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Restrict the search for
lidocaine
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There is one exact (name or code) match for lidocaine
Status:
US Approved OTC
Source:
21 CFR 348.10(a)(2) external analgesic:male genital desensitizer lidocaine
Source URL:
First approved in 1948
Source:
NDA006488
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Lidocaine is a local anesthetic and cardiac depressant used to numb tissue in a specific area and for management of cardiac arrhythmias, particularly those of ventricular origins, such as occur with acute myocardial infarction. Lidocaine alters signal conduction in neurons by blocking the fast voltage-gated Na+ channels in the neuronal cell membrane responsible for signal propagation. With sufficient blockage, the membrane of the postsynaptic neuron will not depolarize and will thus fail to transmit an action potential. This creates the anesthetic effect by not merely preventing pain signals from propagating to the brain, but by stopping them before they begin. Careful titration allows for a high degree of selectivity in the blockage of sensory neurons, whereas higher concentrations also affect other modalities of neuron signaling. Lidocaine exerts an antiarrhythmic effect by increasing the electrical stimulation threshold of the ventricle during diastole. In usual therapeutic doses, lidocaine hydrochloride produces no change in myocardial contractility, in systemic arterial pressure, or an absolute refractory period. The efficacy profile of lidocaine as a local anesthetic is characterized by a rapid onset of action and intermediate duration of efficacy. Therefore, lidocaine is suitable for infiltration, block, and surface anesthesia. Longer-acting substances such as bupivacaine are sometimes given preference for spinal and epidural anesthesias; lidocaine, though, has the advantage of a rapid onset of action. Lidocaine is also the most important class-1b antiarrhythmic drug; it is used intravenously for the treatment of ventricular arrhythmias (for acute myocardial infarction, digoxin poisoning, cardioversion, or cardiac catheterization) if amiodarone is not available or contraindicated. Lidocaine should be given for this indication after defibrillation, CPR, and vasopressors have been initiated. A routine preventative dose is no longer recommended after a myocardial infarction as the overall benefit is not convincing. Inhaled lidocaine can be used as a cough suppressor acting peripherally to reduce the cough reflex. This application can be implemented as a safety and comfort measure for patients who have to be intubated, as it reduces the incidence of coughing and any tracheal damage it might cause when emerging from anesthesia. Adverse drug reactions (ADRs) are rare when lidocaine is used as a local anesthetic and is administered correctly. Most ADRs associated with lidocaine for anesthesia relate to administration technique (resulting in systemic exposure) or pharmacological effects of anesthesia, and allergic reactions only rarely occur. Systemic exposure to excessive quantities of lidocaine mainly result in a central nervous system (CNS) and cardiovascular effects – CNS effects usually occur at lower blood plasma concentrations and additional cardiovascular effects present at higher concentrations, though cardiovascular collapse may also occur with low concentrations.
Status:
US Approved OTC
Source:
21 CFR 348.10(a)(2) external analgesic:male genital desensitizer lidocaine
Source URL:
First approved in 1948
Source:
NDA006488
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Lidocaine is a local anesthetic and cardiac depressant used to numb tissue in a specific area and for management of cardiac arrhythmias, particularly those of ventricular origins, such as occur with acute myocardial infarction. Lidocaine alters signal conduction in neurons by blocking the fast voltage-gated Na+ channels in the neuronal cell membrane responsible for signal propagation. With sufficient blockage, the membrane of the postsynaptic neuron will not depolarize and will thus fail to transmit an action potential. This creates the anesthetic effect by not merely preventing pain signals from propagating to the brain, but by stopping them before they begin. Careful titration allows for a high degree of selectivity in the blockage of sensory neurons, whereas higher concentrations also affect other modalities of neuron signaling. Lidocaine exerts an antiarrhythmic effect by increasing the electrical stimulation threshold of the ventricle during diastole. In usual therapeutic doses, lidocaine hydrochloride produces no change in myocardial contractility, in systemic arterial pressure, or an absolute refractory period. The efficacy profile of lidocaine as a local anesthetic is characterized by a rapid onset of action and intermediate duration of efficacy. Therefore, lidocaine is suitable for infiltration, block, and surface anesthesia. Longer-acting substances such as bupivacaine are sometimes given preference for spinal and epidural anesthesias; lidocaine, though, has the advantage of a rapid onset of action. Lidocaine is also the most important class-1b antiarrhythmic drug; it is used intravenously for the treatment of ventricular arrhythmias (for acute myocardial infarction, digoxin poisoning, cardioversion, or cardiac catheterization) if amiodarone is not available or contraindicated. Lidocaine should be given for this indication after defibrillation, CPR, and vasopressors have been initiated. A routine preventative dose is no longer recommended after a myocardial infarction as the overall benefit is not convincing. Inhaled lidocaine can be used as a cough suppressor acting peripherally to reduce the cough reflex. This application can be implemented as a safety and comfort measure for patients who have to be intubated, as it reduces the incidence of coughing and any tracheal damage it might cause when emerging from anesthesia. Adverse drug reactions (ADRs) are rare when lidocaine is used as a local anesthetic and is administered correctly. Most ADRs associated with lidocaine for anesthesia relate to administration technique (resulting in systemic exposure) or pharmacological effects of anesthesia, and allergic reactions only rarely occur. Systemic exposure to excessive quantities of lidocaine mainly result in a central nervous system (CNS) and cardiovascular effects – CNS effects usually occur at lower blood plasma concentrations and additional cardiovascular effects present at higher concentrations, though cardiovascular collapse may also occur with low concentrations.
Status:
US Approved Rx
(1995)
Source:
ANDA074413
(1995)
Source URL:
First approved in 1984
Source:
NDA019050
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Sufentanil is a synthetic opioid analgesic. Sufentanil interacts predominately with the opioid mu-receptor. These mu-binding sites are discretely distributed in the human brain, spinal cord, and other tissues. In clinical settings, sufentanil exerts its principal pharmacologic effects on the central nervous system. Its primary actions of therapeutic value are analgesia and sedation. Sufentanil may increase the patient's tolerance for pain and decrease the perception of suffering, although the presence of the pain itself may still be recognized. In addition to analgesia, alterations in mood, euphoria and dysphoria, and drowsiness commonly occur. Sufentanil depresses the respiratory centers, depresses the cough reflex, and constricts the pupils. Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Sufentanil's analgesic activity is, most likely, due to its conversion to morphine. Opioids open calcium-dependent inwardly rectifying potassium channels (OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability. Sufentanil is used as an analgesic adjunct in anesthesia and as a primary anesthetic drug in procedures requiring assisted ventilation and in the relief of pain.
Status:
US Approved Rx
(2003)
Source:
ANDA076320
(2003)
Source URL:
First approved in 1965
Source:
CITANEST PLAIN DENTAL by DENTSPLY PHARM
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Prilocaine is a local anesthetic that is similar pharmacologically to lidocaine. Prilocaine binds to the intracellular surface of sodium channels which blocks the subsequent influx of sodium into the cell. Action potential propagation and never function is, therefore, prevented. This block is reversible and when the drug diffuses away from the cell, sodium channel function is restored and nerve propagation returns. Prilocaine acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. The antiarrhythmic actions are mediated through effects on sodium channels in Purkinje fibers. Currently, Prilocaine is used most often for infiltration anesthesia in dentistry.
Status:
US Approved OTC
Source:
21 CFR 346.12(a) anorectal:vasoconstrictor ephedrine sulfate
Source URL:
First marketed in 1928
Source:
Ephetonine by Merck
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Ephedrine (l-form) is an alkaloid, which was initially purified from Ephedra plant. The extract form Ephedra has been used in China for medicinal purposes for several thousand years. Ephedrine acts as an agonist at alpha- and beta-adrenergic receptors and indirectly causes the release of norepinephrine from sympathetic neurons. The drug crosses the blood brain barrier and stimulates the central nervous system. Ephedrine products are now banned in many countries, as they are a major source for the production of the addictive compound methamphetamine. FDA has approved ephedrine only for the treatment of clinically important hypotension occurring in the setting of anesthesia.
Status:
US Approved OTC
Source:
21 CFR 331.11(k)(1) antacid:sodium-containing sodium bicarbonate
Source URL:
First marketed in 1921
Source:
Potassium Bicarbonate U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Diammonium carbonate is a salt with the chemical formula (NH4)2CO3. Since it readily degrades to gaseous ammonia and carbon dioxide upon heating, it is used as a leavening agent and also as smelling salt. Ammonium carbonate may be used as a leavening agent in traditional recipes, particularly those from northern Europe and Scandinavia (e.g. Speculoos, Tunnbröd or Lebkuchen). It also serves as an acidity regulator and has the E number E503. Ammonium carbonate is the main component of smelling salts, although the commercial scale of their production is small. Buckley's cough syrup from Canada today uses ammonium carbonate as an active ingredient intended to help relieve symptoms of bronchitis. Ammonium carbonate is also used as an emetic.
Status:
US Approved OTC
Source:
21 CFR 331.11(a)(5) antacid:aluminum-containing dihydroxyaluminum sodium carbonate
Source URL:
First marketed in 1921
Source:
Potassium Carbonate U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Potash (Dihydroxyaluminum Sodium Carbonate), a component of
Kompensan-S Forte in Germany, is a basic inorganic salt that acts by neutralizing hydrochloric acid in gastric secretions. Kompensan-S Forte is slowly solubilized in the stomach and reacts with hydrochloric acid to form aluminum chloride and water. It also inhibits the action of pepsin by increasing the pH and via adsorption. Cytoprotective effects may occur through increases in bicarbonate ion (HCO3-) and prostaglandins.
Status:
US Approved OTC
Source:
21 CFR 346.10(a) anorectal:local anesthetic benzocaine
Source URL:
First marketed in 1895
Class (Stereo):
CHEMICAL (ACHIRAL)
Benzocaine is a local anesthetic. It acts by blocking voltage-gated sodium ion channels in nerve endings. Benzocaine is available over-the counter for local anesthesia of oral and pharyngeal mucous membranes (sore throat, cold sores, mouth ulcers, toothache, sore gums, denture irritation), otic pain, and as a local anesthetic for surgical or diagnostic procedures. As a spray, benzocaine is used for temporary relief of pain and itching associated with minor burns, sunburn, minor cuts or scrapes, insect bites, or minor skin irritations. Topical application of benzocaine to gums or mouth may cause rare, but serious and potentially fatal adverse effect methemoglobinemia.
