A centrally active muscarinic antagonist that has been used in the symptomatic treatment of PARKINSON DISEASE. Benztropine also inhibits the uptake of dopamine.
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.
A thioxanthene with therapeutic actions similar to the phenothiazine antipsychotics. It is an antagonist at D1 and D2 dopamine receptors.
Sodium chloride-dependent neurotransmitter symporters located primarily on the PLASMA MEMBRANE of dopaminergic neurons. They remove DOPAMINE from the EXTRACELLULAR SPACE by high affinity reuptake into PRESYNAPTIC TERMINALS and are the target of DOPAMINE UPTAKE INHIBITORS.
N-methyl-8-azabicyclo[3.2.1]octanes best known for the ones found in PLANTS.
Drugs that block the transport of DOPAMINE into axon terminals or into storage vesicles within terminals. Most of the ADRENERGIC UPTAKE INHIBITORS also inhibit dopamine uptake.
An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake.

Developing hypothalamic dopaminergic neurones as potential targets for environmental estrogens. (1/48)

Environmental chemicals which mimic the actions of estrogen have the potential to affect any estrogen responsive tissue. The aim of the present study was to investigate their potential to mimic the effects of 17beta-estradiol (E2) on developing primary rat hypothalamic dopaminergic (DA) neurones maintained in a chemically defined medium. We now show that both E2 and octylphenol (OP), but not the non-aromatizable androgen, dihydrotestosterone, enhanced the uptake of [3H]DA by the cultured cells, whereas they had no effect on the uptake of [14C]GABA. Although the sensitivity of responses may change with the age of the developing cultures, the dose response curves for E2 and OP were typically 'bell-shaped', with a rise in response followed by a decline to control levels with increasing concentrations. Effects were seen as low as 10(-14) M for E2 and 10(-11) M for OP. Responses to E2 (10(-12) M) and OP (10(-9) M) were reversed in the presence of the antiestrogen, ZM 182780 (10(-5) M). This study thus provides direct evidence, using a mechanistic rather than toxicological end-point, in support of the hypothesis that inappropriate exposure to environmental estrogens at critically sensitive stages of development, could potentially perturb the organisational activities of estrogen on selected neuronal populations in the CNS.  (+info)

Behavioral and neurochemical effects of the dopamine transporter ligand 4-chlorobenztropine alone and in combination with cocaine in vivo. (2/48)

The current studies evaluated the novel diphenylmethoxytropane analog 4-chlorobenztropine (4-Cl-BZT), cocaine, and combinations of the two drugs for their abilities to stimulate locomotor activity, produce cocaine-like discriminative stimulus effects, and elevate extracellular dopamine (DA) in the nucleus accumbens (NAc) as measured by in vivo microdialysis. Peripherally administered cocaine was approximately twice as efficacious as 4-Cl-BZT as a locomotor stimulant and was behaviorally active at a lower dose than was 4-Cl-BZT. Cocaine also was more efficacious than 4-Cl-BZT in producing discriminative-stimulus effects in rats trained to discriminate i.p. injections of 10 mg/kg cocaine from saline. The time course of behavioral activation differed markedly between the two drugs, with much shorter onset and duration of locomotor stimulant effects for cocaine relative to 4-Cl-BZT. Similarly, i.p. cocaine (10 and 40 mg/kg) induced a pronounced, rapid, and short-lived increase in DA in the NAc, whereas i.p. 4-Cl-BZT was effective only at the higher dose and produced a more gradual, modest, and sustained (>/=2 h) elevation in accumbens DA. In contrast to i.p. administration, local infusion of 4-Cl-BZT (1-100 microM) into the NAc through the microdialysis probe elevated extracellular DA to a much greater extent than did local cocaine (nearly 2000% of baseline maximally for 4-Cl-BZT versus 400% of baseline for cocaine) and displayed a much longer duration of action than cocaine. However, when microinjected bilaterally into the NAc at 30 or 300 nmol/side, cocaine remained a more efficacious locomotor stimulant than 4-Cl-BZT. Finally, pretreatment with i.p. 4-Cl-BZT dose dependently enhanced the locomotor stimulant, discriminative stimulus effects, and NAc DA response to a subsequent low-dose i.p. cocaine challenge. The diphenylmethoxytropane analog also facilitated the emergence of stereotyped behavior and convulsions induced by high-dose cocaine. The current results demonstrate that DA transporter ligands that do not share the neurochemical and behavioral profiles of cocaine nevertheless may enhance the effects of cocaine in vivo.  (+info)

The uptake inhibitors cocaine and benztropine differentially alter the conformation of the human dopamine transporter. (3/48)

The binding affinity of the cocaine analog [(3)H]2 beta-carbomethoxy-3beta-(4-fluorophenyl) tropane (WIN) for the dopamine transporter (DAT) is increased by the reaction of Cys-90, at the extracellular end of the first transmembrane segment, with methanethiosulfonate (MTS) reagents. Cocaine enhances the reaction of Cys-90 with the sulfhydryl reagents, thereby augmenting the increase in binding. In contrast, cocaine decreases the reaction of Cys-135 and Cys-342, endogenous cysteines in cytoplasmic loops, with MTS reagents. Because this reaction inhibits [(3)H]WIN binding, cocaine protects against the loss of binding caused by reaction of these cysteines. In the present work, we compare the abilities of DAT inhibitors and substrates to affect the reaction of Cys-90, Cys-135, and Cys-342 with MTS ethyltrimethylammonium (MTSET). The results indicate that the different abilities of compounds to protect against the MTSET-induced inhibition of binding are attributable to differences in their abilities to attenuate the inhibitory effects of modification of Cys-135 and Cys-342 as well as to enhance the reaction with Cys-90 and the resulting potentiation of binding. The inhibitor benztropine was unique in its inability to protect Cys-135. Moreover, whereas cocaine, WIN, mazindol, and dopamine enhanced the reaction of Cys-90 with MTSET, benztropine had no effect on this reaction. These two features combine to give benztropine its weak potency in protecting ligand binding to wild-type DAT from MTSET. These results indicate that different inhibitors of DAT, such as cocaine and benztropine, produce different conformational changes in the transporter. There are differences in the psychomotor stimulant-like effects of these compounds, and it is possible that the different behavioral effects of these DAT inhibitors stem from their different molecular actions on DAT.  (+info)

Neuroleptic effects on autonomic activity in schizophrenia: between-group and within-subject paradigms and comparisons with controls. (4/48)

Effects of fluphenazine on electrodermal activity (EDA) and heart rate (HR) were studied in patients with schizophrenia and normal control subjects during rest periods, presentation of innocuous tones, and a reaction time (RT) task. Two types of analyses were used: (1) between-group analyses-patients taking placebo were compared with patients taking fluphenazine and with control subjects using only data from the first test session; and (2) within-subject analyses-the same patients were tested when taking fluphenazine and when taking placebo. Results showed higher resting EDA and HR and smaller increments to task performance in placebo patients than in control subjects. Fluphenazine attenuated EDA levels but not the tonic response. Fluphenazine attenuated the HR response but did not affect HR level. Placebo patients were electrodermally hyporesponsive to the RT stimuli but not to simple tones. Fluphenazine markedly attenuated responsivity to simple tones but it attenuated responsivity less for RT stimuli. Testing medicated patients may thus produce misleading results with respect to many, but not all, purported autonomic markers of diagnosis in schizophrenia studies.  (+info)

Gene expression deficits in a subclass of GABA neurons in the prefrontal cortex of subjects with schizophrenia. (5/48)

Markers of inhibitory neurotransmission are altered in the prefrontal cortex (PFC) of subjects with schizophrenia, and several lines of evidence suggest that these alterations may be most prominent in the subset of GABA-containing neurons that express the calcium-binding protein, parvalbumin (PV). To test this hypothesis, we evaluated the expression of mRNAs for PV, another calcium-binding protein, calretinin (CR), and glutamic acid decarboxylase (GAD67) in postmortem brain specimens from 15 pairs of subjects with schizophrenia and matched control subjects using single- and dual-label in situ hybridization. Signal intensity for PV mRNA expression in PFC area 9 was significantly decreased in the subjects with schizophrenia, predominantly in layers III and IV. Analysis at the cellular level revealed that this decrease was attributable principally to a reduction in PV mRNA expression per neuron rather than by a decreased density of PV mRNA-positive neurons. In contrast, the same measures of CR mRNA expression were not altered in schizophrenia. These findings were confirmed by findings from cDNA microarray studies using different probes. Across the subjects with schizophrenia, the decrease in neuronal PV mRNA expression was highly associated (r = 0.84) with the decrease in the density of neurons containing detectable levels of GAD67 mRNA. Furthermore, simultaneous detection of PV and GAD67 mRNAs revealed that in subjects with schizophrenia only 55% of PV mRNA-positive neurons had detectable levels of GAD67 mRNA. Given the critical role that PV-containing GABA neurons appear to play in regulating the cognitive functions mediated by the PFC, the selective alterations in gene expression in these neurons may contribute to the cognitive deficits characteristic of schizophrenia.  (+info)

Evaluation of the blood-brain barrier transport, population pharmacokinetics, and brain distribution of benztropine analogs and cocaine using in vitro and in vivo techniques. (6/48)

The N-substituted 3alpha-[bis(4'-fluorophenyl)methoxy]tropanes (AHN 2-003, AHN 1-055, AHN 2-005, and JHW 007) bind with high affinity to the dopamine transporter and inhibit dopamine uptake more potently than cocaine, but they demonstrate behavioral profiles in animal models of psychostimulant abuse that are unlike that of cocaine. The objective of this study was to characterize the in vitro permeability, brain distribution, and pharmacokinetics of the benztropine (BZT) analogs. Transport studies of cocaine and the BZT analogs (10-4 M) were conducted across bovine brain microvessel endothelial cells. Male Sprague-Dawley rats (approximately 300 g) were administered BZT analogs (10 mg/kg) or cocaine (5 mg/kg) via the tail vein. Blood and brain samples were collected over 36 h and assayed using UV-high-performance liquid chromatography. Transport of both AHN 1-055 (2.15 x 10-4 cm/s) and JHW 007 (2.83 x 10-4 cm/s) was higher (p < 0.05) than that of cocaine (1.63 x 10-4 cm/s). The volume of distribution (12.3-30.5 l/kg) of the analogs was significantly higher than cocaine (0.9 l/kg). The BZT analogs displayed a > or =8-fold higher elimination half-life (4.12-16.49 h) compared with cocaine (0.49 h). The brain-to-plasma partition coefficients were at least two-fold higher for the BZTs versus cocaine, except for AHN 2-003. The BZT analogs are highly permeable across the blood-brain barrier and possess a pharmacokinetic profile different from that of cocaine. These characteristics, in addition to their distinctive behavioral profiles, suggest that the BZT analogs may be promising candidates for the treatment of cocaine abuse.  (+info)

Effects of N-substituted analogs of benztropine: diminished cocaine-like effects in dopamine transporter ligands. (7/48)

Previous studies demonstrated that analogs of benztropine (BZT) possess high affinity for the dopamine transporter, inhibit dopamine uptake, but generally have behavioral effects different from those of cocaine. One hypothesis is that muscarinic-M(1) receptor actions interfere with cocaine-like effects. Several tropane-nitrogen substitutions of 4',4"-diF-BZT have reduced M(1) affinity compared with the CH(3)-analog (AHN 1-055; 3alpha-[bis-(4-fluorophenyl)methoxy]tropane). All of the compounds displaced [(3)H]WIN 35,428 (2beta-carbomethoxy-3beta-(4-fluorophenyl)tropane) binding with affinities ranging from 11 to 108 nM. Affinities at norepinephrine ([(3)H]nisoxetine) and serotonin ([(3)H]citalopram) transporters ranged from 457 to 4810 and 376 to 3260 nM, respectively, and at muscarinic M(1) receptors ([(3)H]pirenzepine) from 11.6 (AHN 1-055) to higher values, reaching 1030 nM for the other BZT-analogs. Cocaine and AHN 1-055 produced dose-related increases in locomotor activity in mice, with AHN 1-055 less effective than cocaine. The other compounds were ineffective in stimulating activity. In rats discriminating cocaine (29 micromol/kg i.p.) from saline, WIN 35,428 fully substituted for cocaine, whereas AHN 1-055 produced a maximal substitution of 79%. None of the other analogs fully substituted for cocaine. WIN 35,428 produced dose-related leftward shifts in the cocaine dose-effect curve, whereas selected BZT analogs produced minimal changes in the effects of cocaine. The results suggest that reducing M(1) affinity of 4',4"-diF-BZT with N-substitutions reduces effectiveness in potentiating the effects of cocaine. Furthermore, although the BZT-analogs bind with high affinity at the dopamine transporter, their behavioral effects differ from those of cocaine. These compounds have reduced efficacy compared with cocaine, a long duration of action, and may serve as leads for the development of medications to treat cocaine abuse.  (+info)

Analogue functional analysis of movements associated with tardive dyskinesia. (8/48)

We studied whether movements associated with tardive dyskinesia (TD) served operant functions in 2 men with developmental disabilities. We found that TD-related movements occurred more frequently in the alone and attention conditions and less frequently in control and demand conditions. Our findings suggest that TD-related movements may not be maintained by social reinforcers and that decreases in TD movements are possibly a result of engagement in activities that are incompatible with TD movements.  (+info)

Benztropine is an anticholinergic medication that is primarily used to treat the symptoms of Parkinson's disease, such as rigidity, tremors, and muscle spasms. It works by blocking the action of acetylcholine, a neurotransmitter in the brain that is involved in the regulation of motor function.

Benztropine is also used to treat side effects caused by certain medications, such as antipsychotics, that can cause Parkinson-like symptoms. It may be prescribed to help reduce drooling or to manage muscle stiffness and restlessness.

The medication comes in the form of tablets or a solution for injection and is typically taken orally once or twice a day. Common side effects of benztropine include dry mouth, blurred vision, dizziness, and constipation. More serious side effects may include hallucinations, confusion, and irregular heartbeat.

It's important to note that benztropine can interact with other medications, so it's essential to inform your healthcare provider of all the drugs you are taking before starting this medication. Additionally, benztropine should be used cautiously in older adults, people with glaucoma or enlarged prostate, and those with a history of heart problems.

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.

Clopenthixol is a type of antipsychotic medication that is primarily used to manage and treat symptoms associated with various mental health disorders, such as schizophrenia and other psychotic disorders. It belongs to a class of drugs known as "typical" or "first-generation" antipsychotics, which work by blocking dopamine receptors in the brain.

Clopenthixol has potent activity at both dopamine D2 and serotonin 5-HT2 receptors, which contributes to its efficacy in treating positive symptoms of schizophrenia, such as hallucinations and delusions, as well as negative symptoms, like apathy and social withdrawal. It is also used off-label for the treatment of agitation and aggression in individuals with dementia or intellectual disabilities.

The medication is available in two forms: immediate-release tablets (Clopenthixol decanoate) and a long-acting injectable form (Clopenthixol decanoate). The long-acting injection is typically administered every 2-4 weeks, while the oral tablet is taken daily.

Like all medications, clopenthixol can have side effects, which may include extrapyramidal symptoms (EPS), such as Parkinsonism, akathisia, and dystonia; weight gain; metabolic changes; sexual dysfunction; and cardiovascular issues. It is essential to monitor patients taking clopenthixol for these potential adverse effects and adjust the treatment plan accordingly.

It's important to note that clopenthixol should only be prescribed and administered under the supervision of a qualified healthcare professional, and patients should follow their instructions carefully to ensure safe and effective use.

Dopamine plasma membrane transport proteins, also known as dopamine transporters (DAT), are a type of protein found in the cell membrane that play a crucial role in the regulation of dopamine neurotransmission. They are responsible for the reuptake of dopamine from the synaptic cleft back into the presynaptic neuron, thereby terminating the signal transduction of dopamine and regulating the amount of dopamine available for further release.

Dopamine transporters belong to the family of sodium-dependent neurotransmitter transporters and are encoded by the SLC6A3 gene in humans. Abnormalities in dopamine transporter function have been implicated in several neurological and psychiatric disorders, including Parkinson's disease, attention deficit hyperactivity disorder (ADHD), and substance use disorders.

In summary, dopamine plasma membrane transport proteins are essential for the regulation of dopamine neurotransmission by mediating the reuptake of dopamine from the synaptic cleft back into the presynaptic neuron.

Tropane alkaloids are a class of naturally occurring compounds that contain a tropane ring in their chemical structure. This ring is composed of a seven-membered ring with two nitrogen atoms, one of which is part of a piperidine ring. Tropane alkaloids are found in various plants, particularly those in the Solanaceae family, which includes nightshade, belladonna, and datura. Some well-known tropane alkaloids include atropine, scopolamine, and cocaine. These compounds have diverse pharmacological activities, such as anticholinergic, local anesthetic, and central nervous system stimulant effects.

Dopamine uptake inhibitors are a class of medications that work by blocking the reuptake of dopamine, a neurotransmitter, into the presynaptic neuron. This results in an increased concentration of dopamine in the synapse, leading to enhanced dopaminergic transmission and activity.

These drugs are used in various medical conditions where dopamine is implicated, such as depression, attention deficit hyperactivity disorder (ADHD), and neurological disorders like Parkinson's disease. They can also be used to treat substance abuse disorders, such as cocaine addiction, by blocking the reuptake of dopamine and reducing the rewarding effects of the drug.

Examples of dopamine uptake inhibitors include:

* Bupropion (Wellbutrin), which is used to treat depression and ADHD
* Methylphenidate (Ritalin, Concerta), which is used to treat ADHD
* Amantadine (Symmetrel), which is used to treat Parkinson's disease and also has antiviral properties.

It's important to note that dopamine uptake inhibitors can have side effects, including increased heart rate, blood pressure, and anxiety. They may also have the potential for abuse and dependence, particularly in individuals with a history of substance abuse. Therefore, these medications should be used under the close supervision of a healthcare provider.

Cocaine is a highly addictive stimulant drug derived from the leaves of the coca plant (Erythroxylon coca). It is a powerful central nervous system stimulant that affects the brain and body in many ways. When used recreationally, cocaine can produce feelings of euphoria, increased energy, and mental alertness; however, it can also cause serious negative consequences, including addiction, cardiovascular problems, seizures, and death.

Cocaine works by increasing the levels of dopamine in the brain, a neurotransmitter associated with pleasure and reward. This leads to the pleasurable effects that users seek when they take the drug. However, cocaine also interferes with the normal functioning of the brain's reward system, making it difficult for users to experience pleasure from natural rewards like food or social interactions.

Cocaine can be taken in several forms, including powdered form (which is usually snorted), freebase (a purer form that is often smoked), and crack cocaine (a solid form that is typically heated and smoked). Each form of cocaine has different risks and potential harms associated with its use.

Long-term use of cocaine can lead to a number of negative health consequences, including addiction, heart problems, malnutrition, respiratory issues, and mental health disorders like depression or anxiety. It is important to seek help if you or someone you know is struggling with cocaine use or addiction.

... benztropine) • Bromantane • 2-Butyl-3-(p-tolyl)quinuclidine (BTQ) • BTS-74,398 • Bupropion (amfebutamone) • Ciclazindol • ...
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Studies of the structure-activity relationships of benztropine have shown that DAT affinity and selectivity over other ... Modification of the tropane n-substituent was found to mitigate the anticholinergic effects of benztropine analogues by ... Rothman, RB; Baumann, MH; Prisinzano, TE; Newman, AH (2008). "Dopamine transport inhibitors based on GBR12909 and benztropine ... ɑInhibition at 10 μM The binding of benztropine analogues to the DAT differs significantly from that of cocaine and the ...
Anticholinergics such as benztropine and diphenhydramine are commonly prescribed to treat the EPS. 4% of users develop rabbit ...
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Benztropine Daturaolone 2-Carbomethoxytropinone (2-CMT) an intermediate in the creation of ecgonine cocaine analogues ...
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Amantadine Amphetamine Amylone Atropine Benztropine Benzydamine Benzylpiperazine Bromocriptine Bupropion Cathinone Cocaine ...
The molecular formula C21H25NO (molar mass: 307.429 g/mol) may refer to: Benzatropine, or benztropine Hepzidine 2β-Propanoyl-3β ...
A number of medications have also been tried including anticholinergics (such as benztropine) which have been found to be ...
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Unisom: Diphenhydramine belongs to a group of medications known as antihistamines. Antihistamines are used to treat symptoms caused by allergies, including itchy and watery eyes, sneezing, runny nose, and skin irritation. Diphenhydramine also causes drowsiness, and can be used by adults and children 12 years of age and older who occasionally have trouble sleeping (insomnia). The effects of diphenhydramine can last for up to 6 hours.
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Be sure to mention any of the following: anticoagulants (blood thinners) such as warfarin (Coumadin, Jantoven); benztropine ( ...
ONSTRYV™ and Benztropine approved by Health Canada. Company Announces Significant Increase in Revenues and Licenses Six ... Marketing approval received from Health Canada for Benztropine, an anticholinergic agent for the treatment of Parkinsons ...
Benztropine mesylate (USP). D00779 Biperiden (JAN/USP/INN). D00782 Procyclidine hydrochloride (USP). ...
Benztropine • Cogentin. Bromocriptine • Parlodel. Carbamazepine • Equetro, others. Chlorpromazine • Thorazine. Clozapine • ... The anticholinergic benztropine, 2 mg bid, also is ineffective.. Combination quetiapine, 300 mg/d, and the antiviral amantadine ...
amantadine benztropine. biperiden trihexyphenidyl. ANTIPSYCHOTIC MEDICATIONS. chlorpromazine clozapine. olanzapine thioridazine ...
Benztropine pretreatment does not affect responses to acute cocaine administration in human volunteers. Human ... Dopamine Transporter-Dependent and -Independent Striatal Binding of the Benztropine Analog JHW 007, a Cocaine Antagonist with ... Transport, Metabolism, and in Vivo Population Pharmacokinetics of the Chloro Benztropine Analogs, a Class of Compounds ... The novel N‐substituted benztropine analog GA2‐50 possesses pharmacokinetic and pharmacodynamic profiles favorable for a ...
Benztropine (Benzatropine) 6. Tetrabenazine (Nitoman) 7. Botulinum Toxins (Botulinum Toxin) 8. Scopolamine (Hyoscine) ...
  • Hypersensitivity to benztropine mesylate tablets. (nih.gov)
  • BENZTROPINE MESYLATE TABLETS USP are white coloured, circular, biconvex tablets with break line on one side and "SGP" embossed on the other side. (sgpharma.com)
  • BENZTROPINE MESYLATE TABLETS USP is recommended for all forms of parkinsonism including arteriosclerotic, postencephalitic, idiopathic, as well as medicine-induced extrapyramidal disorders (except tardive dyskinesia). (sgpharma.com)
  • BENZTROPINE MESYLATE TABLETS USP often is helpful in patients who have become unresponsive to other agents. (sgpharma.com)
  • BENZTROPINE MESYLATE TABLETS USP is a powerful anticholinergic agent which is mainly effective in relieving tremor and rigidity. (sgpharma.com)
  • Because of cumulative action of BENZTROPINE MESYLATE TABLETS USP, therapy should be initiated with a low dose which is increased gradually at five or six-day intervals to the smallest amount necessary for optimal relief. (sgpharma.com)
  • When BENZTROPINE MESYLATE TABLETS USP is started, do not terminate therapy with other antiparkinsonian agents abruptly. (sgpharma.com)
  • Shall be Benztropine Mesylate Tablets, USP. (emilspec.com)
  • For Type I, the tablets must be considered by the FDA to be therapeutically equivalent with Benztropine Mesylate Tablets, USP, by Quantum Pharmics of the same dosage and administration schedule. (emilspec.com)
  • Benztropine is a centrally acting anticholinergic agent with antihistaminic properties resulting from the combination of the tropine portion of the atropine molecule and the benzohydryl portion of diphenhydramine. (sgpharma.com)
  • Marketing approval received from Health Canada for Benztropine, an anticholinergic agent for the treatment of Parkinson's Disease. (newswire.ca)
  • Tablets shall contain 2 mg benztropine mesylate per tablet, within the applicable assayl limits for the tablets. (emilspec.com)
  • Benztropine is a medication that treats symptoms that affect your movement caused by Parkinson's disease and other conditions. (clevelandclinic.org)
  • BENZTROPINE (BENZ troe peen) is for certain movement problems due to Parkinson's disease, certain medicines, or other causes. (clevelandclinic.org)
  • Benztropine partially blocks cholinergic activity in the CNS, which is responsible for the symptoms of Parkinson's disease. (aksci.com)
  • Benztropine antagonises the effect of acetylcholine, decreasing the imbalance between the neurotransmitters acetylcholine and dopamine, which may improve the symptoms of early parkinson's disease. (sgpharma.com)
  • Ironically, the drug identified by Scripps Institute scientist Luke Lairson and his colleagues, is benztropine, which has been used for years to treat tremor in people with Parkinson's Disease. (thenakedscientists.com)
  • What Medicine is used for: ​Benztropine is used to reduce tremors, muscle stiffness and movement problems that are associated with Parkinson's disease and side effects of some medications used to treat mental conditions. (nhcs.com.sg)
  • When benztropine mesylate is given concomitantly with phenothiazines, haloperidol, or other drugs with anticholinergic or antidopaminergic activity, patients should be advised to report gastrointestinal complaints, fever or heat intolerance promptly. (nih.gov)
  • Synthesis, Fluorine-18 Radiolabeling, and Biological Evaluation of N-((E)-4-Fluorobut-2-en-1-yl)-2β-carbomethoxy-3β-(4′-halophenyl)nortropanes: Candidate Radioligands for In Vivo Imaging of the Brain Dopamine Transporter with Positron Emission Tomography. (acs.org)
  • Benztropine Mesylate is a synthetic compound containing structural features found in atropine and diphenhydramine. (nih.gov)
  • tell your doctor and pharmacist if you are allergic to benztropine, any other medications, or any of the ingredients in the benztropine preparation. (medlineplus.gov)
  • Before taking this medication, advise your doctor if you are allergic to Benztropine, or if you have any other allergies. (mydrugcenter.com)
  • Benztropine mesylate possesses both anticholinergic and antihistaminic effects, although only the former have been established as therapeutically significant in the management of parkinsonism. (nih.gov)
  • The recommended adult dose of benztropine to treat Parkinsonism is usually 1 mg to 2 mg daily, although the dose can range from 0.5 mg to 6 mg daily depending on circumstances. (medbroadcast.com)
  • Benztropine is in a class of medications called anticholinergics. (medlineplus.gov)
  • Do not stop taking benztropine suddenly without talking with your doctor, especially if you are also taking other medications. (medlineplus.gov)
  • Older adults should not usually take benztropine because it is not as safe or effective as other medications that can be used to treat the same condition. (medlineplus.gov)
  • Benztropine, rash, talk with your doctor or pharmacist. (njacs.org)
  • Benztropine is a selective M1 muscarinic acetylcholine receptor antagonist. (aksci.com)
  • Can you mix Benztropine Mesylate and Cocaine? (worldsbest.rehab)
  • Honestly, we don't recommend mixing Benztropine Mesylate with Cocaine. (worldsbest.rehab)
  • Benztropine Mesylate does nothing to enhance the effects of Cocaine and can cause serious complications that are really going to put a downer on your evening. (worldsbest.rehab)
  • Like death for example, which is always a risk when using Cocaine or mixing Cocaine and Benztropine Mesylate. (worldsbest.rehab)
  • When mixed with Benztropine Mesylate, Cocaine can affect the body's ability to keep the correct temperature and heart function. (worldsbest.rehab)
  • Indeed, this can also be caused by taking Cocaine in higher quantities without mixing it with Benztropine Mesylate. (worldsbest.rehab)
  • Even taking Cocaine without Benztropine Mesylate has a negative effect on the heart, and then taking Benztropine Mesylate with it increases the risk exponentially. (worldsbest.rehab)
  • While common, combining cocaine and Benztropine Mesylate together or even hours apart can be extremely risky because it increases heart rate and blood pressure, further increasing the risk of a heart attack. (worldsbest.rehab)
  • Cocaine and Benztropine Mesylate also react inside the liver to form a chemical known as cocaethylene, which is toxic to the heart, liver, and other organs. (worldsbest.rehab)
  • This can also happen even if cocaine and Benztropine Mesylate are used separately for several consecutive days. (worldsbest.rehab)
  • Mixing cocaine with Benztropine Mesylate will cause great harm to your heart, liver and other organs. (worldsbest.rehab)
  • Taking Cocaine and Benztropine Mesylate actually increases the risk of a heart attack. (worldsbest.rehab)
  • Some Cocaine addicts say it's better to mix Cocaine and Benztropine Mesylate as they believe it helps to improve the overall psychoactive experience. (worldsbest.rehab)
  • When mixing Cocaine and Benztropine Mesylate the interaction 'tricks' the brain into taking increased amounts of either the Cocaine, the Benztropine Mesylate or both simultaneously. (worldsbest.rehab)
  • Benztropine belongs to a class of medication called anticholinergics that work by blocking a certain natural substance (acetylcholine). (mydrugcenter.com)
  • Since benztropine mesylate has cumulative action, continued supervision is advisable. (nih.gov)
  • Animal studies have indicated that anticholinergic activity of benztropine is approximately half that of atropine, while antihistaminic activity approaches that of pyrilamine. (sgpharma.com)
  • If you become pregnant while taking benztropine , call your doctor. (medlineplus.gov)
  • Since benztropine mesylate contains structural features of atropine, it may produce anhidrosis. (nih.gov)
  • Paralytic ileus, hyperthermia and heat stroke, all of which have sometimes been fatal, have occurred in patients taking anticholinergic-type antiparkinsonism drugs, including benztropine mesylate, in combination with phenothiazines and/or tricyclic antidepressants. (nih.gov)
  • Allow at least 1-2 hours between doses of benztropine and certain drugs for diarrhea (adsorbent antidiarrheals such as kaolin, pectin, attapulgite). (mydrugcenter.com)
  • Antacids and some drugs for diarrhea may prevent the full absorption of benztropine, and this product may prevent the complete absorption of ketoconazole when these products are taken together. (mydrugcenter.com)
  • Study uncovers alarming overprescribing of benztropine, an anticholinergic drug, in patients with movement disorders. (psychiatrist.com)
  • Benztropine works by blocking the action of a nerve signalling chemical called acetyl choline, which also keeps the oligodendrocyte precursors cells that make myelin in a quiescent state. (thenakedscientists.com)
  • talk to your doctor about the risks and benefits of taking benztropine if you are 65 years of age or older. (medlineplus.gov)
  • A search of the medical literature using PubMed, however, found no further recent published reports of Benztropine in the treatment of hyperhidrosis. (sweathelp.org)
  • Benztropine mesylate may impair mental and/or physical abilities required for performance of hazardous tasks, such as operating machinery or driving a motorvehicle. (nih.gov)
  • Each tablet, for oral administration, contains 0.5 mg, 1 mg or 2 mg of benztropine mesylate. (nih.gov)
  • Buprenorphine Hydrochloride Injection, the Adriamycin (DOXOrubicin HCl) Injection, and the BENZTROPINE Mesylate Injection, USP are part of Hikma Pharmaceuticals' product portfolio. (globenewswire.com)
  • They point out in their paper in Nature , where the work is published, that, "benztropine has significant neurological and psychiatric side effects," emphasising that further preclinical and clinical evalution will be needed before the findings can be translated to the clinic. (thenakedscientists.com)
  • When benztropine emerged as the most powerful candidate tested, the team then administered the agent to mice with the rodent equivalent of MS. (thenakedscientists.com)
  • Benztropine is absorbed from the GI tract, crosses the blood-brain-barrier, and may cross the placenta. (sgpharma.com)
  • Your doctor may start with a small dose and increase it slowly after seeing your response to benztropine. (medlineplus.gov)