Nisshin Pharma · Small Molecule · Small Molecule
nitroglycerin is a small molecule developed by Nisshin Pharma. It is approved for therapeutic indications via transdermal.
| Brand Names | Minitro Tape |
| Company | Nisshin Pharma |
| Drug Class | Small Molecule |
| Route | Transdermal |
| Status | Approved |
nitroglycerin is developed for 1 unique indication across 1 therapeutic area.
| Therapeutic Area | Condition | Phase |
|---|---|---|
| Cardiac disorders | Angina pectoris | ✓ Approved |
Tomaselli Federica F, Albanese Roberta R, Blessent Claudio Gio Francesco CGF, Montes Christian C et al.
Iddir Samir S, Kemel Nouara N
Lohsiriwat Varut V, Gosoom Navarat N, Ovartchaiyapong Pornraksa P
Chronic anal fissure is associated with elevated resting anal pressure and impaired tissue healing. Promoting fissure healing with the mucoprotective agent sucralfate could be an alternative pharmacologic approach to medical sphincterotomy. We aimed to evaluate the efficacy of topical sucralfate versus topical nitroglycerin for chronic anal fissure. This single-center, double-blind, randomized controlled trial enrolled adult with chronic anal fissure. Participants were randomly assigned in a 1:1 ratio to receive either 3% sucralfate-containing topical formulation or 0.2% nitroglycerin ointment, applied onto the fissure twice daily. The primary outcome was fissure healing at 2 weeks. Secondary outcomes included healing at 4 weeks, changes in pain score and quality-of-life score, and recurrence. This study included 82 patients (42 in the sucralfate-containing formulation group) with a median age of 46 years and median fissure symptom duration of 8 weeks. Patients' demographics were comparable between groups. At 2 weeks, fissure healing occurred in 21 of 42 patients (50%) in the sucralfate-containing formulation group and 9 of 40 (23%) in the nitroglycerin group (P=0.010; RR 2.22; 95% CI 1.16-4.26). At 4 weeks, healing occurred in 33 of 42 patients (79%) and 19 of 40 (48%), respectively (P=0.004; RR 1.65; 95% CI 1.15-2.38). Pain reduction and quality-of-life improvement were comparable between groups. Recurrence occurred in 5 of 27 patients (19%) in the sucralfate-containing formulation group and 4 of 17 (24%) in the nitroglycerin group (P=0.716). Sucralfate-containing formulation was superior to nitroglycerin in achieving fissure healing at 2 and 4 weeks.
Kawaji Tetsuma T, Okubo Saki S, Naka Misaki M, Ishida Ryuta R et al.
Cavotricuspid isthmus(CTI) using pulsed field ablation(PFA) is still challenging. We prospectively enrolled 90 consecutive patients with atrial fibrillation(AF) and atrial flutter(AFL), who received CTI ablation using a linear-shaped PulseSelect PFA Loop catheter. Coronary angiography of the right coronary artery was performed before and just after PFA application. During the CTI ablation following PVI, the initial 45 patients did not receive prophylactic nitroglycerin administration (control group), and the latter 45 patients received systemic nitroglycerin administration of 1.5 mg before the applications (NTG group). All patients achieved an acute line of block using only the PFA catheter, with 91.1% requiring two or fewer applications. Operators performed additional "bonus" applications, resulting in an average of 4.4 ± 1.4 applications per patient. After a mean waiting period of 24.7 min, high-density mapping revealed a re-conduction gap in 20 patients (22.2%). Of these 20 patients with reconduction, four had an epicardial bridge. Coronary artery spasm was observed in 51.1% of the control group. In contrast, prophylactic nitroglycerin administration significantly reduced the incidence of coronary spasm to 15.6% in the NTG group. No severe spasms were observed in the NTG group. Among nine patients who underwent a repeat ablation procedure due to clinical AF recurrence, CTI reconduction was found in five (55.6%). Linear-shaped PulseSelect CTI ablation readily achieves acute block, but early reconduction limits long-term durability despite consolidation applications. Without prophylactic NTG, there is a notable risk of coronary spasm, necessitating its routine use. Additionally, systematic postprocedural follow-up is needed to assess delayed coronary safety.
Šinigoj Porčnik Petra P, Kabaklić Amela A
Coexistence of neurogenic orthostatic hypotension with supine or nocturnal hypertension creates a therapeutic challenge because treatment of either component may aggravate the other. This case illustrates a clinical management framework based on characterization of the full hemodynamic phenotype, repeated reassessment, and treatment adaptation according to posture and time of day, integrating postural blood pressure (BP) responses, 24-hour BP monitoring, symptoms, functional status, comorbidities, and safety findings. A 63-year-old man with hypertension and insulin-treated type 2 diabetes presented with orthostatic dizziness and presyncope. Antihypertensive therapy was intensified for elevated seated BP. After intensification, upright tolerance worsened, with recurrent syncope, a rib fracture, and loss of functional independence. Symptoms remained disabling despite antihypertensive withdrawal and nonpharmacological measures. Supine-to-seated-to-standing assessment showed a BP fall from 197/99 mm Hg supine to 122/81 mm Hg seated and 79/56 mm Hg standing, with presyncope and heart rate increasing from 72 to 86 beats/min. Supine measurements and 24-hour BP monitoring documented severe supine and nocturnal hypertension, reverse dipping, and mean asleep BP 203/107 mm Hg. Autonomic testing demonstrated combined cardiovagal and adrenergic dysfunction, supporting neurogenic orthostatic hypotension due to diabetic autonomic neuropathy. Management was tailored to upright and recumbent periods. A removable transdermal nitroglycerin patch was used overnight. Nonpharmacological measures included repeated encouragement to increase fluid intake, but daily intake generally remained below 2 L. Clinical assessment suggested relative volume depletion. Low-dose morning fludrocortisone was introduced cautiously despite severe supine/nocturnal hypertension. After upright tolerance improved, morning lercanidipine was added. Subsequent 24-hour BP monitoring showed a more balanced profile. Orthostatic symptoms and upright tolerance improved. No further syncope or falls occurred, and functional independence improved. Later 24-hour BP monitoring showed reduced nocturnal predominance, with mean awake/asleep BP 164/86 and 165/89 mm Hg, respectively. Mild peripheral edema was managed with intermittent torasemide. This case illustrates how integrating postural BP responses with 24-hour BP patterns can identify competing hemodynamic phenotypes that may require different management during upright and recumbent periods. Repeated reassessment and individualized treatment adaptation according to the documented BP pattern and clinical context may help balance competing risks of upright hypoperfusion and supine/nocturnal hypertension.
Ann Mathew Aparna A, Sithara M S MS, Unni Ashok R AR, Anand Kumar A A et al.
Migraine is a neurovascular disorder characterized by recurrent headaches and sensitivity to light, sound and movement. Magnesium has therapeutic potential in migraine, but poor brain bioavailability may limit its efficacy. This study evaluated lactoferrin conjugated liposome loaded with magnesium sulfate (LMGPLS) as a targeted brain delivery system. Acute toxicity was assessed in male and female rats with graded doses of LMGPLS. Haematological and biochemical findings of LMGPLS showed no observable toxicity up to 200 mg/kg of magnesium sulfate. Antimigraine activity was evaluated in a nitroglycerin-induced rat model (10 mg/kg, s.c.) using behavioral, biomarker, magnesium distribution and histopathological analyses. LMGPLS (100 mg/kg) improved locomotor activity and reduced anxiety-like behavior compared with migraine-induced controls. It also reduced glutamate, nNOS, CGRP, and substance P while increasing magnesium in brain tissue and cerebrospinal fluid, with minimal plasma change. These findings support enhanced brain delivery of magnesium by LMGPLS and an antimigraine effect associated with modulation of glutamate, nNOS, and vasoactive neuropeptides.
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