at 20W and incremental cycling to exhaustion, with placebo or sublingual nitroglycerin in a single-blind, cross-over design. Ratings of perceived breathlessness and its unpleasantness, and ventilation and arterial blood gas measurements, were completed at rest, during the final minute of constant-load cycling, and immediately after incremental cycling. ASI scores predicted Dyspnoea-12, but not mMRC scores. Across rest and exercise, PaCO2 and ventilatory efficiency was lower, and minute ventilation, dead space, and breathlessness ratings were higher, under nitroglycerin challenge. Under this condition, patients with higher ASI also reported more breathlessness across the exercise protocol, required greater E to eliminate CO2 (E/ CO2), and had lower PaCO2 at pre-exercise while waiting for the nitroglycerin to take effect. Overreporting of dyspnea and mild hyperventilation need to be considered when testing patients with HFpEF that are high in anxiety sensitivity in unusual medical situations that elicit symptoms.

PubMedThe journal of headache and pain2026-07-18

IRAK-M attenuates pain hypersensitivity and anxiety-like behaviors in a nitroglycerin-induced chronic migraine mouse model with concomitant reductions in microglial activation and neuroinflammation.

Liang Xiao-Tao XT, Xie Shi-Ru SR, Liu Xi-Mao XM, Zhu Xiao-Yu XY et al.

Chronic migraine (CM) is a disabling neurological disorder in which neuroinflammatory mechanisms and central sensitization are thought to contribute to disease pathophysiology. Interleukin-1 receptor-associated kinase M (IRAK-M), which is predominantly expressed in microglia in the central nervous system (CNS), is an endogenous negative regulator of innate immune signaling. Previous studies have linked IRAK-M to the restraint of Toll-like receptor 4 (TLR4) signaling and NLR family pyrin domain-containing 3 (NLRP3) inflammasome-related responses. However, the role of IRAK-M in CM-related pathophysiology and associated neuropsychiatric comorbidities remains unclear. This study aimed to investigate the function of IRAK-M and its underlying molecular mechanisms in a mouse model of chronic migraine. Mice were repeatedly given intraperitoneal injections of nitroglycerin (NTG; 10 mg/kg) to create a chronic migraine model. Mechanical and thermal sensitivity were assessed using von Frey filaments and the hot-plate test, respectively; light aversion and anxiety-like behaviors were evaluated using the light-aversion test, open-field test, and elevated plus-maze test. To further clarify the role of IRAK-M, both transgenic genetic engineering approaches and adeno-associated virus (AAV)-mediated expression strategies were employed. The underlying molecular mechanisms were further investigated using quantitative PCR, immunoblotting, immunofluorescence, and three-dimensional reconstruction. Repeated administration of NTG increased IRAK-M protein in the trigeminal nucleus caudalis (TNC). IRAK-M deficiency exacerbated mechanical and thermal hyperalgesia, increased c-Fos and CGRP expression, and enhanced microglial activation; these changes were accompanied by increased TLR4/NF-κB-related signaling, NLRP3 inflammasome activation, and GSDMD cleavage. Conversely, TNC-targeted IRAK-M overexpression attenuated pain hypersensitivity and anxiety-like behavioral alterations and was accompanied by corresponding reductions in neuroinflammatory molecular and cellular readouts. These findings support IRAK-M as an important regulator of central sensitization and neuroinflammatory responses in a chronic migraine model. Our findings identify IRAK-M as an important preclinical regulator of microglial reactivity and neuroinflammatory responses in the NTG-induced chronic migraine model. IRAK-M manipulation was accompanied by bidirectional changes in TLR4/NF-κB- and NLRP3/GSDMD-related signaling, pain hypersensitivity, and anxiety-like behavioral alterations. These findings provide a preclinical rationale for further investigation of IRAK-M-related neuroimmune signaling in migraine. Not applicable.

PubMedFrontiers in cardiovascular medicine2026-07-17

Case Report: Spontaneous coronary artery dissection presenting as MINOCA in uncontrolled Graves' disease.

Pan Yunfeng Y, Han Hao H, Chen Jijie J, Zhang Shiyi S

Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of myocardial infarction with non-obstructive coronary arteries (MINOCA). Although Graves' disease is a well-established cause of coronary vasospasm, its potential association with structural coronary arterial injury remains incompletely understood. We report a case of hyperthyroidism-associated SCAD that provides clinical insight into a possible link between severe thyrotoxicosis and coronary arterial vulnerability. We report a 56-year-old female with uncontrolled Graves' disease presenting with an acute ST-segment elevation myocardial infarction (STEMI). Despite prominent inferior ST-segment elevations, emergent coronary angiography revealed a long narrowing extending from the mid to the distal tip of the left anterior descending (LAD) artery with preserved TIMI 3 flow. The lesion's lack of response to intracoronary nitroglycerin supported a working diagnosis of MINOCA. Given the concurrent severe thyrotoxicosis and the substantial risk of precipitating thyroid storm during invasive evaluation, a staged diagnostic approach was adopted: acute-phase management prioritized conservative cardiovascular and antithyroid therapy, while definitive intravascular imaging was deferred. Follow-up intravascular ultrasound (IVUS) at three months demonstrated a persistent intramural hematoma, confirming the diagnosis of SCAD. The patient remained asymptomatic at the one-year follow-up. This case suggests that severe thyrotoxicosis may contribute to coronary arterial vulnerability and the development of SCAD. It also highlights the diagnostic challenges of complex MINOCA presentations in patients with uncontrolled hyperthyroidism. In selected cases, a staged diagnostic strategy with deferred intracoronary imaging after endocrinological stabilization may provide a safe and effective approach to diagnostic confirmation while minimizing procedural risk.

PubMedCureus2026-07-16

Survival and Favorable Neurological Outcome Following Home Delivery at 22 Weeks of Gestation: A Case Report.

Haga Mitsuhiro M, Oshima Ayumi A, Nagashima Yasuhisa Y, Kanai Masayo M

We encountered a male infant with extremely low birth weight born at 22 weeks and 0 days of gestational age in the toilet at home. He was resuscitated with chest compression and bag-valve-mask ventilation by the emergency medical service crew and was transported to our institution 50 minutes after birth. The patient was intubated and given intratracheal artificial surfactant after admission. After he recovered from the initial hypotensive phase, we maintained the blood pressure at an appropriate level using nitroglycerin to avoid cerebral overcirculation. He was discharged home at 170 days of life with no signs of intraventricular hemorrhage or periventricular leukomalacia. His overall developmental quotient at one year and seven months of corrected age was 104, and he showed no apparent developmental delay. This case demonstrates that appropriate medical management can save the lives of extremely preterm infants born outside medical institutions.

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