Delving into the Latest Updates on Molsidomine with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Molisidomine, Molsidomine (JAN/USAN/INN)

+ [1]

Target-

Mechanism

Nitric oxide donors

Therapeutic Areas

Nervous System DiseasesCardiovascular Diseases

Active Indication

Angina PectorisHeart FailureMyocardial Infarction

Inactive Indication-

Originator Organization

THERABEL Pharma NV

Active Organization

THERABEL Pharma NV

Inactive Organization-

Drug Highest PhaseApproved

First Approval Date

BE (10 Feb 2004),

Angina Pectoris

Regulation-

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Structure

Molecular FormulaC9H14N4O4

InChIKeyXLFWDASMENKTKL-UHFFFAOYSA-N

CAS Registry25717-80-0

There is a lack of data on the prognostic importance of silent ischemia in totally asymptomatic subjects without history of coronary artery disease (CAD), and, particularly, on a possible benefit of medical therapy in such patients. SWISSI 1 therefore recruits totally asymptomatic subjects older than 40 years of age without any history of CAD but one cardiovascular risk factor with documented silent ischemia. Participants are randomized to open antianginal drug therapy and risk factor control versus only risk factor management and followed up for ≥ 10 years.

Start Date01 Feb 1992

Sponsor / Collaborator

Luzerner Kantonsspital AG

100 Clinical Results associated with Molsidomine

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100 Translational Medicine associated with Molsidomine

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100 Patents (Medical) associated with Molsidomine

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735

Literatures (Medical) associated with Molsidomine

01 Nov 2024·Biomedicine & Pharmacotherapy

Histamine H3 receptor antagonist/nitric oxide donors as novel promising therapeutic hybrid-tools for glaucoma and retinal neuroprotection

Article

Author: Khanfar, Mohammad A ; Khanfar, Mohammad A. ; Villano, Serafina ; Marri, Silvia ; Sgambellone, Silvia ; Stark, Holger ; Lucarini, Laura ; Nardini, Patrizia ; Reiner-Link, David ; Frank, Annika

Glaucoma is a degenerative optic neuropathy in which the degeneration of optic nerve and blindness occur. The main cause is a malfunction of ciliary processes (protrusions of the ciliary bodies) resulting in increased intraocular pressure (IOP). Ocular hypertension (OHT) causes ischemic events leading to retinal ganglion cell (RGC) depletion and blindness. Histaminergic and nitrergic systems are involved in the regulation of IOP. Therefore, we developed novel hybrid compounds that target histamine H₃ receptor (H₃R) with nitric oxide (NO) releasing features (ST-1989 and ST-2130). After H₃R binding was proven in vitro, we investigated their effects in two OHT models in New Zealand White rabbits. Compound ST-1989 showed the highest NO elevation, together with antioxidative and anti-inflammatory features partly superior to the co-administered H₃R antagonist (ciproxifan) and NO donor (molsidomine). This hybrid compound demonstrated IOP reduction in both OHT models induced by intravitreal injection of hypertonic saline and carbomer into the anterior chamber of the eye, respectively. Ocular perfusion and photoreceptor neuroprotection were evaluated in a model of ischemia/reperfusion (I/R) of the ophthalmic artery induced by repeated sub-tenon injections of endothelin-1 (ET-1), twice a week for six weeks. Compound ST-1989 counteracts retinal degeneration reducing ophthalmic artery resistance index and increasing photoreceptor responses, thus rescuing RGCs. Our results indicate that compound ST-1989 is a promising molecule with long-lasting hypotensive effects and good effectiveness in reducing inflammation, oxidative stress, and RGCs apoptosis. In conclusion, these hybrid compounds could be a novel strategy to combat glaucomatous blindness and RGC depletion for ocular diseases involving retinal damage.

01 Nov 2023·Biomeditsinskaya Khimiya

Contribution of the gasotransmitter nitric oxide to the structural and functional organization of erythrocytes under conditions of hypoxia/reoxygenation

Article

Author: Zinchuk, V V ; Akulich, N V

Hypoxia is accompanied by changes in metabolism and cell functioning. Erythrocyte hemoglobin can be involved in adaptation to hypoxia by acting as an oxygen sensor, providing a link between oxygen content and blood circulation. The mechanisms providing this function have not been completely established. The purpose of this study was to evaluate the effect of the gasotransmitter nitric oxide on the structural and functional organization of erythrocytes under conditions of hypoxia/reoxygenation. NO participated in adaptive reactions under hypoxia/reoxygenation conditions by changing hemoglobin conformation, followed by changes in hemoprotein spectral characteristics and hemoglobin affinity to oxygen together with increasing anisocytosis, volume and cell surface. The increase in intracellular NO concentrations under hypoxic conditions was provided by extracellular fluid nitrites. Molsidomine (a NO donor) induced a higher NO increase without involvement of the nitrite reductase mechanism, it caused an increase in the average erythrocyte volume, anisocytosis, and an increase in the cell surface.

01 Oct 2023·Pediatric Research

Molsidomine decreases hyperoxia-induced lung injury in neonatal rats

Article

Author: Gul, Cemile Ceren ; Gokce, Ismail Kursat ; Deveci, Mehmet Fatih ; Turgut, Hatice ; Tanbek, Kevser ; Tekin, Suat ; Ozdemir, Ramazan ; Aslan, Mehmet ; Cetin Taslidere, Asli ; Kaya, Huseyin

BACKGROUNDThe study's objective is to evaluate if Molsidomine (MOL), an anti-oxidant, anti-inflammatory, and anti-apoptotic drug, is effective in treating hyperoxic lung injury (HLI).METHODSThe study consisted of four groups of neonatal rats characterized as the Control, Control+MOL, HLI, HLI + MOL groups. Near the end of the study, the lung tissue of the rats were evaluated with respect to apoptosis, histopathological damage, anti-oxidant and oxidant capacity as well as degree of inflammation.RESULTSCompared to the HLI group, malondialdehyde and total oxidant status levels in lung tissue were notably reduced in the HLI + MOL group. Furthermore, mean superoxide dismutase, glutathione peroxidase, and glutathione activities/levels in lung tissue were significantly higher in the HLI + MOL group as compared to the HLI group. Tumor necrosis factor-α and interleukin-1β elevations associated with hyperoxia were significantly reduced following MOL treatment. Median histopathological damage and mean alveolar macrophage numbers were found to be higher in the HLI and HLI + MOL groups when compared to the Control and Control+MOL groups. Both values were increased in the HLI group when compared to the HLI + MOL group.CONCLUSIONSOur research is the first to demonstrate that bronchopulmonary dysplasia may be prevented through the protective characteristics of MOL, an anti-inflammatory, anti-oxidant, and anti-apoptotic drug.IMPACTMolsidomine prophylaxis significantly decreased the level of oxidative stress markers. Molsidomine administration restored the activities of antioxidant enzymes. Molsidomine prophylaxis significantly reduced the levels of inflammatory cytokines. Molsidomine may provide a new and promising therapy for BPD in the future. Molsidomine prophylaxis decreased lung damage and macrophage infiltration in the tissue.

100 Deals associated with Molsidomine

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