A centrally active drug that apparently both blocks serotonin uptake and provokes transport-mediated serotonin release.
A FENFLURAMINE analog that inhibits serotonin uptake and may provoke release of serotonin. It is used as an appetite depressant and an experimental tool in animal studies.
Agents that are used to suppress appetite.
A dopamine agonist and serotonin antagonist. It has been used similarly to BROMOCRIPTINE as a dopamine agonist and also for MIGRAINE DISORDERS therapy.
Drugs used for their effects on serotonergic systems. Among these are drugs that affect serotonin receptors, the life cycle of serotonin, and the survival of serotonergic neurons.
The S-isomer of FENFLURAMINE. It is a serotonin agonist and is used as an anorectic. Unlike fenfluramine, it does not possess any catecholamine agonist activity.
Chlorinated analog of AMPHETAMINE. Potent neurotoxin that causes release and eventually depletion of serotonin in the CNS. It is used as a research tool.
An amphetamine-like anorectic agent. It may cause pulmonary hypertension.
A appetite depressant considered to produce less central nervous system disturbance than most drugs in this therapeutic category. It is also considered to be among the safest for patients with hypertension. (From AMA Drug Evaluations Annual, 1994, p2290)
A sympathomimetic agent that was formerly used as an anorectic. It has properties similar to those of DEXTROAMPHETAMINE. It has been implicated in lipid storage disorders and pulmonary hypertension. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1223)
A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.
A tricyclic antidepressant that has actions and uses similar to those of AMITRIPTYLINE, but has only weak antimuscarinic and sedative effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p257)
Compounds that specifically inhibit the reuptake of serotonin in the brain.
Process of preserving a dead body to protect it from decay.
A sympathomimetic drug used primarily as an appetite depressant. Its actions and mechanisms are similar to DEXTROAMPHETAMINE.
Cyclobutanes are saturated hydrocarbons consisting of a four-carbon ring with only carbon-carbon sigma bonds, making up the smallest cycloalkane ring that can adopt a puckered conformation to alleviate angle strain. (25 words)
Biogenic amines having only one amine moiety. Included in this group are all natural monoamines formed by the enzymatic decarboxylation of natural amino acids.
A homolog of ERGONOVINE containing one more CH2 group. (Merck Index, 11th ed)
Tricyclic anorexigenic agent unrelated to and less toxic than AMPHETAMINE, but with some similar side effects. It inhibits uptake of catecholamines and blocks the binding of cocaine to the dopamine uptake transporter.
An N-substituted amphetamine analog. It is a widely abused drug classified as a hallucinogen and causes marked, long-lasting changes in brain serotonergic systems. It is commonly referred to as MDMA or ecstasy.
A nonmetallic, diatomic gas that is a trace element and member of the halogen family. It is used in dentistry as flouride (FLUORIDES) to prevent dental caries.
A tricyclic antidepressant similar to IMIPRAMINE that selectively inhibits the uptake of serotonin in the brain. It is readily absorbed from the gastrointestinal tract and demethylated in the liver to form its primary active metabolite, desmethylclomipramine.
A serotonin receptor subtype found in the BRAIN; HEART; LUNGS; PLACENTA and DIGESTIVE SYSTEM organs. A number of functions have been attributed to the action of the 5-HT2B receptor including the development of cardiac myocytes (MYOCYTES, CARDIAC) and the contraction of SMOOTH MUSCLE.
Drugs that inhibit the transport of neurotransmitters into axon terminals or into storage vesicles within terminals. For many transmitters, uptake determines the time course of transmitter action so inhibiting uptake prolongs the activity of the transmitter. Blocking uptake may also deplete available transmitter stores. Many clinically important drugs are uptake inhibitors although the indirect reactions of the brain rather than the acute block of uptake itself is often responsible for the therapeutic effects.
An amphetamine derivative that inhibits uptake of catecholamine neurotransmitters. It is a hallucinogen. It is less toxic than its methylated derivative but in sufficient doses may still destroy serotonergic neurons and has been used for that purpose experimentally.
A group of compounds that are derivatives of beta- aminoethylbenzene which is structurally and pharmacologically related to amphetamine. (From Merck Index, 11th ed)
Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters.
Drugs that bind to but do not activate serotonin receptors, thereby blocking the actions of serotonin or SEROTONIN RECEPTOR AGONISTS.
An antihyperlipoproteinemic agent and uricosuric agent.
A serotonin receptor subtype found at high levels in the BASAL GANGLIA and the frontal cortex. It plays a role as a terminal autoreceptor that regulates the rate of SEROTONIN release from nerve endings. This serotonin receptor subtype is closely related to and has similar drug binding properties as the 5-HT1D RECEPTOR. It is particularly sensitive to the agonist SUMATRIPTAN and may be involved in mediating the drug's antimigraine effect.
Cell-surface proteins that bind SEROTONIN and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action.
Hydroxyindoleacetic acid (5HIAA) is a major metabolite of serotonin, a neurotransmitter, formed by the action of monoamine oxidase and aldehyde dehydrogenase, and its measurement in urine is often used as a biomarker for serotonin synthesis in clinical and research settings.
A series of structurally-related alkaloids that contain the ergoline backbone structure.
Analogs or derivatives of AMPHETAMINE. Many are sympathomimetics and central nervous system stimulators causing excitation, vasopressin, bronchodilation, and to varying degrees, anorexia, analepsis, nasal decongestion, and some smooth muscle relaxation.
An indirect sympathomimetic. Tyramine does not directly activate adrenergic receptors, but it can serve as a substrate for adrenergic uptake systems and monoamine oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals. Tyramine may be a neurotransmitter in some invertebrate nervous systems.
A derivative of benzodiazepine that acts on the cholecystokinin A (CCKA) receptor to antagonize CCK-8's (SINCALIDE) physiological and behavioral effects, such as pancreatic stimulation and inhibition of feeding.
Pathological conditions involving any of the various HEART VALVES and the associated structures (PAPILLARY MUSCLES and CHORDAE TENDINEAE).

d,l-fenfluramine response in impulsive personality disorder assessed with [18F]fluorodeoxyglucose positron emission tomography. (1/227)

Reduced serotonergic activity has been associated with impulsive aggression in personality disordered patients in metabolite and pharmacologic challenge studies. This study used positron emission tomography to explore whether reduced serotonergic function occurs in critical brain regions such as orbital frontal and cingulate cortex that, may play a role in modulating aggression. Six impulsive-aggressive patients and five healthy volunteers were evaluated for changes in regional glucose metabolism after administration of the serotonergic releasing agent d,l-fenfluramine (60 mg, p.o.) or placebo. Volunteers demonstrated increases in orbital frontal and adjacent ventral medial frontal cortex, cingulate, and inferior parietal cortex, whereas impulsive-aggressive patients showed no significant increases in glucose metabolism after fenfluramine in any region. Compared with volunteers, patients showed significantly blunted metabolic responses in orbital frontal, adjacent ventral medial and cingulate cortex, but not in inferior parietal lobe. These results are consistent with reduced serotonergic modulation of orbital frontal, ventral medial frontal, and cingulate cortex in patients with impulsive-aggressive personality disorders.  (+info)

Operant methodology in the study of learning. (2/227)

A series of experiments is described in which operant methodology is used to study the effects of drugs on "learning." Emphasis is placed on the technique of repeated acquisition as a behavioral baseline for studying this type of transition state. In this technique, each subject is required to learn a new discrimination each session. Multiple-schedule procedures are also described in which acquisition is compared to a "performance" task, where the discrimination is the same each session. The learning baseline is more sensitive to the disruptive effects of a variety of drugs (e.g., cocaine, d-amphetamine, haloperidol) than is the performance baseline. This general finding obtains across procedural variations and species (pigeons and monkeys). The potential usefulness of these procedures for studying both acute and chronic behavioral toxicity is discussed.  (+info)

Use of dexfenfluramine, fenfluramine and phentermine and the risk of stroke. (3/227)

AIMS: To estimate the incidence of newly diagnosed idiopathic stroke among users of fenfluramine, dexfenfluramine and phentermine compared to obese nonusers. METHODS: We conducted a cohort study with nested case-control analysis utilizing data from the General Practice Research Database in the UK. Eight thousand four hundred and twenty-three subjects aged 69 years or less at the start of follow-up were exposed to at least one of the three study drugs and 17 225 similarly obese subjects were not exposed to any of the study drugs. RESULTS: We identified 45 incident cases of idiopathic CVA in this cohort of subjects. The incidence of CVA among all current users of a diet drug was 1.3/1000 person-years (95% CI 0.5, 3.5). The incidence for current fenfluramine users (n=2) was 2.6/1000 person-years (95% CI 0.7, 9.6), for current dexfenfluramine users (n=1) 1.1/1000 person-years (95% CI 0.3, 3.8), and for current phentermine users 0/1000 person-years (95% CI 0.0, 12.9). The incidence in obese nonusers was 0.6/1000 person-years (95% CI 0.4, 0. 9). The adjusted matched odds ratio (OR) for thrombotic stroke from the case-control analysis comparing current use of a diet drug to nonuse was 2.4 (95% CI 0.6, 9.1). There was only one exposed subject among seven who had haemorrhagic stroke. CONCLUSIONS: The incidence of CVA in generally young obese subjects during use of fenfluramine, dexfenfluramine or phentermine is low. Although we found an OR of 2. 4 comparing users of any of the anorexiants with nonusers, this is based on only three exposed cases and the confidence limits are wide. We conclude that our study does not support a substantial increased risk of stroke attributable to the use of fenfluramine, dexfenfluramine or phentermine.  (+info)

Pharmacologic induction of weight loss to treat type 2 diabetes. (4/227)

OBJECTIVE: Most individuals with type 2 diabetes are overweight, and weight loss for them is an important therapeutic objective. However, usual weight-loss strategies have generally not produced sustained weight loss. Pharmacologic agents to assist weight loss might be useful, but no long-term data on their effectiveness and safety in patients with type 2 diabetes are available. We therefore initiated a 2-year placebo-controlled trial of the weight-loss medications fenfluramine and phentermine in type 2 diabetic subjects. RESEARCH DESIGN AND METHODS: A total of 44 overweight (> 120% ideal body weight) subjects with type 2 diabetes were enrolled in a randomized, placebo-controlled, double-blind trial of fenfluramine and phentermine. All subjects received intensive nutrition counseling, an exercise prescription, and instruction in behavior modification. Subjects were randomly assigned to 20 mg fenfluramine three times a day and 37.5 mg phentermine daily (n = 23) or dual placebos (n = 21). Diabetes medications were adjusted as necessary to achieve glycemic goals. Changes in weight, glycemia, lipemia, and blood pressure were assessed every 2 months, as were adverse events. In September 1997, when fenfluramine was withdrawn from the U.S. market, fenfluramine was stopped in all subjects. Thus the length of drug treatment varied, but 16 subjects (8 in each group) reached 12 months of treatment. Only data obtained before the withdrawal of fenfluramine are included in this report. RESULTS: A study termination, diabetes medications had been reduced in 1 subject in the placebo group (5%) and 11 subjects in the drug treatment group (52%) (P = 0.005). Drug treatment resulted in significant reductions in body weight, BMI, and HbA1c at all time points through 6 months. Changes in weight at 6 months were -2.7 +/- 1.4 kg (mean +/- SEM) with placebo treatment and -9.6 +/- 1.5 kg with drug treatment (P = 0.003). Even though more subjects in the drug treatment group required reductions in diabetes medications, at 6 months, changes in HbA1c were -0.3 +/- 0.2% with placebo treatment and -1.6 +/- 0.3% with drug treatment (P = 0.002). Fasting plasma glucose and triglycerides were significantly reduced at some time points with drug treatment. No serious adverse events attributable to study medications were observed. CONCLUSIONS: Premature study termination decreased the power of our study at later time points. However, our data suggest that weight loss medications are an effective treatment for type 2 diabetes during active weight loss. Whether the benefit persists after weight loss has stopped remains to be determined.  (+info)

Direct agonists for serotonin receptors enhance locomotor function in rats that received neural transplants after neonatal spinal transection. (5/227)

We analyzed whether acute treatment with serotonergic agonists would improve motor function in rats with transected spinal cords (spinal rats) and in rats that received transplants of fetal spinal cord into the transection site (transplant rats). Neonates received midthoracic spinal transections within 48 hr of birth; transplant rats received fetal (embryonic day 14) spinal cord grafts at the time of transection. At 3 weeks, rats began 1-2 months of training in treadmill locomotion. Rats in the transplant group developed better weight-supported stepping than spinal rats. Systemic administration of two directly acting agonists for serotonergic 5-HT(2) receptor subtypes, quipazine and (+/-)-1-[2, 5]-dimethoxy-4-iodophenyl-2-aminopropane), further increased weight-supported stepping in transplant rats. The improvement was dose-dependent and greatest in rats with poor to moderate baseline weight support. In contrast, indirectly acting serotonergic agonists, which block reuptake of 5-HT (sertraline) or release 5-HT and block its reuptake (D-fenfluramine), failed to enhance motor function. Neither direct nor indirect agonists significantly improved locomotion in spinal rats as a group, despite equivalent upregulation of 5-HT(2) receptors in the lumbar ventral horn of lesioned rats with and without transplants. The distribution of immunoreactive serotonergic fibers within and caudal to the transplant did not appear to correspond to restoration of motor function. Our results confirm our previous demonstration that transplants improve motor performance in spinal rats. Additional stimulation with agonists at subtypes of 5-HT receptors produces a beneficial interaction with transplants that further improves motor competence.  (+info)

Aminorex, fenfluramine, and chlorphentermine are serotonin transporter substrates. Implications for primary pulmonary hypertension. (6/227)

BACKGROUND: Coadministration of phentermine and fenfluramine (phen/fen) effectively treats obesity and possibly addictive disorders. The association of fenfluramine and certain other anorexic agents with serious side effects, such as cardiac valvulopathy and primary pulmonary hypertension (PPH), limits the clinical utility of these drugs. Development of new medications that produce neurochemical effects like phen/fen without causing unwanted side effects would be a significant therapeutic breakthrough. METHODS AND RESULTS: We tested the hypothesis that fenfluramine (and other anorexic agents) might increase the risk of PPH through interactions with serotonin (5-HT) transporters. Because 5-HT transporter proteins in the lung and brain are identical, we examined, in rat brain, the effects of selected drugs on 5-HT efflux in vivo and monoamine transporters in vitro as a generalized index of transporter function. Our data show that drugs known or suspected to increase the risk of PPH (eg, aminorex, fenfluramine, and chlorphentermine) are 5-HT transporter substrates, whereas drugs that have not been shown to increase the risk of PPH are less potent in this regard. CONCLUSIONS: We speculate that medications that are 5-HT transporter substrates get translocated into pulmonary cells where, depending on the degree of drug retention, their intrinsic drug toxicity, and individual susceptibility, PPH could develop as a response to high levels of these drugs or metabolites. Emerging evidence suggests that it is possible to develop transporter substrates devoid of adverse side effects. Such medications could have therapeutic application in the management of obesity, drug dependence, depression, and other disorders.  (+info)

The promotion effect of anorectic drugs on aflatoxin B(1)-induced hepatic preneoplastic foci. (7/227)

The ability of three extensively used anorectic drugs, namely fenfluramine (FN), fluoxetine (FX) and amphetamine (AM), to alter the development of aflatoxin B(1) (AFB(1))-induced gamma-glutamyl-positive (GGT(+)) preneoplastic liver foci was investigated in 135 male weanling F344 rats. Following AFB(1) administration, 15 rats were killed, while the rest were divided into four groups and fed diets containing either FN, FX, AM or control diet, with half of the animals in each group subsequently being killed at 4 weeks and half at 10 weeks. All three anorectic drugs as expected suppressed initial food intake, growth rate, body weight gain and food efficiency. They also tended to suppress body fat mass and to decrease plasma levels of T(3) and T(4). FN significantly (P < 0.05) increased GGT(+) foci number/cm(2) and number/cm(3), while FX significantly increased GGT(+) foci number/cm(2) and the volume fraction of foci. Histopathological staining also revealed that FN- and FX-treated animals had more serious morphological alterations in their liver tissue. In contrast, foci development was, if anything, suppressed by AM feeding. These results indicate that serotoninergic drugs (FN and FX), as opposed to dopaminergic drugs (AM), may have tumor promoter activity, at least for liver tissue.  (+info)

Potent depression of stimulus evoked field potential responses in the medial entorhinal cortex by serotonin. (8/227)

1. The entorhinal cortex (EC), main input structure to the hippocampus, gets innervated by serotonergic terminals from the raphe nuclei and expresses 5-HT-receptors at high density. Using extra- and intracellular recording techniques we here investigated the effects of serotonin on population and cellular responses within the EC. 2. Stimulation in the lateral entorhinal cortex resulted in complex field potential responses in the superficial EC. The potentials are composed of an early antidromic and a late orthodromic component reflecting the efferent and afferent circuitry. 3. Serotonin (5-HT) reduced synaptic potentials of the stimulus evoked extracellular field potential at all concentrations tested (0. 1 - 100 microM; 59%-depression by 10 microM serotonin), while the antidromic response was not significantly changed by up to 50 microM 5-HT. Depression of field potential responses by serotonin was associated with a significant increase in paired-pulse facilitation from 1.15 to 1.88. 4. The effects of serotonin on field potential responses were mimicked by 5-HT1A-receptor agonists (8-OH-DPAT, 5-CT) and partially prevented by the 5-HT1A-receptor antagonist (S-UH-301). Moreover, the 5-HT1A-receptor antagonist WAY100635 reduced the effect of 5-CT. 5. Fenfluramine, a serotonin releaser, mimics the effects of serotonin on stimulus-evoked field potential responses, indicating that synaptically released serotonin can produce the changes in reactivity to afferent stimulation. 6. Depression of isolated AMPA-receptor mediated EPSCs by serotonin as well as fenfluramine was associated with an increase in paired pulse facilitation, indicating a presynaptic locus of action. 7. We conclude that physiological concentrations of serotonin potently suppresses excitatory synaptic transmission in the superficial entorhinal cortex by a presynaptic mechanism.  (+info)

Fenfluramine is a drug that was previously used for the short-term treatment of obesity. It works by suppressing appetite and increasing the feeling of fullness. Fenfluramine is an amphetamine derivative and stimulates the release of serotonin, a neurotransmitter in the brain that helps regulate mood, appetite, and sleep.

Fenfluramine was commonly prescribed in combination with phentermine, another appetite suppressant, under the brand name Fen-Phen. However, in 1997, the U.S. Food and Drug Administration (FDA) issued a public health warning about the potential risk of serious heart valve damage associated with the use of fenfluramine and withdrew its approval for the drug's use. Since then, fenfluramine has not been approved for medical use in many countries, including the United States.

Norfenfluramine is not a medication that is currently used in medical practice. It is a serotonin agonist, meaning it binds to and activates serotonin receptors in the body. Norfenfluramine was previously used as an appetite suppressant for the treatment of obesity, but it was withdrawn from the market due to safety concerns. Specifically, it was found to be associated with an increased risk of heart valve damage and primary pulmonary hypertension, a rare but serious lung condition.

The chemical structure of norfenfluramine is similar to that of fenfluramine, another appetite suppressant that was also withdrawn from the market due to safety concerns. Both drugs were found to increase levels of serotonin in the body, which can have harmful effects on the heart and lungs. Norfenfluramine is still occasionally used in research settings to study the effects of serotonin agonists on various physiological processes, but it is not used as a medication.

Appetite depressants are medications or substances that reduce or suppress feelings of hunger and appetite. They can be prescribed to treat various medical conditions, such as obesity or binge eating disorder, where weight loss is a recommended treatment goal. Some common appetite depressants include:

1. Phentermine: This medication works by stimulating the release of certain neurotransmitters in the brain that help suppress appetite and increase metabolism. It is often prescribed for short-term use (up to 12 weeks) as part of a comprehensive weight loss plan.

2. Diethylpropion: Similar to phentermine, diethylpropion stimulates the release of neurotransmitters that suppress appetite and increase metabolism. It is also prescribed for short-term use in treating obesity.

3. Naltrexone-bupropion (Contrave): This combination medication helps manage weight by reducing appetite and increasing feelings of fullness. Naltrexone is an opioid antagonist that blocks the rewarding effects of food, while bupropion is an antidepressant that can help reduce cravings for high-calorie foods.

4. Lorcaserin (Belviq): This medication works by selectively activating serotonin receptors in the brain, which helps promote satiety and reduce appetite. It was withdrawn from the US market in 2020 due to concerns about its potential link to an increased risk of cancer.

5. Topiramate (Topamax): Although primarily used as an anticonvulsant, topiramate has also been found to have appetite-suppressing effects. It is often combined with phentermine in a single formulation (Qsymia) for the treatment of obesity.

6. Cannabis: Some studies suggest that cannabinoids, the active compounds in marijuana, may help reduce hunger and promote weight loss by interacting with the endocannabinoid system in the body. However, more research is needed to fully understand its potential as an appetite depressant.

It's important to note that appetite suppressants should only be used under the guidance of a healthcare professional and as part of a comprehensive weight management plan. These medications can have side effects and potential risks, so it's crucial to discuss their use with your doctor before starting any new treatment regimen.

Methysergide, commonly known as methylergometrine or metergoline, is not typically considered a medication in the medical field. It is actually a derivative of ergot alkaloids, which are fungal metabolites that have been used in medicine for their vasoconstrictive and oxytocic properties.

Methysergide has been used in the past as a migraine prophylaxis medication due to its ability to block serotonin receptors in the brain. However, its use is now limited due to its potential to cause serious side effects such as fibrotic reactions in various organs, including the heart, lungs, and kidneys.

Therefore, methysergide/metergoline is not commonly used in modern medical practice, and its use is typically reserved for highly specific cases under close medical supervision.

Serotonin agents are a class of drugs that work on the neurotransmitter serotonin (5-hydroxytryptamine, 5-HT) in the brain and elsewhere in the body. They include several types of medications such as:

1. Selective Serotonin Reuptake Inhibitors (SSRIs): These drugs block the reabsorption (reuptake) of serotonin into the presynaptic neuron, increasing the availability of serotonin in the synapse to interact with postsynaptic receptors. SSRIs are commonly used as antidepressants and include medications such as fluoxetine, sertraline, and citalopram.
2. Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): These drugs block the reabsorption of both serotonin and norepinephrine into the presynaptic neuron, increasing the availability of these neurotransmitters in the synapse. SNRIs are also used as antidepressants and include medications such as venlafaxine and duloxetine.
3. Serotonin Receptor Agonists: These drugs bind to and activate serotonin receptors, mimicking the effects of serotonin. They are used for various indications, including migraine prevention (e.g., sumatriptan) and Parkinson's disease (e.g., pramipexole).
4. Serotonin Receptor Antagonists: These drugs block serotonin receptors, preventing the effects of serotonin. They are used for various indications, including nausea and vomiting (e.g., ondansetron) and as mood stabilizers in bipolar disorder (e.g., olanzapine).
5. Serotonin Synthesis Inhibitors: These drugs block the enzymatic synthesis of serotonin, reducing its availability in the brain. They are used as antidepressants and include medications such as monoamine oxidase inhibitors (MAOIs) like phenelzine and tranylcypromine.

It's important to note that while these drugs all affect serotonin, they have different mechanisms of action and are used for various indications. It's essential to consult a healthcare professional before starting any new medication.

Dexfenfluramine is a medication that was previously used as an appetite suppressant for weight loss. It is a stereoisomer (enantiomer) of fenfluramine, which is another appetite suppressant. Dexfenfluramine works by increasing the levels of serotonin in the brain, which helps to reduce appetite and promote weight loss.

However, dexfenfluramine was withdrawn from the market in 1997 due to concerns about its safety. Studies found that long-term use of dexfenfluramine was associated with an increased risk of primary pulmonary hypertension, a rare but serious condition that can lead to heart failure. Additionally, when dexfenfluramine was used in combination with phentermine (a different appetite suppressant), there was an increased risk of valvular heart disease.

Therefore, dexfenfluramine is no longer available for medical use and its prescription is not recommended due to these safety concerns.

P-Chloroamphetamine, also known as PCA or 4-chloroamphetamine, is a synthetic stimulant drug that has been used in scientific research but is not commonly used medically. It is a derivative of amphetamine and has similar effects, such as increasing heart rate, blood pressure, and alertness. However, it also has hallucinogenic properties and can cause psychological disturbances.

PCA acts as a releasing agent for the neurotransmitters dopamine, norepinephrine, and serotonin, which are involved in regulating mood, appetite, and other physiological processes. It is classified as a Schedule I controlled substance in the United States due to its high potential for abuse and lack of accepted medical use.

It's important to note that PCA is not approved for any medical use in humans and should only be used in a controlled research setting with appropriate safety measures in place.

Aminorex is a stimulant drug that was previously used as an appetite suppressant for weight loss. It is a derivative of amphetamine and has a similar chemical structure and pharmacological effects. Aminorex works by increasing the levels of certain neurotransmitters in the brain, such as dopamine and norepinephrine, which can lead to increased alertness, energy, and mood.

However, the use of Aminorex has been associated with serious health risks, including pulmonary hypertension, a rare but potentially life-threatening condition that affects the blood vessels in the lungs. As a result, Aminorex was banned in many countries in the 1970s and is no longer used medically.

It's important to note that the use of any appetite suppressant or weight loss drug should be done under the close supervision of a healthcare provider, as these medications can have serious side effects and interactions with other drugs.

Diethylpropion is a sympathomimetic amine, which is a type of medication that stimulates the nervous system. It is primarily used as an appetite suppressant for the short-term treatment of obesity. Diethylpropion works by affecting the neurotransmitters in the brain that regulate appetite, leading to a decrease in food intake and an increase in weight loss.

Diethylpropion is available in immediate-release and extended-release forms, and it is typically taken two to three times a day, about one hour before meals. Common side effects of diethylpropion include dry mouth, constipation, difficulty sleeping, and increased heart rate. More serious side effects can include high blood pressure, irregular heartbeat, and seizures.

Diethylpropion is a controlled substance in many countries due to its potential for abuse and dependence. It should only be used under the close supervision of a healthcare provider and for a limited period of time.

Chlorphentermine is a sympathomimetic amine, which is a type of medication that stimulates the nervous system. It was used as an appetite suppressant for the short-term treatment of obesity, although it is no longer widely available or used in clinical practice due to its potential for serious side effects and addiction.

Like other sympathomimetic amines, chlorphentermine works by stimulating the release of certain neurotransmitters in the brain, such as norepinephrine and dopamine, which can help to suppress appetite and increase metabolism. However, long-term use or abuse of these medications can lead to a number of serious health problems, including cardiovascular issues, addiction, and psychiatric disorders.

Chlorphentermine has been associated with a range of side effects, including dry mouth, constipation, difficulty sleeping, irritability, and increased heart rate and blood pressure. In some cases, it may also cause more serious adverse reactions, such as seizures, hallucinations, or cardiac arrhythmias.

Due to these risks, chlorphentermine is no longer approved for use in many countries, and its prescription is tightly controlled in those where it is still available. Today, other medications and lifestyle interventions are typically used to manage obesity and promote weight loss.

Serotonin, also known as 5-hydroxytryptamine (5-HT), is a monoamine neurotransmitter that is found primarily in the gastrointestinal (GI) tract, blood platelets, and the central nervous system (CNS) of humans and other animals. It is produced by the conversion of the amino acid tryptophan to 5-hydroxytryptophan (5-HTP), and then to serotonin.

In the CNS, serotonin plays a role in regulating mood, appetite, sleep, memory, learning, and behavior, among other functions. It also acts as a vasoconstrictor, helping to regulate blood flow and blood pressure. In the GI tract, it is involved in peristalsis, the contraction and relaxation of muscles that moves food through the digestive system.

Serotonin is synthesized and stored in serotonergic neurons, which are nerve cells that use serotonin as their primary neurotransmitter. These neurons are found throughout the brain and spinal cord, and they communicate with other neurons by releasing serotonin into the synapse, the small gap between two neurons.

Abnormal levels of serotonin have been linked to a variety of disorders, including depression, anxiety, schizophrenia, and migraines. Medications that affect serotonin levels, such as selective serotonin reuptake inhibitors (SSRIs), are commonly used to treat these conditions.

Iprindole is a tricyclic antidepressant that was used for the treatment of depression. It works by increasing the levels of neurotransmitters (chemical messengers) in the brain, such as serotonin and noradrenaline, which help to regulate mood and emotion.

Iprindole has been discontinued in many countries due to its limited efficacy and unfavorable side effect profile compared to other antidepressants. Some of the common side effects associated with iprindole include dry mouth, blurred vision, constipation, dizziness, drowsiness, and weight gain.

It is important to note that iprindole should only be taken under the supervision of a healthcare provider, as it can interact with other medications and have serious side effects if not used properly.

Serotonin uptake inhibitors (also known as Selective Serotonin Reuptake Inhibitors or SSRIs) are a class of medications primarily used to treat depression and anxiety disorders. They work by increasing the levels of serotonin, a neurotransmitter in the brain that helps regulate mood, appetite, and sleep, among other functions.

SSRIs block the reuptake of serotonin into the presynaptic neuron, allowing more serotonin to be available in the synapse (the space between two neurons) for binding to postsynaptic receptors. This results in increased serotonergic neurotransmission and improved mood regulation.

Examples of SSRIs include fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), citalopram (Celexa), and escitalopram (Lexapro). These medications are generally well-tolerated, with side effects that may include nausea, headache, insomnia, sexual dysfunction, and increased anxiety or agitation. However, they can have serious interactions with other medications, so it is important to inform your healthcare provider of all medications you are taking before starting an SSRI.

Embalming is a process used in mortuary science, where the preservation and disinfection of human remains are carried out for the purpose of delaying decomposition and preserving the appearance of the body. This procedure typically involves the removal of bodily fluids and replacement with chemical preservatives, such as formaldehyde, which help to prevent the decay of tissues.

The goal of embalming is to make it possible to view the deceased person during funerals or memorial services, allowing friends and family members an opportunity for closure and remembrance. It also enables the body to be transported over long distances without risking health hazards associated with decomposition.

There are different methods of embalming, but all share the common objective of maintaining the dignity and integrity of the deceased while providing a safe and respectful way to handle and display the body.

Phenmetrazine is a stimulant drug that was previously used for the treatment of obesity, but its use has been discontinued in many countries due to its addictive potential and adverse effects. It acts as a central nervous system stimulant, increasing heart rate, blood pressure, and alertness, and decreasing appetite.

The medical definition of Phenmetrazine is:

A psychostimulant drug that has been used in the treatment of obesity but has been discontinued in many countries due to its addictive potential and adverse effects. It is a phenylpropylamine derivative, structurally related to amphetamine and methamphetamine, and acts as a central nervous system stimulant, increasing heart rate, blood pressure, and alertness, and decreasing appetite. Phenmetrazine has sympathomimetic effects, releasing catecholamines from presynaptic nerve endings and blocking their reuptake, resulting in increased concentrations of these neurotransmitters in the synaptic cleft. It also inhibits monoamine oxidase, further increasing the concentration of catecholamines in the brain.

Phenmetrazine is classified as a Schedule II controlled substance in the United States due to its high potential for abuse and dependence. Its use is limited to research purposes only and requires a special license from the Drug Enforcement Administration (DEA).

Cyclobutanes are a class of organic compounds that contain a four-membered carbon ring. The carbons in this ring are bonded to each other in a cyclic arrangement, forming a square-like structure. These compounds can be found naturally or synthesized in the laboratory and play important roles in various chemical reactions and biological processes.

Cyclobutanes are relatively uncommon in nature due to the strain associated with having four carbons in a small ring. This strain makes the molecules more reactive, which can lead to interesting chemical properties. For example, cyclobutanes can undergo ring-opening reactions when exposed to heat or light, leading to the formation of new chemical bonds and the release of energy.

In biology, cyclobutane rings are found in certain types of DNA damage, such as those caused by ultraviolet (UV) radiation. These damages can lead to mutations and may contribute to the development of skin cancer. However, cells have mechanisms for repairing this type of DNA damage, helping to prevent these negative outcomes.

Overall, while cyclobutanes are relatively simple molecules, they have important implications in chemistry and biology, making them a fascinating area of study.

Biogenic monoamines are a type of neurotransmitter, which are chemical messengers that transmit signals in the brain and other parts of the nervous system. They are called "biogenic" because they are derived from biological substances, and "monoamines" because they contain one amine group (-NH2) and are derived from the aromatic amino acids: tryptophan, tyrosine, and phenylalanine.

Examples of biogenic monoamines include:

1. Serotonin (5-hydroxytryptamine or 5-HT): synthesized from the amino acid tryptophan and plays a crucial role in regulating mood, appetite, sleep, memory, and learning.
2. Dopamine: formed from tyrosine and is involved in reward, motivation, motor control, and reinforcement of behavior.
3. Norepinephrine (noradrenaline): also derived from tyrosine and functions as a neurotransmitter and hormone that modulates attention, arousal, and stress responses.
4. Epinephrine (adrenaline): synthesized from norepinephrine and serves as a crucial hormone and neurotransmitter in the body's fight-or-flight response to stress or danger.
5. Histamine: produced from the amino acid histidine, it acts as a neurotransmitter and mediates allergic reactions, immune responses, and regulates wakefulness and appetite.

Imbalances in biogenic monoamines have been linked to various neurological and psychiatric disorders, such as depression, anxiety, Parkinson's disease, and schizophrenia. Therefore, medications that target these neurotransmitters, like selective serotonin reuptake inhibitors (SSRIs) for depression or levodopa for Parkinson's disease, are often used in the treatment of these conditions.

Methylergonovine is a medication that belongs to a class of drugs called ergot alkaloids. It is primarily used to prevent and treat uterine bleeding after childbirth. Medically, it is defined as a semi-synthetic ergopeptide analog with oxytocic properties, which stimulates myometrial contractions and reduces postpartum hemorrhage.

Methylergonovine works by stimulating the smooth muscle of the uterus, causing it to contract. This helps to return the uterus to its pre-pregnancy size and also helps to control bleeding after childbirth. It is important to note that methylergonovine should only be used under the supervision of a healthcare provider, as it can have serious side effects if not used properly.

Mazindol is a prescription medication that belongs to a class of drugs known as sympathomimetic amines or anorectics. It has been used in the treatment of obesity, as it works by reducing appetite and increasing the amount of energy that the body uses. Mazindol affects certain chemicals in the brain that control appetite.

It's important to note that mazindol is not commonly used today due to its potential for abuse and serious side effects. It should only be used under the close supervision of a healthcare provider, and its use is typically reserved for individuals with severe obesity who have not responded to other treatment options.

N-Methyl-3,4-methylenedioxyamphetamine (also known as MDA) is a synthetic psychoactive drug that belongs to the class of amphetamines. It acts as a central nervous system stimulant and hallucinogen. Chemically, it is a derivative of amphetamine with an additional methylenedioxy ring attached to the 3,4 positions on the aromatic ring. MDA is known for its empathogenic effects, meaning that it can produce feelings of empathy, emotional openness, and euphoria in users. It has been used recreationally as a party drug and at raves, but it also has potential therapeutic uses. However, MDA can have serious side effects, including increased heart rate and blood pressure, hyperthermia, dehydration, and in some cases, serotonin syndrome. As with other psychoactive drugs, MDA should only be used under medical supervision and with a clear understanding of its potential risks and benefits.

Fluorine is not a medical term itself, but it is a chemical element that is often discussed in the context of dental health. Here's a brief scientific/chemical definition:

Fluorine is a chemical element with the symbol F and atomic number 9. It is the most reactive and electronegative of all elements. Fluorine is never found in its free state in nature, but it is abundant in minerals such as fluorspar (calcium fluoride).

In dental health, fluoride, which is a compound containing fluorine, is used to help prevent tooth decay. It can be found in many water supplies, some foods, and various dental products like toothpaste and mouthwash. Fluoride works by strengthening the enamel on teeth, making them more resistant to acid attacks that can lead to cavities.

Clomipramine is a tricyclic antidepressant drug that is primarily used to treat obsessive-compulsive disorder (OCD). It works by increasing the levels of certain neurotransmitters, such as serotonin and norepinephrine, in the brain. These neurotransmitters are involved in regulating mood and behavior.

Clomipramine is also used off-label to treat other conditions, including panic disorder, depression, chronic pain, and sleep disorders. It is available as a tablet or capsule and is typically taken one to three times a day. Common side effects of clomipramine include dry mouth, constipation, blurred vision, dizziness, and drowsiness.

As with all medications, clomipramine should be used under the close supervision of a healthcare provider, who can monitor its effectiveness and potential side effects. It is important to follow the dosage instructions carefully and to report any unusual symptoms or concerns to the healthcare provider promptly.

A serotonin receptor, specifically the 5-HT2B receptor, is a type of G protein-coupled receptor (GPCR) that binds to the neurotransmitter serotonin (5-hydroxytryptamine or 5-HT). These receptors are located on the cell membrane of certain cells, including neurons and other cell types in various organs.

The 5-HT2B receptor is involved in a variety of physiological functions, such as regulating mood, appetite, sleep, and sensory perception. In the cardiovascular system, activation of 5-HT2B receptors can lead to the proliferation of cardiac fibroblasts and changes in the extracellular matrix, which may contribute to heart valve abnormalities.

In the central nervous system, 5-HT2B receptors have been implicated in several neurological conditions, including migraine, depression, and schizophrenia. However, their precise roles in these disorders are not yet fully understood.

Pharmacologically targeting 5-HT2B receptors has led to the development of drugs for various indications, such as antimigraine medications (e.g., telcagepant) and potential treatments for heart failure (e.g., mavacamten). However, some 5-HT2B receptor agonists have also been associated with serious side effects, such as valvular heart disease, which has limited their clinical use.

Neurotransmitter uptake inhibitors are a class of drugs that work by blocking the reuptake of neurotransmitters, such as serotonin, norepinephrine, and dopamine, into the presynaptic neuron after they have been released into the synapse. This results in an increased concentration of these neurotransmitters in the synapse, which can enhance their signal transduction and lead to therapeutic effects.

These drugs are commonly used in the treatment of various psychiatric disorders, such as depression, anxiety, and attention deficit hyperactivity disorder (ADHD). They include selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and norepinephrine reuptake inhibitors (NRIs).

It's important to note that while neurotransmitter uptake inhibitors can be effective in treating certain conditions, they may also have potential side effects and risks. Therefore, it is essential to use them under the guidance and supervision of a healthcare professional.

3,4-Methylenedioxyamphetamine (MDA) is a psychoactive drug that belongs to the amphetamine class. It is also known as "ecstasy" or "molly." MDA acts as a stimulant, hallucinogen, and entactogen, which means it can produce feelings of increased energy, emotional warmth, and empathy.

MDA is illegal in many countries, including the United States, due to its potential for abuse and the risk of serious adverse effects. Some of the negative consequences associated with MDA use include nausea, vomiting, muscle tension, teeth grinding, increased heart rate and blood pressure, and hyperthermia (elevated body temperature). In high doses or when used in combination with other substances, MDA can cause seizures, coma, and even death.

It is important to note that the use of illegal drugs like MDA carries significant legal and health risks. If you are concerned about your own or someone else's drug use, it is recommended that you seek help from a qualified healthcare professional.

Phenethylamines are a class of organic compounds that share a common structural feature, which is a phenethyl group (a phenyl ring bonded to an ethylamine chain). In the context of pharmacology and neuroscience, "phenethylamines" often refers to a specific group of psychoactive drugs, including stimulants like amphetamine and mescaline, a classic psychedelic. These compounds exert their effects by modulating the activity of neurotransmitters in the brain, such as dopamine, norepinephrine, and serotonin. It is important to note that many phenethylamines have potential for abuse and are controlled substances.

Sympathomimetic drugs are substances that mimic or stimulate the actions of the sympathetic nervous system. The sympathetic nervous system is one of the two divisions of the autonomic nervous system, which regulates various automatic physiological functions in the body. The sympathetic nervous system's primary function is to prepare the body for the "fight-or-flight" response, which includes increasing heart rate, blood pressure, respiratory rate, and metabolism while decreasing digestive activity.

Sympathomimetic drugs can exert their effects through various mechanisms, including directly stimulating adrenergic receptors (alpha and beta receptors) or indirectly causing the release of norepinephrine and epinephrine from nerve endings. These drugs are used in various clinical settings to treat conditions such as asthma, nasal congestion, low blood pressure, and attention deficit hyperactivity disorder (ADHD). Examples of sympathomimetic drugs include epinephrine, norepinephrine, dopamine, dobutamine, albuterol, pseudoephedrine, and methylphenidate.

It is important to note that sympathomimetic drugs can also have adverse effects, particularly when used in high doses or in individuals with certain medical conditions. These adverse effects may include anxiety, tremors, palpitations, hypertension, arrhythmias, and seizures. Therefore, these medications should be used under the close supervision of a healthcare provider.

Serotonin antagonists are a class of drugs that block the action of serotonin, a neurotransmitter, at specific receptor sites in the brain and elsewhere in the body. They work by binding to the serotonin receptors without activating them, thereby preventing the natural serotonin from binding and transmitting signals.

Serotonin antagonists are used in the treatment of various conditions such as psychiatric disorders, migraines, and nausea and vomiting associated with cancer chemotherapy. They can have varying degrees of affinity for different types of serotonin receptors (e.g., 5-HT2A, 5-HT3, etc.), which contributes to their specific therapeutic effects and side effect profiles.

Examples of serotonin antagonists include ondansetron (used to treat nausea and vomiting), risperidone and olanzapine (used to treat psychiatric disorders), and methysergide (used to prevent migraines). It's important to note that these medications should be used under the supervision of a healthcare provider, as they can have potential risks and interactions with other drugs.

Halofenate is not typically considered a medication with a primary use in modern medical practice. However, historically it has been used as a treatment for gout and hyperuricemia (high levels of uric acid in the blood). It is a compound with both uricosuric and anti-inflammatory properties.

The uricosuric action of halofenate helps to lower serum uric acid levels by increasing its excretion in the urine, while its anti-inflammatory effects may help alleviate symptoms associated with gout attacks. It is important to note that due to its limited use and potential side effects, other medications are often preferred for managing gout and hyperuricemia.

Please consult a healthcare professional or pharmacist for more information about specific medications and treatment options.

A serotonin receptor, specifically the 5-HT1B receptor, is a type of G protein-coupled receptor found in the cell membrane. It binds to the neurotransmitter serotonin (also known as 5-hydroxytryptamine or 5-HT) and plays a role in regulating various physiological functions, including neurotransmission, vasoconstriction, and smooth muscle contraction.

The 5-HT1B receptor is widely distributed throughout the body, but it is particularly abundant in the brain, where it is involved in modulating mood, cognition, and motor control. When serotonin binds to the 5-HT1B receptor, it activates a signaling pathway that ultimately leads to the inhibition of adenylyl cyclase, which reduces the production of cAMP (cyclic adenosine monophosphate) in the cell. This reduction in cAMP levels can have various effects on cellular function, depending on the specific tissue and context in which the 5-HT1B receptor is expressed.

In addition to its role as a serotonin receptor, the 5-HT1B receptor has also been identified as a target for certain drugs used in the treatment of migraine headaches, such as triptans. These medications bind to and activate the 5-HT1B receptor, which leads to vasoconstriction of cranial blood vessels and inhibition of neuropeptide release, helping to alleviate the symptoms of migraines.

Serotonin receptors are a type of cell surface receptor that bind to the neurotransmitter serotonin (5-hydroxytryptamine, 5-HT). They are widely distributed throughout the body, including the central and peripheral nervous systems, where they play important roles in regulating various physiological processes such as mood, appetite, sleep, memory, learning, and cognition.

There are seven different classes of serotonin receptors (5-HT1 to 5-HT7), each with multiple subtypes, that exhibit distinct pharmacological properties and signaling mechanisms. These receptors are G protein-coupled receptors (GPCRs) or ligand-gated ion channels, which activate intracellular signaling pathways upon serotonin binding.

Serotonin receptors have been implicated in various neurological and psychiatric disorders, including depression, anxiety, schizophrenia, and migraine. Therefore, selective serotonin receptor agonists or antagonists are used as therapeutic agents for the treatment of these conditions.

Hydroxyindoleacetic acid (5HIAA) is a major metabolite of the neurotransmitter serotonin, formed in the body through the enzymatic degradation of serotonin by monoamine oxidase and aldehyde dehydrogenase. 5HIAA is primarily excreted in the urine and its measurement can be used as a biomarker for serotonin synthesis and metabolism in the body.

Increased levels of 5HIAA in the cerebrospinal fluid or urine may indicate conditions associated with excessive serotonin production, such as carcinoid syndrome, while decreased levels may be seen in certain neurodegenerative disorders, such as Parkinson's disease. Therefore, measuring 5HIAA levels can have diagnostic and therapeutic implications for these conditions.

Ergolines are a group of ergot alkaloids that have been widely used in the development of various pharmaceutical drugs. These compounds are known for their ability to bind to and stimulate specific receptors in the brain, particularly dopamine receptors. As a result, they have been explored for their potential therapeutic benefits in the treatment of various neurological and psychiatric conditions, such as Parkinson's disease, migraine, and depression.

However, ergolines can also have significant side effects, including hallucinations, nausea, and changes in blood pressure. In addition, some ergot alkaloids have been associated with a rare but serious condition called ergotism, which is characterized by symptoms such as muscle spasms, vomiting, and gangrene. Therefore, the use of ergolines must be carefully monitored and managed to ensure their safety and effectiveness.

Some specific examples of drugs that contain ergolines include:

* Dihydroergotamine (DHE): used for the treatment of migraine headaches
* Pergolide: used for the treatment of Parkinson's disease
* Cabergoline: used for the treatment of Parkinson's disease and certain types of hormonal disorders

It is important to note that while ergolines have shown promise in some therapeutic areas, they are not without their risks. As with any medication, it is essential to consult with a healthcare provider before using any drug containing ergolines to ensure that it is safe and appropriate for an individual's specific needs.

Amphetamines are a type of central nervous system stimulant drug that increases alertness, wakefulness, and energy levels. They work by increasing the activity of certain neurotransmitters (chemical messengers) in the brain, such as dopamine and norepinephrine. Amphetamines can be prescribed for medical conditions such as attention deficit hyperactivity disorder (ADHD) and narcolepsy, but they are also commonly abused for their ability to produce euphoria, increase confidence, and improve performance in tasks that require sustained attention.

Some common examples of amphetamines include:

* Adderall: a combination of amphetamine and dextroamphetamine, used to treat ADHD and narcolepsy
* Dexedrine: a brand name for dextroamphetamine, used to treat ADHD and narcolepsy
* Vyvanse: a long-acting formulation of lisdexamfetamine, a prodrug that is converted to dextroamphetamine in the body, used to treat ADHD

Amphetamines can be taken orally, snorted, smoked, or injected. Long-term use or abuse of amphetamines can lead to a number of negative health consequences, including addiction, cardiovascular problems, malnutrition, mental health disorders, and memory loss.

Tyramine is not a medical condition but a naturally occurring compound called a biogenic amine, which is formed from the amino acid tyrosine during the fermentation or decay of certain foods. Medically, tyramine is significant because it can interact with certain medications, particularly monoamine oxidase inhibitors (MAOIs), used to treat depression and other conditions.

The interaction between tyramine and MAOIs can lead to a hypertensive crisis, a rapid and severe increase in blood pressure, which can be life-threatening if not treated promptly. Therefore, individuals taking MAOIs are often advised to follow a low-tyramine diet, avoiding foods high in tyramine, such as aged cheeses, cured meats, fermented foods, and some types of beer and wine.

Devazepide is not a medical term, but it is a pharmaceutical compound. It is a selective and competitive antagonist of the benzodiazepine site on GABA(A) receptors. This means that devazepide blocks the effects of benzodiazepines by binding to the same site on the GABA(A) receptor without activating it.

Devazepide has been studied in research settings as a potential treatment for alcohol use disorder and anxiety disorders, but it is not currently approved for medical use in any country.

Therefore, there is no official medical definition for 'Devazepide'.

Heart valve diseases are a group of conditions that affect the function of one or more of the heart's four valves (tricuspid, pulmonic, mitral, and aortic). These valves are responsible for controlling the direction and flow of blood through the heart. Heart valve diseases can cause the valves to become narrowed (stenosis), leaky (regurgitation or insufficiency), or improperly closed (prolapse), leading to disrupted blood flow within the heart and potentially causing symptoms such as shortness of breath, fatigue, chest pain, and irregular heart rhythms. The causes of heart valve diseases can include congenital defects, age-related degenerative changes, infections, rheumatic heart disease, and high blood pressure. Treatment options may include medications, surgical repair or replacement of the affected valve(s), or transcatheter procedures.

The fenfluramine REMS requires health care professionals who prescribe fenfluramine and pharmacies that dispense fenfluramine ... Fenfluramine was approved for medical use in the European Union in December 2020. Fenfluramine is a prescription medication in ... In overdose, fenfluramine can cause serotonin syndrome and rapidly result in death. Fenfluramine acts primarily as a serotonin ... Fenfluramine was approved in the United States in 1973. The combination of fenfluramine and phentermine was proposed in 1984. ...
"Fenfluramine". Archived from the original on 27 September 2013. Retrieved 24 September 2013. "Withdrawal of pain medicine ...
Rothman, RB; Elmer, GI; Shippenberg, TS; Rea, W; Baumann, MH (1998). "Phentermine and fenfluramine. Preclinical studies in ...
Anonymous (1997). "Fenfluramine and dexfenfluramine withdrawn. Further cases of valvular heart disease". Current Problems in ... The chiral switches of fluoxetine and fenfluramine are classical examples. The development of (R )-fluoxetine was terminated ... The chiral switch of fenfluramine, dexfenfluramine was withdrawn from world marker due to pulmonary hypertension. The table ... Thompson PD (December 1997). "Valvular heart disease associated with fenfluramine-phentermine". The New England Journal of ...
It is related to fenfluramine. Benfluorex Fludorex Tiflorex Ganellin CR, Triggle DJ (21 November 1996). Dictionary of ...
... fenfluramine-associated; 178600; BMPR2 Pulmonary veno occlusive disease; 265450; BMPR2 Pycnodysostosis; 265800; CTSK Pyogenic ...
... (INN), or (−)-3-trifluoromethyl-N-ethylamphetamine, also known as (−)-fenfluramine or (R)-fenfluramine, is a ... Both fenfluramine and dexfenfluramine are anorectic agents that have been used clinically in the treatment of obesity (and ... Fenfluramine Dexfenfluramine Norfenfluramine Chapman and Hall (1996). Dictionary of Organic Compounds. CRC Press. p. 3141. ISBN ... Ni W, Li MW, Thakali K, Fink GD, Watts SW (May 2004). "The fenfluramine metabolite (+)-norfenfluramine is vasoactive". The ...
Both fenfluramine and benfluorex form norfenfluramine as a metabolite. This side effect led to the withdrawal of fenfluramine ... Fenfluramine, a related drug, had been withdrawn from the market in 1997 after reports of heart valve disease, pulmonary ... fenfluramine-like cardiovascular side effects), are greater than their benefits. Thus Frachon et al. showed a higher rate of ... is an anorectic and hypolipidemic agent that is structurally related to fenfluramine (a substituted amphetamine). It may ...
Sachdev M, Miller WC, Ryan T, Jollis JG (December 2002). "Effect of fenfluramine-derivative diet pills on cardiac valves: a ... The drugs most classically associated with the condition are weight loss drugs such as fenfluramine and chlorphentermine, and ... Hopkins PN, Polukoff GI (June 2003). "Risk of valvular heart disease associated with use of fenfluramine". BMC Cardiovascular ... Some appetite suppressant drugs such as fenfluramine (which in combination with phentermine was marketed as Pondimin and ...
Fenfluramine repurposing from weight loss to epilepsy; what we do and do not know. Pharmacol Ther.226, 107866 (2021). M. Bilaer ... Lorcaserin for Dravet Syndrome- A potential advance over fenfluramine? CNS Drugs, 21:115-122 (2022). "Professor Meir Bialer". ...
In 2020, fenfluramine was approved for the medical treatment in the European Union and the USA. Approaching seizures in adults ... Fintepla, on ema.europa.eu Fintepla (fenfluramine). An overview of Fintepla and why it is authorised in the EU, on ema.europa. ... RCTs are now only available for the drugs fenfluramine (FFA), cannabidiol (CBD), and stiripentol (STP). A North American ...
"Untoward effects of fenfluramine in autistic children". Journal of Clinical Psychopharmacology. 6 (6): 350-355. doi:10.1097/ ... "Fenfluramine treatment of autism: UCLA collaborative study of 81 patients at nine medical centers". Psychopharmacology Bulletin ...
Early anorectics (appetite suppressants) were fenfluramine and phentermine. A more recent addition is sibutramine which ...
"FDA Announces Withdrawal Fenfluramine and Dexfenfluramine (Fen-Phen)". Fda.gov. Retrieved 12 July 2013. Weigle DS (June 2003 ... In 1997, after 24 cases of heart valve disease in fen-phen users, fenfluramine and dexfenfluramine were voluntarily taken off ... Studies later showed nearly 30% of people taking fenfluramine or dexfenfluramine for up to 24 months had abnormal valve ... Phentermine was marketed with fenfluramine or dexfenfluramine as a combination appetite suppressant and fat burning agent under ...
Rothman RB, Ayestas MA, Dersch CM, Baumann MH (August 1999). "Aminorex, fenfluramine, and chlorphentermine are serotonin ... Aminorex Cericlamine Cloforex Clortermine Etolorex Fenfluramine Methylenedioxyphentermine Phentermine Anvisa (2023-03-31). "RDC ... as it has a serotonergic effects profile similar to other withdrawn appetite suppressants such as fenfluramine and aminorex ...
FDA Announces Withdrawal Fenfluramine and Dexfenfluramine (Fen-Phen) "Dexfenfluramine". PubChem. U.S. Library of Medicine. ... It is the d-enantiomer of fenfluramine and is structurally similar to amphetamine, but lacks any psychologically stimulating ... Benfluorex Fenfluramine Levofenfluramine Norfenfluramine Anvisa (24 July 2023). "RDC Nº 804 - Listas de Substâncias ... Drug description Dexfenfluramine hydrochloride Questions and Answers about Withdrawal of Fenfluramine (Pondimin) and ...
Fenfluramine binds to the serotonin transporter, blocking serotonin reuptake. However, fenfluramine also acts to induce non- ... Wang YX, Bowersox SS, Pettus M, Gao D (1999). "Antinociceptive properties of fenfluramine, a serotonin reuptake inhibitor, in a ... Fenfluramine is an indirect agonist of serotonin receptors. ... and the mechanism of fenfluramine neurotoxicity". Ann. N. Y. ... exocytotic serotonin release; in a mechanism similar to that of methamphetamine in dopamine neurons, fenfluramine binds to ...
Tifluorex is claimed to be a more potent anorectic than fenfluramine, with twice its potency in humans and 4 times its potency ... Fenfluramine in particular causes very similar side effects and appetite suppression at therapeutically relevant doses. In rats ... It is structurally related to fenfluramine and 4-MTA. Tiflorex went to phase II clinical trials. The extended release ... Similar compounds such as fenfluramine, norfenfluramine and 4-MTA act as selective serotonin releasing agents and 5-HT2 ...
Cozzi NV, Frescas S, Marona-Lewicka D, Huang X, Nichols DE (March 1998). "Indan analogs of fenfluramine and norfenfluramine ... It functions as a selective serotonin releasing agent (SSRA). ETAI is the aminoindane analogue of fenfluramine and is ...
... as both fenfluramine and benfluorex form norfenfluramine as an active metabolite. It is a human TAAR1 agonist. Fenfluramine ... This side effect led to the withdrawal of fenfluramine as an anorectic agent worldwide, and to the withdrawal of benfluorex in ...
Reimann W, Schneider F (May 1998). "Induction of 5-hydroxytryptamine release by tramadol, fenfluramine and reserpine". European ... which is in accordance with other serotonin releasing agents such as fenfluramine and MDMA. However, two more recent studies ... similar in effect to fenfluramine. The serotonin releasing effects of tramadol could be blocked by sufficiently high ...
... enantiomer of fenfluramine) Etolorex (prodrug of chlorphentermine; never marketed) Fenfluramine (Pondimin, Fen-Phen) Flucetorex ... Fenfluramine, chlorphentermine, and aminorex, which are also amphetamines and relatives, were formerly used as appetite ... enantiomer of fenfluramine) Carbamazepine (Equetro, Epitol, and many other variations) Amiflamine (FLA-336) Viqualine (PK-5078 ...
3-Fluoroethamphetamine 4-Methoxyethamphetamine Fenfluramine Freudenmann RW, Spitzer M (2004). "The Neuropsychopharmacology and ...
Cozzi NV, Frescas S, Marona-Lewicka D, Huang X, Nichols DE (March 1998). "Indan analogs of fenfluramine and norfenfluramine ...
Cozzi NV, Frescas S, Marona-Lewicka D, Huang X, Nichols DE (March 1998). "Indan analogs of fenfluramine and norfenfluramine ...
Fluminorex Fludorex Fenfluramine TFMPP Befiradol J. Elks (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical ...
Reimann W, Schneider F (May 1998). "Induction of 5-hydroxytryptamine release by tramadol, fenfluramine and reserpine". European ...
In 1959, phentermine had been FDA approved and fenfluramine in 1973. The two were no more popular than other medications until ... Dexfenfluramine (Redux) was developed in the mid-1990s as an alternative to fenfluramine with fewer side-effects, and received ... Bachorik L. "FDA Announces Withdrawal Fenfluramine and Dexfenfluramine (Fen-Phen)". U.S. Food and Drug Administration. FDA. ...
Hegadoren KM, Baker GB, Coutts RT, Dewhurst WG (March 1991). "Interactions of iprindole with fenfluramine metabolism in rat ... fenfluramine, phenelzine, tranylcypromine, trimipramine, and fluoxetine, likely via inactivating cytochrome P450 enzymes. It ...
Oxaflozane Befiradol Fenfluramine Fludorex Fluminorex TFMPP Elks J (14 November 2014). The Dictionary of Drugs: Chemical Data: ...
The fenfluramine REMS requires health care professionals who prescribe fenfluramine and pharmacies that dispense fenfluramine ... Fenfluramine was approved for medical use in the European Union in December 2020. Fenfluramine is a prescription medication in ... In overdose, fenfluramine can cause serotonin syndrome and rapidly result in death. Fenfluramine acts primarily as a serotonin ... Fenfluramine was approved in the United States in 1973. The combination of fenfluramine and phentermine was proposed in 1984. ...
... the FDA has approved fenfluramine to treat seizures associated with Dravet syndrome in persons 2 years of age and older. Learn ... The risks of fenfluramine taken during pregnancy are not known. Breastfeeding: No information is available on fenfluramine in a ... Fenfluramine is approved for use:. *In the US, the FDA has approved fenfluramine to treat seizures associated with Dravet ... Importantly, clinical trials of fenfluramine have not found any heart problems, when fenfluramine is used at the doses ...
Find everything you need to know about Fenfluramine, including what it is used for, warnings, reviews, side effects, and ... You should not use fenfluramine if you are allergic to it.. Do not use fenfluramine if you have used an MAO inhibitor in the ... What happens if I overdose on Fenfluramine (Fintepla)?. If you think you or someone else may have overdosed on: Fenfluramine ( ... How to take Fenfluramine (Fintepla)?. Use Fenfluramine (Fintepla) exactly as directed on the label, or as prescribed by your ...
... were randomly assigned to fenfluramine 0.7 mg/kg/day (n = 25 and 62, respectively), fenfluramine 0.2 mg/kg/day (n = 25 and 64 ... Antiseizure Therapy Fenfluramine Continues to Show Pronounced Benefits in Rare, Developmental Epilepsies. September 28, 2023. ... Impact of fenfluramine on drop seizure frequency in adults or dose-capped patients with Lennox-Gastaut syndrome: comparative ... In the open-label extension of the trial, 75% of patients received less than 0.5 mg/kg/day of fenfluramine. Using Wilcoxon rank ...
Cardiac Valvulopathy Associated with Exposure to Fenfluramine or Dexfenfluramine: U.S. Department of Health and Human Services ... Percentage of persons who had received fenfluramine .... Article. Fenfluramine and dexfenfluramine are appetite suppressants ... used fenfluramine alone; 16 (14%), dexfenfluramine alone; 89 (79%), a combination of fenfluramine and phentermine; and six (5 ... Recently, fenfluramine has been widely used both in combination with phentermine (fen-phen) and for periods longer than a few ...
Serotonin releasing agent fenfluramine improves executive function in healthy volunteers: an experimental medicine study ... Serotonin releasing agent fenfluramine improves executive function in healthy volunteers: an experimental medicine study ...
Both fenfluramine dose groups showed significant decreases in generalized tonic-clonic seizures, whereas those on placebo ... In the fenfluramine 0.7- and 0.2-mg/kg/day groups, the estimated median difference in GTC seizure frequency was -50.3% (95% CI ... Full Dataset Shows Fenfluramines Significant Treatment Effect in Lennox-Gastaut Syndrome. May 10, 2022. Marco Meglio ... Also approved for the treatment of Dravet syndrome (DS), in this study of LGS, fenfluramine 0.7 mg/kg/day resulted in a median ...
Post your question or story about Fenfluramine and connect with others who have experience with the same medications. No ... Recently active Fenfluramine forums and community discussion threads. ... Home › Drugs: F › Fenfluramine › Discussions Fenfluramine Forums. Recently active Fenfluramine forums and community discussion ... Fenfluramine availability Does anyone know about the availability of fenfluramine? I would like to purchase fenfluramine. ## I ...
Fenfluramine Fenfluramine is indicated for treatment of seizures associated with Dravet syndrome in patients aged 2 years and ... Fenfluramine hydrochloride for the treatment of seizures in Dravet syndrome: a randomised, double-blind, placebo-controlled ... Fenfluramine for treatment-resistant seizures in patients with Dravet syndrome receiving stiripentol-inclusive regimens: a ... Fenfluramine and its metabolite, norfenfluramine, increase extracellular levels of serotonin through interaction with serotonin ...
Fenfluramine and cerebral glucose. Biol Psychiatry. 1992 Jun 01; 31(11):1173-4. ...
A new publication on the efficacy of Fenfluramine was issued recently in Epilepsia, acknowledging how the registry RESIDRAS can ... New study on Fenfluramine using Residras registry. Posted at 23:11h in News, Specialist Area by DSEF ... The study concludes that after administering Fenfluramine to 52 patients, 53% of them had a reduction in seizures of at least ... A new publication on the efficacy of Fenfluramine was issued recently in Epilepsia, acknowledging how the registry RESIDRAS can ...
Fintepla Fenfluramine. Sale! $191.03. $175.97. Add to cart. Sort by popularity. Sort by latest. Sort by price: low to high. ...
Fintepla Fenfluramine. Sale! $191.03. $175.97. Add to cart. Sort by popularity. Sort by latest. Sort by price: low to high. ...
... fenfluramine hydrochloride;Formulanor is C12H17ClF3N;Synonyms (+)-Fenfluramine hydrochloride;More Molecular information Lookup ... Synonyms:(+)-Fenfluramine hydrochloride Molecular Weight:267.718. Tags: (+)-Fenfluramine hydrochloride, (S)-fenfluramine ... S)-fenfluramine hydrochloride. Cas No,Cas Number,CAS Registry Number:3239-45-0 .. Chemical Name,Molecular Name:(S)-fenfluramine ...
Dive into the research topics of Timing of neuroendocrine responses and effect of m-CPP and fenfluramine plasma levels in OCD ... Timing of neuroendocrine responses and effect of m-CPP and fenfluramine plasma levels in OCD. ...
... d-fenfluramine (d-FEN), in ten healthy male volunteers. Pindolol pretreatment lowered baseline PRL levels but, when this effect ... Adult, Dose-Response Relationship, Drug, Double-Blind Method, Fenfluramine, Humans, Male, Middle Aged, Pindolol, Prolactin, ... d-fenfluramine (d-FEN), in ten healthy male volunteers. Pindolol pretreatment lowered baseline PRL levels but, when this effect ...
Fenfluramine damage to the brain and mind. *April 21, 1998. */ Admin. */ children-articles,psychiatry-racism-coercion-and- ...
Fenfluramine-induced loss of serotonin transporters in baboon brain visualized with PET. In: Synapse. 1996 ; Vol. 24, No. 4. pp ... Fenfluramine-induced loss of serotonin transporters in baboon brain visualized with PET. / Scheffel, Ursula; Szabo, Zsolt; ... Fenfluramine-induced loss of serotonin transporters in baboon brain visualized with PET. Synapse. 1996 Dec;24(4):395-398. doi: ... keywords = "Fenfluramine, Neurotoxicity, Positron Emission Tomography, Serotonin",. author = "Ursula Scheffel and Zsolt Szabo ...
N2 - Fenfluramine therapy has been reported to improve behavior in infantile autism and has been associated with a decrease in ... AB - Fenfluramine therapy has been reported to improve behavior in infantile autism and has been associated with a decrease in ... Fenfluramine therapy has been reported to improve behavior in infantile autism and has been associated with a decrease in ... abstract = "Fenfluramine therapy has been reported to improve behavior in infantile autism and has been associated with a ...
Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
Detailed drug Information for Duo-Vil 2-25. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
a. Fenfluramine. For this compound, the term isomer includes the optical, positional, or geometric isomer. ...
This medicine comes with a patient information insert. Read and follow these instructions carefully. Ask your doctor or pharmacist if you have any questions. The solution comes in small containers that are only used one time. Throw the empty container away after putting the medicine into your ear(s). This medicine should be used only inside the ear. Do not put it in the eyes or nose, and do not take it by mouth. If this medicine is swallowed by accident or gets into your eyes, call your doctor right away. It is important that the infected ear remain clean and dry. When bathing, avoid getting the infected ear wet. Avoid swimming unless your doctor has instructed you otherwise. To use the ear drops:. ...
Detailed drug Information for Xolox. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
Assessing the effects of fenfluramine, quipazine and d-amphetamine on self-control in pigeons. / Woods, J. H.; Reilly, Mark P. ... Woods, J. H., & Reilly, M. P. (1998, May). Assessing the effects of fenfluramine, quipazine and d-amphetamine on self-control ... Woods, JH & Reilly, MP 1998, Assessing the effects of fenfluramine, quipazine and d-amphetamine on self-control in pigeons.. ... Dive into the research topics of Assessing the effects of fenfluramine, quipazine and d-amphetamine on self-control in pigeons ...
97-1, repealed paragraph (4)(w) effective upon the removal of fenfluramine from the schedules of controlled substances in 21 C. ... Drug Enforcement Administration of the United States Department of Justice filed a proposed final rule removing fenfluramine ... 97-1, added paragraph (4)(w) listing fenfluramine. Section 5, ch. ...
Activation of central melanocortin pathways by fenfluramine. Science 2002; 297: 609-611. ...
MDMA, PMA, Fenfluramine & AMT. Difficult Experiences. [6]. Ecstacy Nightmare. Ska Girl. PMA (sold as Ecstasy). ...
IN-VIVO EVIDENCE THAT D-FENFLURAMINE RELEASES 5-HT FROM NERVE-TERMINALS OF BOTH THE DORSAL AND MEDIAN RAPHE NUCLEI ... IN-VIVO EVIDENCE THAT D-FENFLURAMINE RELEASES 5-HT FROM NERVE-TERMINALS OF BOTH THE DORSAL AND MEDIAN RAPHE NUCLEI ...
  • Fenfluramine, sold under the brand name Fintepla, is a serotonergic medication used for the treatment of seizures associated with Dravet syndrome and Lennox-Gastaut syndrome. (wikipedia.org)
  • Fenfluramine is the generic name (non-brand name) of a seizure medicine with the brand name Fintepla® from Zogenix. (epilepsy.com)
  • What is Fenfluramine (Fintepla) used for? (everydayhealth.com)
  • Can I take Fenfluramine (Fintepla) if I'm pregnant or breastfeeding? (everydayhealth.com)
  • Use Fenfluramine (Fintepla) exactly as directed on the label, or as prescribed by your doctor. (everydayhealth.com)
  • At the recently concluded 35th International Epilepsy Congress (IEC), held September 2-6, in Dublin, Ireland, UCB Pharma presented several posters showcasing the clinical benefits of Fintepla (fenfluramine) across multiple forms of epilepsy, including rare epileptic disorders such as Dravet syndrome (DS), Lennox-Gastaut syndrome (LGS), and cyclin-dependent kinase-like 5 (CDKL5) deficiency disorder. (ajmc.com)
  • The effects of fenfluramine in children are as described above. (epilepsy.com)
  • If you are pregnant, your name may be listed on a pregnancy registry to track the effects of fenfluramine on the baby. (everydayhealth.com)
  • Fenfluramine acts as a serotonin releasing agent, agonist of the serotonin 5-HT2 receptors, and σ1 receptor positive modulator. (wikipedia.org)
  • Since fenfluramine and its active metabolite norfenfluramine stimulate serotonin receptors, this may have led to the valvular abnormalities found in patients using fenfluramine. (wikipedia.org)
  • Use of these medications together with fenfluramine can increase the risk of a potentially serious reaction called serotonin syndrome. (epilepsy.com)
  • An interaction with fenfluramine could cause a serious condition called serotonin syndrome. (everydayhealth.com)
  • The present study sought to determine whether or not Positron Emission Tomography (PET) with the newly developed positron emitting serotonin (5-HT) transporter ligand, (+)[ 11 C]McN-5652, could be used to detect fenfluramine- induced 5-HT neurotoxicity in the brain of living primates (baboons). (johnshopkins.edu)
  • Fenfluramine therapy has been reported to improve behavior in infantile autism and has been associated with a decrease in abnormally increased blood serotonin content. (elsevierpure.com)
  • Fenfluramine is indicated for the treatment of seizures associated with Dravet syndrome and Lennox-Gastaut syndrome in people age two and older. (wikipedia.org)
  • In the US, the FDA has approved fenfluramine to treat seizures associated with Dravet syndrome and Lennox-Gastaut syndrome in persons 2 years of age and older. (epilepsy.com)
  • Fenfluramine is used to treat seizures caused by Dravet syndrome and Lennox-Gastaut syndrome in people at least 2 years old. (everydayhealth.com)
  • Both fenfluramine dose groups showed significant decreases in generalized tonic-clonic seizures, whereas those on placebo showed worsening of their condition. (neurologylive.com)
  • Additionally, a subgroup analysis showed that fenfluramine was highly effective in reducing the frequency of generalized tonic-clonic seizures (GTCs) in nearly 50% of patients. (neurologylive.com)
  • The study concludes that after administering Fenfluramine to 52 patients, 53% of them had a reduction in seizures of at least or over 75%, while 11.1% were seizure-free. (dravet.eu)
  • The authors of "Efficacy and safety of Fenfluramine hydrochloride for the treatment of seizures in Dravet syndrome: A real-world study" - Specchio et al. (dravet.eu)
  • Although there are differences in antiseizure activity and pharmacokinetics among the enantiomers of fenfluramine and norfenfluramine, all compounds tested are effective in protecting against MES-induced seizures in rodents. (austin.org.au)
  • Fenfluramine and dexfenfluramine are appetite suppressants that were in widespread use in the United States. (cdc.gov)
  • Subsequently, reports of fenfluramine- or dexfenfluramine-associated valvulopathy increased. (cdc.gov)
  • Therefore, in this analysis, a case of fenfluramine- or dexfenfluramine-associated cardiac valvulopathy was defined as documented AR of mild or greater severity and/or MR of moderate or greater severity after exposure to these drugs. (cdc.gov)
  • In early September, FDA received echocardiographic reports from five independent, unpublished echocardiographic prevalence surveys of patients who had received dexfenfluramine or fenfluramine alone or in combination with phentermine ( Table 1 ). (cdc.gov)
  • Fenfluramine and its active metabolite norfenfluramine affect the 5-HT2B receptors, which are plentiful in human cardiac valves. (wikipedia.org)
  • Comparative Activity of the Enantiomers of Fenfluramine and Norfenfluramine in Rodent Seizure Models, and Relationship with their Concentrations in Plasma and Brain. (austin.org.au)
  • To investigate the comparative antiseizure activity of the individual enantiomers of fenfluramine and its major active primary metabolite norfenfluramine in rodent seizure models, and its relationship with the pharmacokinetics of these compounds in plasma and brain. (austin.org.au)
  • The antiseizure potency of d,l-fenfluramine (racemic fenfluramine) was compared with the respective potencies of its individual enantiomers and the individual enantiomers of norfenfluramine using the maximal electroshock (MES) test in rats and mice, and the 6-Hz 44 mA test in mice. (austin.org.au)
  • In the light of the evidence linking the d-enantiomers to cardiovascular and metabolic adverse effects, these data suggest that l-fenfluramine and l-norfenfluramine are potentially attractive candidates for a chiral switch approach leading to development of a novel, enantiomerically-pure antiseizure medication. (austin.org.au)
  • The dose of fenfluramine used in this study (5 mg/kg) is known to produce 5-HT neurotoxicity in primates, and to be approximately two times higher than a dose of fenfluramine reported to produce small and inconsistent weight loss in baboons (2 mg/kg). (johnshopkins.edu)
  • Also approved for the treatment of Dravet syndrome (DS) , in this study of LGS, fenfluramine 0.7 mg/kg/day resulted in a median reduction of 26.5% in MDSF compared with 14.2% reduction in the 0.2-mg/kg/day group and 7.6% reduction in the placebo group. (neurologylive.com)
  • p-Chloroamphetamine (PCA), 3,4-methylenedioxy-methamphetamine (MDMA) and d-fenfluramine pretreatment attenuates d-fenfluramine-evoked release of 5-HT in vivo. (ox.ac.uk)
  • Previous work has suggested that repeated treatment with substituted amphetamines including PCA, MDMA and d-fenfluramine produces a persistent neurodegeneration which is relatively selective for the fine serotoninergic terminals arising from the dorsal raphe nucleus. (ox.ac.uk)
  • The aim of the present study was to investigate whether the acute releasing effect of d-fenfluramine might also be sensitive to lesions produced by PCA, MDMA and d-fenfluramine itself. (ox.ac.uk)
  • Basal and 5-HT release evoked by d-fenfluramine or 100 mM KCl was measured by microdialysis in frontal or parietal cortex of rats 2 weeks after they had been treated with a neurodegenerative regime of PCA, MDMA, d-fenfluramine, or vehicle. (ox.ac.uk)
  • MDMA (20 mg/kg x 8) and d-fenfluramine (1.25 mg/kg x 8) pretreatment reduced d-fenfluramine-evoked release of 5-HT in frontal cortex by 45.2% and 72.0%, respectively. (ox.ac.uk)
  • Overall, the present data are consistent with the hypothesis that the acute release of 5-HT evoked by d-fenfluramine occurs via those terminals destroyed by pretreatment with PCA, MDMA and d-fenfluramine, while KCl evokes release from both PCA-sensitive and PCA-insensitive terminals. (ox.ac.uk)
  • As part of the REMS requirements, prescribers and patients must adhere to the required cardiac monitoring with echocardiograms to receive fenfluramine. (wikipedia.org)
  • However, persons taking fenfluramine should undergo regular heart follow-up with echocardiograms. (epilepsy.com)
  • Fenfluramine is usually started at a dose of 0.2 mg/kg/day divided into 2 equal doses and may be increased by 0.2 mg/kg/d every 4 days to a maximum dose of 0.7 mg/kg/d (maximum 25.9 mg/day). (epilepsy.com)
  • The dose should be reduced in patients on stiripentol, as co-therapy with stiripentol increases the blood levels of fenfluramine. (epilepsy.com)
  • If using with stiripentol, the fenfluramine should be started at 0.2 mg/kg/d and increased gradually as needed over approximately 3 weeks to a maximum dose of 0.4 mg/kg/day (to a maximum 17 mg/day). (epilepsy.com)
  • These results suggest that PET imaging with (+)[ 11 C]McN- 5652 will be useful for evaluating the 5-HT neurotoxic potential of fenfluramine and related drugs in living humans. (johnshopkins.edu)
  • In the randomized controlled trial, 76 adults (aged 18-35 years) and 187 children/adolescents (aged 2-17 years) were randomly assigned to fenfluramine 0.7 mg/kg/day (n = 25 and 62, respectively), fenfluramine 0.2 mg/kg/day (n = 25 and 64), or placebo (n = 26 and 61). (ajmc.com)
  • Study 1601 was a double-blind, placebo-controlled, parallel-group trial that included 263 patients aged 2 to 35 years with LGS who were randomly assigned to either fenfluramine 0.7 mg/kg/day (n = 87), fenfluramine 0.2 mg/kg/day (n = 89), or placebo (n = 87). (neurologylive.com)
  • The suggested mechanism by which fenfluramine causes damage is through over or inappropriate stimulation of these receptors leading to inappropriate valve cell division. (wikipedia.org)
  • Fenfluramine works by binding to serotonergic receptors, as well as by positively modulating a receptor called sigma 1, which itself further modulates how brain cells communicate with each other. (epilepsy.com)
  • Effect of pindolol on the prolactin response to d-fenfluramine. (ox.ac.uk)
  • We studied the effect of the 5-HT1A receptor antagonist, pindolol, on the prolactin (PRL) response to the 5-HT releasing agent, d-fenfluramine (d-FEN), in ten healthy male volunteers. (ox.ac.uk)
  • The significance of these results for the interpretation of neuroendocrine data from d-fenfluramine challenge tests is discussed. (ox.ac.uk)
  • Importantly, clinical trials of fenfluramine have not found any heart problems, when fenfluramine is used at the doses prescribed. (epilepsy.com)
  • Previously, fenfluramine was used in much higher doses, and in combination with another medication called phentermine for weight loss. (epilepsy.com)
  • All told, the primary end point was met, with a 19.9% estimated mean difference (95% CI, -31.0 to -8.7) in monthly drop seizure frequency reduction (MDSF) between the fenfluramine 0.7-mg/kg/day group and placebo ( P = .001), while the 0.2-mg/kg/day group reported an estimated mean difference of 10.5% (95% CI, -25.0 to 4.0) in MDSF reduction compared with placebo ( P = .09). (neurologylive.com)
  • In total, 25% of patients in the fenfluramine 0.7-mg/kg/day group achieved at least a 50% response compared with 10% of those on placebo ( P = .02). (neurologylive.com)
  • There have been reports associating chronic fenfluramine treatment with emotional instability, cognitive deficits, depression, psychosis, exacerbation of pre-existing psychosis (schizophrenia), and sleep disturbances. (wikipedia.org)
  • Fenfluramine was formerly used as an appetite suppressant in the treatment of obesity, but was withdrawn for this use due to cardiovascular toxicity. (wikipedia.org)
  • Six PET imaging studies were performed: three before treatment with fenfluramine (5 mg/kg, s.c., twice daily for 4 days) and three after (18, 45, and 81 days after treatment). (johnshopkins.edu)
  • Following fenfluramine treatment, marked lasting reductions in regional brain specific binding of (+)[ 11 C]McN-5652 were found by means of PET. (johnshopkins.edu)
  • Beta-endorphin-like immunoreactivity was determined in lumbar cerebrospinal fluid of patients during and before or after treatment with fenfluramine and then was compared to normal controls. (elsevierpure.com)
  • 005) and was reduced toward control values during fenfluramine treatment. (elsevierpure.com)
  • The results are consistent with a role for beta-endorphin in infantile autism and in the mechanism of fenfluramine treatment. (elsevierpure.com)
  • The U.S. Food and Drug Administration (FDA) fenfluramine labeling includes a boxed warning stating the drug is associated with valvular heart disease (VHD) and pulmonary arterial hypertension (PAH). (wikipedia.org)
  • The distinctive valvular abnormality seen with fenfluramine is a thickening of the leaflet and chordae tendineae. (wikipedia.org)
  • On July 8, 1997, 24 cases of valvular heart disease in women who had been treated with fenfluramine and phentermine were publicly reported (1). (cdc.gov)
  • Fenfluramine was developed in the early 1960s and was first introduced for medical use as an appetite suppressant in France in 1963 followed by approval in the United States in 1973. (wikipedia.org)
  • Do not use fenfluramine if you have used an MAO inhibitor in the past 14 days. (everydayhealth.com)
  • Fenfluramine was used for weight loss both alone under the brand name Pondimin and in combination with phentermine. (wikipedia.org)
  • Fenfluramine was previously a schedule IV controlled substance in the United States. (wikipedia.org)
  • Ensure your healthcare provider knows what other medications are being taken together with fenfluramine. (epilepsy.com)
  • Post your question or story about Fenfluramine and connect with others who have experience with the same medications. (medschat.com)
  • Effect of d-fenfluramine on human experimental anxiety. (bvsalud.org)
  • The fenfluramine REMS requires health care professionals who prescribe fenfluramine and pharmacies that dispense fenfluramine to be specially certified in the fenfluramine REMS and that patients be enrolled in the REMS. (wikipedia.org)
  • Most patients (70.6%) experienced GTCS or TCS at baseline, and fenfluramine was typically initiated at 0.2 mg/day and titrated per protocol or through physician discretion. (ajmc.com)
  • In addition, 5 studies reported more than half of patients were GTCS free after fenfluramine. (ajmc.com)
  • Such behavior is possible but rare with fenfluramine. (epilepsy.com)
  • Beta-endorphin is involved in the anorexic effect of fenfluramine and may play a role in autism. (elsevierpure.com)
  • Because of the risks of VHD and PAH, fenfluramine is available only through a restricted drug distribution program, under a risk evaluation and mitigation strategy (REMS). (wikipedia.org)
  • A new publication on the efficacy of Fenfluramine was issued recently in Epilepsia, acknowledging how the registry RESIDRAS can serve as a useful tool for systematic data collection to carry out new analyses. (dravet.eu)
  • Recently active Fenfluramine forums and community discussion threads. (medschat.com)
  • The time course of seizure protection in rats was compared with the concentration profiles of d-fenfluramine, l-fenfluramine and their primary active metabolites in plasma and brain. (austin.org.au)
  • Both d- and l-fenfluramine were absorbed and distributed rapidly to the brain, suggesting that seizure protection at early time points (≤2 h) was mainly related to the parent compound. (austin.org.au)
  • Fenfluramine is best taken with food to reduce the chance of stomach upset. (epilepsy.com)
  • Fenfluramine can affect weight or growth in children. (everydayhealth.com)
  • Nine children with infantile autism were treated with fenfluramine in double-blind, placebocrossover design. (elsevierpure.com)
  • Does anyone know about the availability of fenfluramine? (medschat.com)

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