L-NMMA Acetate

L-NMMA acetate is a nitric oxide synthase inhibitor of all NOS isoforms, like NOS1, NOS2, and NOS3.

Designed for biological research and industrial applications, not intended for individual clinical or medical purposes.

CAT No: 10-101-117

CAS No:17035-90-4 (net), 53308-83-1 (acetate)

Synonyms/Alias:Tilarginine Acetate; Targinine Acetate

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M.F/Formula
C9H20N4O4
M.W/Mr.
248.28
Sequence
H-Arg(Me)-OH acetate salt
Labeling Target
Tilarginine
Application
L-NMMA is a useful clinical tool as NO synthase inhibitor to study the role and the effects of NO in cardiovascular and gastrointestinal disorders, hypertension, septic shock, inflammation, infection, stroke and neurodegenerative disorders.
Activity
Inhibitor
Areas of Interest
Cardiovascular Disease
Target
NO Synthase

L-NMMA Acetate, also known as NG-Monomethyl-L-arginine acetate, is a widely utilized arginine analog recognized for its capacity to modulate nitric oxide synthase (NOS) activity in various biological systems. This compound is distinguished by its ability to selectively inhibit the production of nitric oxide (NO), a pivotal signaling molecule involved in numerous physiological and biochemical pathways. Researchers value L-NMMA Acetate for its high specificity and effectiveness in experimental settings, making it an essential tool for probing NO-dependent mechanisms within cellular and molecular biology. Its solubility and stability further enhance its suitability for in vitro and in vivo studies, providing consistent results and facilitating accurate interpretation of experimental data. The unique properties of L-NMMA Acetate support its adoption across multiple research disciplines, where precise modulation of NO pathways is required for advancing scientific understanding.

Vascular Biology Research: L-NMMA Acetate plays a critical role in vascular biology investigations by serving as a potent inhibitor of nitric oxide synthase. By attenuating NO synthesis in endothelial cells, this compound enables researchers to dissect the intricate mechanisms underlying vascular tone regulation, endothelial function, and blood flow dynamics. Utilizing NG-Monomethyl-L-arginine acetate in experimental models helps clarify the contribution of NO to vasodilation and vasoconstriction, thereby advancing knowledge in hypertension, atherosclerosis, and other vascular disorders. Its application in these studies provides insight into the molecular interplay between NO and other vasoactive agents, supporting the development of targeted therapeutic strategies.

Neuroscience Studies: In neuroscience research, L-NMMA Acetate is employed to investigate the role of nitric oxide as a neurotransmitter and neuromodulator within the central and peripheral nervous systems. By selectively inhibiting NOS activity, it allows scientists to evaluate the impact of NO on synaptic plasticity, neuronal communication, and neurovascular coupling. This tool is instrumental in elucidating the signaling pathways involved in learning, memory, and neurodegenerative processes. The use of L-NMMA Acetate in cultured neurons or brain tissue preparations helps delineate the functional significance of NO in neural development and response to injury.

Immunological Research: NG-Monomethyl-L-arginine acetate is integral to studies examining the immunomodulatory effects of nitric oxide in both innate and adaptive immune responses. Its ability to suppress NO synthesis in immune cells such as macrophages and lymphocytes facilitates detailed analysis of NO's involvement in pathogen defense, inflammation, and immune regulation. By modulating NO levels, researchers can investigate the molecular mechanisms through which NO influences cytokine production, cell signaling, and the resolution of inflammatory processes. This application is invaluable for exploring the balance between protective and pathological immune responses.

Cardiac Physiology Investigations: In the field of cardiac physiology, L-NMMA Acetate is utilized to probe the regulatory functions of nitric oxide in myocardial contractility, electrophysiology, and coronary blood flow. By inhibiting NOS, it enables precise assessment of NO's role in cardiac muscle performance and the adaptation to stressors such as ischemia or hypoxia. The compound's use in isolated heart preparations or cardiac cell cultures helps unravel the complex interactions between NO signaling and other cardiac regulatory pathways, contributing to a deeper understanding of heart function under physiological and pathological conditions.

Metabolic Pathways Analysis: Researchers employ NG-Monomethyl-L-arginine acetate to study the influence of nitric oxide on metabolic processes such as glucose uptake, lipid metabolism, and energy homeostasis. Through targeted inhibition of NO synthesis, it becomes possible to investigate how NO modulates cellular metabolism and the cross-talk between metabolic and signaling networks. This approach aids in clarifying the role of NO in metabolic adaptation, insulin sensitivity, and the development of metabolic disorders. The versatility of L-NMMA Acetate makes it a valuable asset for metabolic research across diverse biological models.

Biochemical Mechanism Elucidation: L-NMMA Acetate is also pivotal in studies focused on the biochemical mechanisms underlying nitric oxide synthase function and regulation. By serving as a competitive substrate analog, it allows for detailed kinetic analyses and the identification of key residues involved in enzyme activity. This application supports the rational design of novel NOS inhibitors and enhances the understanding of structure-function relationships within the enzyme family. Collectively, the diverse applications of L-NMMA Acetate underscore its significance as a research tool in the exploration of nitric oxide biology and its far-reaching implications in science.

Source#
Synthetic
Solubility
−20°C
InChI
InChI=1S/C7H16N4O2.C2H4O2/c1-10-7(9)11-4-2-3-5(8)6(12)13;1-2(3)4/h5H,2-4,8H2,1H3,(H,12,13)(H3,9,10,11);1H3,(H,3,4)/t5-;/m0./s1
InChI Key
IKPNWIGTWUZCKM-JEDNCBNOSA-N
Isomeric SMILES
CC(=O)O.CN=C(N)NCCC[C@@H](C(=O)O)N
References

Cardiogenic shock complicating acute myocardial infarction (MI) remains a common and lethal disorder despite aggressive use of early revascularization. Systemic inflammation, including expression of inducible nitric oxide synthase (NOS) and generation of excess nitric oxide, is believed to contribute to the pathogenesis and inappropriate vasodilatation of persistent cardiogenic shock. Preliminary, single-center studies suggested a beneficial effect of NOS inhibition on hemodynamics, renal function, and survival in patients with cardiogenic shock.

Alexander, J. H., Reynolds, H. R., Stebbins, A. L., Dzavik, V., Harrington, R. A., Van de Werf, F., & Hochman, J. S. (2007). Effect of tilarginine acetate in patients with acute myocardial infarction and cardiogenic shock: the TRIUMPH randomized controlled trial. Jama, 297(15), 1657-1666.

Syncope is sudden transient loss of consciousness and postural tone with spontaneous recovery; the most common form is vasovagal syncope(VVS). We previously demonstrated impaired post-synaptic adrenergic responsiveness in young VVS patientswas reversed by blocking nitric oxide synthase(NOS). We hypothesised that nitric oxide may account for reduced orthostatic tolerance in young recurrent VVS patients.

Stewart, J. M., Sutton, R., Kothari, M. L., Goetz, A. M., Visintainer, P., & Medow, M. S. (2017). Nitric oxide synthase inhibition restores orthostatic tolerance in young vasovagal syncope patients. Heart, heartjnl-2017.

Guidelines recommend β-blockers and renin-angiotensin-aldosterone system blockers to improve long-term survival in hemodynamically stable myocardial infarction patients with a reduced left ventricular ejection fraction. The prevalence and outcomes associated with β and renin-angiotensin-aldosterone system blocker therapy in patients with ongoing cardiogenic shock is unknown.

van Diepen, S., Reynolds, H. R., Stebbins, A., Lopes, R. D., Džavík, V., Ruzyllo, W., ... & Dauerman, H. L. (2014). Incidence and outcomes associated with early heart failure pharmacotherapy in patients with ongoing cardiogenic shock. Critical care medicine, 42(2), 281-288.

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