Vmn2r2 Inhibitors
Vmn2r2 inhibitors encompass a diverse array of chemical compounds that indirectly attenuate the activity of the Vmn2r2 receptor by modulating various physiological systems and cellular processes. Amiloride, for example, through its antagonism of epithelial sodium channels, disrupts the ionic balance crucial for Vmn2r2 signaling, leading to a dampened receptor response. Similarly, the application of copper sulfate may interfere with Vmn2r2's metal ion dependency, hindering its capacity to properly transduce signals. Methimazole's impact on thyroid hormone levels can indirectly suppress Vmn2r2 function by altering the metabolic state of chemosensory tissues, which in turn affects the receptor's activity. Quinine, with its ability to block specific ion channels, could diminish Vmn2r2's signaling by altering the local ionic milieu, while lidocaine's sodium channel blockade can reduce neuronal excitability and consequently Vmn2r2 signaling. Additionally, ouabain and nifedipine indirectly inhibit Vmn2r2 by respectively disrupting Na+/K+-ATPase pump activity, altering membrane potentials, and blocking calcium channels that may influence intracellular signaling pathways associated with the receptor.
Moreover, the influence of hormonal pathways on Vmn2r2 is evident with compounds like mifepristone and propranolol, which alter the hormonal and adrenergic environment, potentially affecting Vmn2r2's functional state. Atropine's muscarinic receptor blockade may suppress parasympathetic activity, thus impacting Vmn2r2 regulation. Tetrodotoxin's blockade of voltage-gated sodium channels impedes action potential generation, a necessary precursor for Vmn2r2's activation in neuronal pathways. The presence of zinc sulfate, which is recognized for its modulatory effect on taste receptors, suggests that Vmn2r2 may also be sensitive to zinc ion concentrations, providing an additional indirect pathway for inhibition. Collectively, these Vmn2r2 inhibitors demonstrate the intricacy of pharmacological modulation, where altering various physiological and molecular parameters can converge to attenuate the functional activity of this specific receptor.
SEE ALSO...
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Amiloride • HCl | 2016-88-8 | sc-3578 sc-3578A | 25 mg 100 mg | $22.00 $56.00 | 6 | |
Amiloride is a diuretic that acts as an antagonist to epithelial sodium channels. Vmn2r2, being a chemosensory receptor, may have its signaling modulated by ionic changes in the environment. By reducing sodium reabsorption, amiloride can alter the ionic composition of extracellular fluids, potentially affecting Vmn2r2's ability to bind its ligands or transduce signals, leading to reduced functional activity. | ||||||
Copper(II) sulfate | 7758-98-7 | sc-211133 sc-211133A sc-211133B | 100 g 500 g 1 kg | $45.00 $120.00 $185.00 | 3 | |
Copper sulfate is a chemical compound that can bind to and inhibit a variety of proteins. If Vmn2r2 requires metal cofactors for proper function or is sensitive to metal-induced conformational changes, copper ions could bind to the protein or its associated signaling partners, leading to an inhibition of Vmn2r2 signaling. | ||||||
Methimazole | 60-56-0 | sc-205747 sc-205747A | 10 g 25 g | $69.00 $110.00 | 4 | |
Methimazole is a thiourea derivative that acts as an inhibitor of the enzyme thyroid peroxidase. Given Vmn2r2's expression in chemosensory tissues, changes in thyroid hormone levels, which can be influenced by methimazole, might indirectly affect Vmn2r2 function by altering the metabolic state of these tissues and modulating sensory receptor expression or activity. | ||||||
Quinine | 130-95-0 | sc-212616 sc-212616A sc-212616B sc-212616C sc-212616D | 1 g 5 g 10 g 25 g 50 g | $77.00 $102.00 $163.00 $347.00 $561.00 | 1 | |
Quinine is a natural compound known for its bitter taste and is a blocker of certain ion channels. If Vmn2r2's function is modulated by the activity of nearby ionic currents, quinine could indirectly inhibit Vmn2r2 activity by altering the ionic environment, thus affecting the receptor's signaling capabilities. | ||||||
Lidocaine | 137-58-6 | sc-204056 sc-204056A | 50 mg 1 g | $50.00 $128.00 | ||
Lidocaine is a local anesthetic and sodium channel blocker. By inhibiting sodium channels, lidocaine could hinder action potential generation and propagation in neurons expressing Vmn2r2. This indirect effect could lead to decreased signaling through Vmn2r2 due to reduced neuronal excitability. | ||||||
Ouabain-d3 (Major) | sc-478417 | 1 mg | $506.00 | |||
Ouabain is a cardiac glycoside that inhibits the Na+/K+-ATPase pump. Inhibition of this pump can lead to alterations in the ionic gradients across cell membranes, which could affect the activity of ion-sensitive proteins like Vmn2r2. This could result in an indirect decrease in Vmn2r2 signaling due to altered membrane potentials and cellular excitability. | ||||||
Nifedipine | 21829-25-4 | sc-3589 sc-3589A | 1 g 5 g | $58.00 $170.00 | 15 | |
Nifedipine is a calcium channel blocker. By blocking calcium channels, Nifedipine can affect calcium-mediated signaling pathways, which may indirectly influence Vmn2r2 activity if Vmn2r2 signaling is modulated by intracellular calcium levels. | ||||||
Mifepristone | 84371-65-3 | sc-203134 | 100 mg | $60.00 | 17 | |
Mifepristone is a glucocorticoid and progesterone receptor antagonist. By antagonizing these hormone receptors, it can modify the hormonal environment that could indirectly influence Vmn2r2 expression or activity, particularly if Vmn2r2 function is sensitive to hormonal regulation. | ||||||
Propranolol | 525-66-6 | sc-507425 | 100 mg | $180.00 | ||
Propranolol is a non-selective beta-adrenergic receptor antagonist. By inhibiting beta-adrenergic receptors, it could dampen the adrenergic signaling that might modulate Vmn2r2 activity or expression indirectly, especially if Vmn2r2 is expressed in cells that are responsive to catecholamines. | ||||||
Atropine | 51-55-8 | sc-252392 | 5 g | $200.00 | 2 | |
Atropine is a muscarinic acetylcholine receptor antagonist. It can indirectly decrease Vmn2r2 function by inhibiting parasympathetic nervous system activity, which could affect the regulation of Vmn2r2 through cholinergic signaling pathways. | ||||||