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General Description:

Nylidrin, identified by CAS number 447-41-6, is a notable compound with significant therapeutic applications. Nylidrin, also known as _buphenine_ belongs to the category of drugs called _vasodilators_, which relax blood vessels and increase blood flow. Nylidrin is a peripheral vasodilator. Some studies show the evidence of improving cognitive impairment in selected individuals, such as geriatric patients with mild to moderate symptoms of cognitive, emotional and physical impairment . Nylidrin is utilized to treat several disorders that may benefit from increased blood flow (for example, certain mental disorders, blood vessel disease due to diabetes, frostbite, night leg cramps, and certain types of ulcers). This medication works by dilating (widening) blood vessels to help increase blood flow (improving circulation) throughout the body, including the extremities and central nervous system. This effect may help to improve memory/judgment, improve walking ability, and support the healing of frostbite/ulcers . FDA has considered nylidrin as "lacking substantial evidence of effectiveness" in cerebral ischemia, cerebral arteriosclerosis, and other cerebral circulatory insufficiencies. Therefore, the FDA has withdrawn nylidrin from the U.S. market .

Indications:

This drug is primarily indicated for: Nylidrin is mainly indicated in conditions like arteriosclerosis, cerebrovascular disease, peripheral vascular disease, Raynaud's disease, thrombo-angitis obliterans, and thrombophlebitis . It may sometimes be used in the treatment of peripheral vascular disorders in addition premature labor (however, the drug is not approved for premature labor). Its use in specific medical scenarios underscores its importance in the therapeutic landscape.

Absorption:

The absorption characteristics of Nylidrin are crucial for its therapeutic efficacy: Readily absorbed from the gastrointestinal tract . The drug's ability to rapidly penetrate into cells ensures quick onset of action.

Half-life:

The half-life of Nylidrin is an important consideration for its dosing schedule: Duration of action is 10h . This determines the duration of action and helps in formulating effective dosing regimens.

Pharmacodynamics:

Nylidrin exerts its therapeutic effects through: Nylidrin hydrochloride acts mainly by beta-receptor stimulation , . Beta stimulation with nylidrin has been studied and confirmed in a variety of isolated tissues from rabbits, guinea pigs, as well as dogs. This drug has been shown to dilate arterioles in skeletal muscle and to increase cardiac output in the anesthetized dog and cat as well as the unanesthetized man. An increase in cerebral blood flow and a decrease in vascular resistance has also been reported. The result of this combination of mechanisms is an improved blood supply to ischemic tissues, with minimal change in blood pressure (generally) . Nylidrin causes peripheral vasodilation, a positive inotropic effect, and an increased volume of gastric acid. , . According to one study, there are two primary effects of this agent following the intra‐arterial route of administration: one, to decrease total peripheral resistance; and two, a direct effect on the heart tissue to increase cardiac output . It also acts directly on the arteries and arterioles of the skeletal muscles. Additionally, it suppresses uterine contractility thereby preventing or halting premature labor . The drug's ability to modulate various physiological processes underscores its efficacy in treating specific conditions.

Mechanism of Action:

Nylidrin functions by: This drug is classified as a beta receptor agonist .The β2-adrenergic receptor belongs to the widely expressed _7-transmembrane receptors superfamily_, which signals through heterotrimeric _G-proteins_. They are frequently referred to as G-protein-coupled receptors because they accomplish signal transduction to the interior of the cell by interactions with _guanine nucleotide regulatory binding proteins_. The receptor-coupled G-proteins work as “molecular switches” which alternate from an inactive guanosine-diphosphate to an active guanosine-triphosphate (GTP) state, which then act to modulate all downstream cell processes. Signaling by various hormones and neurotransmitters, as well as photons and odors, follows the same general pathway, (i.e, by binding of an extracellular ligand to the receptor, which then interacts with the membrane-bound G-protein). This complex, often referred to as the ternary complex, then acts through the activated G-protein to regulate an effector, such as _adenylyl cyclase_, _phospholipase C_, or ion channels . The main effects of Nylidrin may be divided into 3 categories: Blood vessels Vascular smooth muscle has β2-adrenoceptors that have a high binding affinity for circulating epinephrine and a lower affinity to norepinephrine released by sympathetic adrenergic nerves . When nylidrin binds to the beta-adrenergic receptors, it prevents the binding of epinephrine, leading to decreased blood vessel contractility as epinephrine is unable to bind . Heart: Increased intracellular cAMP by beta-2-agonists inhibits _myosin light chain kinase_, leading to relaxation These receptors, like the receptors in the heart, are coupled to a Gs-protein, which acts stimulate the formation of cAMP. Although increased cAMP increases cardiac myocyte contraction, in vascular smooth muscle, an increase in cAMP causes smooth muscle relaxation. The reason for this is the fact that cAMP inhibits myosin light chain kinase that is responsible for phosphorylating smooth muscle myosin. Increases in intracellular cAMP caused by β2-agonists inhibit myosin light chain kinase thereby producing less contractile force (i.e, promoting relaxation) . Other tissues Activation of _β2-adrenoceptors_ in the lungs causes bronchodilation. β2-adrenoceptor activation leads to hepatic glycogenolysis and the pancreatic secretion of glucagon, increasing plasma glucose concentrations. β1-adrenoceptor stimulation in the kidneys promotes the release of renin, stimulating the production of angiotensin II and the subsequent release of aldosterone by the adrenal cortex . This mechanism highlights the drug's role in inhibiting or promoting specific biological pathways, contributing to its therapeutic effects.

Toxicity:

Classification:

Nylidrin belongs to the class of organic compounds known as phenylpropanes. These are organic compounds containing a phenylpropane moiety, classified under the direct parent group Phenylpropanes. This compound is a part of the Organic compounds, falling under the Benzenoids superclass, and categorized within the Benzene and substituted derivatives class, specifically within the Phenylpropanes subclass.

Categories:

Nylidrin is categorized under the following therapeutic classes: 2-Amino-1-Phenylethanol Derivatives, Adrenergic Agents, Adrenergic Agonists, Adrenergic beta-Agonists, Agents causing hyperkalemia, Agents producing tachycardia, Agents that produce hypertension, Alcohols, Amines, Amino Alcohols, Antiarrhythmic agents, Autonomic Agents, Bradycardia-Causing Agents, Calcium Channel Blockers, Cardiovascular Agents, Cytochrome P-450 CYP3A Substrates, Cytochrome P-450 CYP3A4 Substrates, Cytochrome P-450 Substrates, Ethylamines, Genito Urinary System and Sex Hormones, Miscellaneous Vasodilatating Agents, Neurotransmitter Agents, Peripheral Nervous System Agents, Peripheral Vasodilators, Phenethylamines, Propanolamines, Propanols, Reproductive Control Agents, Sympathomimetics, Sympathomimetics, Labour Repressants, Tocolytic Agents, Vasodilating Agents. These classifications highlight the drug's diverse therapeutic applications and its importance in treating various conditions.

Experimental Properties:

Further physical and chemical characteristics of Nylidrin include:

• Melting Point: 217