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Symmetrel (Amantadine)

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Generic Symmetrel is an antiviral medication. It blocks the actions of viruses in your body. Generic Symmetrel is used to treat and prevent influenza A (viral infection). Generic Symmetrel is also used to treat Parkinson's disease and "Parkinson-like" symptoms such as stiffness and shaking that may be caused by the use of certain drugs.

Other names for this medication:
Adekin, Aman, Amanta-hcl, Amantadina, Amantadinum, Amantagamma, Amantan, Amazolon, Amentrel, Amixx, Antadine, Atarin, Cerebramed, Endantadine, Influenzol, Lysovir, Mantadan, Mantadix, Paramantin, Paritrel, Protexin, Solu-contenton, Symadine, Tregor, Viregyt, Virofral, Virosol

Similar Products:
Famvir, Rebetol, Sustiva, Combivir, Epivir, Retrovir

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Also known as:  Amantadine.


Generic Symmetrel is an antiviral medication. It blocks the actions of viruses in your body.

Generic name of Generic Symmetrel is Amantadine.

Symmetrel is also known as Amantadine.

Brand name of Generic Symmetrel is Symmetrel.


Take this medicine with a full glass of water. If you are taking Generic Symmetrel to treat influenza A, start taking the medication within 24-48 hours after flu symptoms begin.

Do not stop taking it suddenly.


If you overdose Generic Symmetrel and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Symmetrel are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Be careful with Generic Symmetrel while you are pregnant or have nurseling. Generic Symmetrel can pass in breast milk and harm your baby.

Do not use Generic Symmetrel if you are allergic to Generic Symmetrel components.

Do not use FluMist nasal influenza "live vaccine" while you are being treated with Generic Symmetrel and for at least 48 hours after you stop taking Generic Symmetrel. The nasal vaccine may not be as effective if you receive it while you are taking Generic Symmetrel.

Be careful with Generic Symmetrel if you have epilepsy or other seizure disorder, congestive heart failure, kidney or liver disease, low blood pressure, eczema, glaucoma, or a history of mental illness, suicide attempt, or drug/alcohol addiction.

Be careful with Generic Symmetrel if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Generic Symmetrel if you take atropine (Atreza, Sal-Tropine, and others); dicyclomine (Bentyl); glycopyrrolate (Robinul); hyoscyamine (Anaspaz, Levbid, Levsin, Nulev, and others); mepenzolate (Cantil); methscopolamine (Pamine); propantheline (Pro-Banthine); scopolamine (Maldemar, Scopace, Transderm-Scop); quinine (Qualaquin); quinidine (Cardioquin, Quinaglute); diuretic (water pill) such as triamterene (Dyrenium), hydrochlorothiazide (HCTZ, Dyazide, HydroDiuril, Hyzaar, Lopressor, Vasoretic, Zestoretic); phenothiazines such as prochlorperazine (Compazine), thioridazine (Mellaril), and others.

Avoid alcohol.

Do not stop taking it suddenly.

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Hypertension and comorbid dementia are common illnesses affecting older adults disproportionally. Medication adherence is vital in achieving therapeutic outcomes. Use of antihypertensive and dementia medications may vary by race/ethnicity and has not been well explored.

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The high proportion of influenza A viruses currently circulating in the United States demonstrating adamantane resistance highlights the clinical importance of rapid surveillance for antiviral resistance. Our results indicate that these drugs should not be used for the treatment or prophylaxis of influenza in the United States until susceptibility to adamantanes has been reestablished among circulating influenza A isolates.

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The IOP increased with age in both D2J and B6 mice with a larger increase in the D2J strain. IOPs were not influenced by memantine treatment. The response amplitude of the scotopic flash ERG decreased with age in the D2J strain. This amplitude decrease, particularly that of the b-wave, was smaller in treated D2J mice. The retinae of treated D2J mice exhibited less peripheral degeneration of cone photoreceptors, and optic nerve neuropathy was less frequent.

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Memantine is approved as a treatment for moderate to severe Alzheimer's disease (AD). However, recent studies report that memantine is harmful for AD patients in several ways. This paper will systematically review all the available studies to provide an update regarding memantine as a treatment for AD.

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Eighteen-month-long randomized, placebo-controlled clinical trials are common for phase II and phase III drug development for Alzheimer's disease (AD). Yet, no 18-month trial has shown statistically significant outcomes favoring the test drug. We examined characteristics and underlying assumptions of these trials by assessing the placebo groups.

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Matrix (M) protein genes of 17 H9N2 avian influenza viruses (AIVs) isolated from chickens in northern China during the last 10 years were completely sequenced and phylogenetically analyzed. Homology of nucleotide sequences in the M gene of 17 isolates was 92.7-99.9%. Phylogenetic analysis showed that 11 of the tested M genes belong to the A/chicken/HongKong/Y280/97 (Y280)-like lineage, while the other six belong to the A/Quail/HongKong/G1/97 (G1)-like lineage. This is also the first time that a G1-like M gene of a H9N2 virus was detected in chicken flocks in northern China. These newly appearing changes in M genes may be due to reassortment events of AIVs, or they may have come from the H9N2 strains of southern China which surged in northern China after translocation. An analysis of the viral amino acid sequence of M2 protein has revealed substitution of S31N in two isolates, which is the molecular characterization of amantadine resistance in AIVs. Results of this study suggest that long-term monitoring should be continued to track the transmission and evolution of H9N2 AIVs in chickens in China.

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Platinum was detected in all plasma and ultrafiltrate samples 15 min after oral administration of both compounds and peaked between 3-4 h and 1-3 h, respectively. Similar for LA-12 and satraplatin, the C (max) and AUC values of plasma and ultrafiltrate platinum increased less than in proportion to dose. The mean C (max) and AUC values of plasma platinum observed after administration of LA-12 were from 0.84 to 2.5 mg/l and from 20.2 to 75.9 mg h/l. For ultrafiltrate platinum, the corresponding ranges were 0.16-0.78 mg/l and 0.63-1.8 mg h/l, respectively. The AUC of plasma platinum was higher after satraplatin (P < 0.001). However, administration of LA-12 resulted in significantly higher AUC values of ultrafiltrate platinum after the doses of 150 mg and 300 mg/kg (P < 0.01), respectively, and the C (max) values were significantly higher starting from the dose of 75 mg/kg LA-12 and upward (P < 0.01). Cumulative 72-h urinary recovery of platinum dose was below 5% for both compounds, and it decreased with the dose of satraplatin (P < 0.01), while a numerical decrease was observed after administration of LA-12 that did not reach statistical significance (P = 0.41). The renal clearance of free platinum was similar regardless of the dose and compound administered. Platinum concentrations in the liver homogenate exceeded those in the kidney. Distribution of platinum to tissues was higher after LA-12 compared to satraplatin. The difference in kidney platinum increased with dose and was twofold after 350 mg/kg LA-12. Liver platinum was twofold higher after LA-12 across all four doses.

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We conclude that ApoPep-1 is the effective probe for imaging of apoptosis in the MPTP model and can be applied in brain diseases with apoptosis.

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Since the gene products (M1 and M2) of influenza virus RNA segment 7 have been implicated in host range restriction, sensitivity to the drug amantadine, virus yield in chicken embryos as well as in virus assembly and morphology, we have determined the nucleotide sequence of this RNA segment for an avian [A/FPV/Weybridge (H7N7)] and a human [A/WSN/33 (H1N1)] virus and compared it to that of the other influenza A virus strains. The results show that all ten strains of influenza A virus contain an identical number of nucleotides (1027 bases) in RNA segment 7 and an identical number of amino acids in M1 (252 aa) and M2 (97 aa) proteins. The observed amino acid changes are conservative in nature suggesting the requirement of a critical structure of both proteins in virus assembly. Furthermore, the presence of some consistent amino acid substitutions among different human and avian strains also supports the possible existence of host range and drug resistance determinants in M1 and M2 proteins.

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An interhelical distance has been precisely measured by REDOR solid-state NMR spectroscopy in the transmembrane tetrameric bundle of M2-TMP, from the M2 proton channel of the influenza A viral coat. The high-resolution structure of the helical backbone has been determined using orientational restraints from uniformly aligned peptide preparations in hydrated dimyristoylphosphatidylcholine bilayers. Here, the distance between (15)N(pi) labeled His37 and (13)C(gamma) labeled Trp41 is determined to be less than 3.9 A. Such a short distance, in combination with the known tilt and rotational orientation of the individual helices, permits not only a determination of which specific side chain pairings give rise to the interaction, but also the side chain torsion angles and restraints for the tetrameric bundle can also be characterized. The resulting proton channel structure is validated in a variety of ways. Both histidine and tryptophan side chains are oriented in toward the pore where they can play a significant functional role. The channel appears to be closed by the proximity of the four indoles consistent with electrophysiology and mutagenesis studies of the intact protein at pH 7.0 and above. The pore maintains its integrity to the N terminal side of the membrane, and at the same time, a cavity is generated that appears adequate for binding amantadine. Finally, the observation of a 2 kHz coupling in the PISEMA spectrum of (15)N(pi)His37 validates the orientation of the His37 side chain based on the observed REDOR distance.

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The purposes of this study were to evaluate the co-administration of clonidine with memantine and to determine whether it has a peripheral action in intensifying cutaneous analgesia.

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The retention time for dansylated memantine was 17.1 ± 0.2 minutes. The calibration curve was linear over a concentration range from 5 to 160 ng/mL (n = 8/r² > 0.999). The method had an accuracy of >90%. Intra-assay and inter-assay coefficients of variation were <5% and <13%, respectively, at 3 different concentrations. The limit of quantification and the limit of detection were 2.9 ng/mL and 0.8 ng/mL, respectively. Among 100 substances prescribed as comedications in the treatment of dementia only fluvoxamine and zuclopenthixole showed retention times close to dansylated memantine (17.8 minutes and 18.1 minutes, respectively). However, these 2 drugs were removed from patients' specimens during solid-phase extraction sample preparation.

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symmetrel drug 2017-02-28

Glutamate receptor antagonists with selective action at the N-methyl-D-aspartate (NMDA) receptor are promising agents for the neuroprotective and symptomatic pharmacotherapy of various neuropsychiatric disorders. Although NMDA receptor antagonists of the Flomax Mg phencyclidine (PCP) type are precluded from clinical use because of their psychotomimetic properties, amantadine and memantine have been administered to human patients with idiopathic Parkinson's disease and spasticity for many years without serious adverse effects. The mechanisms underlying these differences in psychotogenicity of different NMDA receptor antagonist are currently being discussed. Different affinity to the PCP binding site of the NMDA receptor, region-specific pharmacology, as well as different binding profiles to neurotransmitter receptors other than the NMDA type glutamate receptor, most likely play a role in determining whether an NMDA receptor antagonist drug will be tolerated clinically or not.

symmetrel user reviews 2015-12-11

In the present study, we investigated the influence of repeated treatment with fluoxetine (FLU, 5 or 10 mg/kg) and amantadine (AMA, 10 mg/kg), given separately or jointly (twice daily for 14 day), at the mRNA level (the Northern blot) in the hippocampus and cerebral cortex. The experiment was carried out on male Wistar rats. The tissue Lipitor Generic Equivalent for biochemical assays was dissected 24 h after the last dose of drug. We also studied the effect of repeated treatment with FLU and AMA on the action of 5-hydroksytryptamine (5-HT)(1A)- and 5-HT(2) receptor agonists (+/-)-8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT) and (+/-)-1-(4-iodo-2,5-dimethoxy-phenyl)-2-aminopropane ((+/-)DOI), respectively, in behavioral tests. The obtained results showed that FLU (10 mg/kg) in the hippocampus, and FLU (5 and 10 mg/kg) and AMA(10 mg/kg) in the cerebral cortex, significantly elevated BDNF mRNA levels. Joint administration of FLU (5 or 10 mg/kg) and AMA(10 mg/kg) induced a more substantial increase in BDNF gene expression in the cerebral cortex (but not in the hippocampus), and inhibited the behavioral syndrome induced by 8-OH-DPAT or (+/-)DOI (compared to treatment with either drug alone). The obtained results suggest that the enhancement of BDNF gene expression may be essential for the therapeutic effect of the co-administration of FLU and AMA in drug-resistant depressed patients, and that among other mechanisms, 5-HT(1A) and 5-HT(2) receptors may play some role in this effect.

symmetrel overdose 2015-03-17

A Medline search was performed to gather information about the safety of the medications approved for the treatment of the motor symptoms of PD. This was supplemented with Avalide Dose Range additional articles obtained from online sources and information provided by the FDA and the manufacturers. The focus of this review is the side-effect and safety profiles of carbidopa/levodopa, dopamine agonists, selective monoamine oxidase inhibitors, catechol-o-methyltransferase inhibitors, anticholinergics and amantadine.

symmetrel en alcohol 2016-09-06

Twenty-four subjects with Huntington disease took amantadine hydrochloride, 100 mg 3 times daily for 2 weeks, and placebo for 2 weeks. Kapikachhu Tablets Benefits

symmetrel dosage forms 2016-03-10

Cardiovascular disorders are the most frequently reported adverse effects of drugs used Tofranil 25mg Medication to treat Alzheimer's disease. They are potentially fatal.

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The change in predominance from influenza B to influenza A in the spring of 1993 emphasizes the importance of annual Prandin E Gel influenza surveillance. Although influenza vaccine is effective against both influenza A and B, the antiviral drugs amantadine and rimantadine are effective only against influenza A. Outbreaks during the summer of 1993 emphasize that influenza should be considered a possible cause of respiratory infections during summer and early autumn.

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There were no significant Nexium Drug Uses differences between the two groups with respect to age, gender, nausea and vomiting, sleep quality, blood pressure, and heart rate. No significant differences were observed between the two groups in pain scores (P = 0.39) and analgesic consumption (P = 0.78).

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To study the inhibitory effects of some agents or drugs (inhibitors) on Cozaar Review benzo(e)pyrene (B(e)P)-induced cell death and apoptosis on human retinal pigment epithelial (ARPE-19) cells in vitro.

symmetrel generic 2017-05-06

There is growing evidence that N-methyl-d-aspartate (NMDA) receptor antagonists Uroxatral Drug may have potential for the treatment of alcohol disorders. Memantine is a selective noncompetitive NMDA receptor antagonist that has been shown to decrease alcohol craving in moderate drinkers. This 16-week double-blind outpatient pilot clinical trial determined if memantine was more effective than placebo at reducing alcohol use in actively drinking alcohol-dependent patients.

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To determine the effects of 28 weeks of memantine treatment for patients with AD on resource utilisation and costs.

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We included subjects with refractory migraine (episodic migraine with 8-14 days of headache per month or transformed migraine, who had previously failed at least 2 trials of adequate preventive therapy). Other preventive drugs were allowed if the patient had been on a stable dose for more than 30 days. MEM dose ranged from 10 mg to 20 mg per day. The treatment phase lasted 3 months. The primary endpoint was number of days with headache at month 3. Cognitive performance was assessed with the trail making tests A and B (TMT-A and B). Statistical analyses were performed on the intent-to-treat (ITT) population, using data subjected to the last observation carried forward algorithm.We also conducted per protocol analyses.

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The objective of the study was to profile a range of psychoactive agents (glutamatergic, dopaminergic, and cholinergic agonists and antagonists) known to be important in cognitive processing on visual discrimination performance using a touch sensitive computer monitor.

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Because of no differences in postoperative pain or opioid consumption, we conclude that a preoperative dose of 200 mg amantadine IV fails to enhance postoperative analgesia in patients undergoing elective abdominal hysterectomy.

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Memantine is an uncompetitive N-methyl-D-aspartate receptor antagonist with moderate affinity. Its mechanism of action is neuroprotective and potentially therapeutic in several neuropsychiatric diseases. It has been approved by the FDA for the treatment of moderate to severe Alzheimer's disease (AD) either as a monotherapy or in combination with cholinesterase inhibitors. This review covers key studies of memantine's safety and efficacy in treating moderate to severe AD. It also covers current research into other dementias including but not exclusively mild AD and vascular dementia. Other studies on the efficacy of memantine for other neuropsychiatric diseases are discussed. Memantine is a safe and effective drug that merits further research on several topics. Clinicians should be aware of new studies and potential uses of memantine because of its safety and efficacy.

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Alzheimer's disease (AD) is a complex medical condition involving abnormalities in multiple biological and environmental domains. Current knowledge suggests that simultaneous intervention in these domains may be the most effective way to help AD patients and their families. Treatments for AD are centered on the inhibition of enzymes responsible for the degradation of acetylcholine--a neurotransmitter that is reduced in AD patients. Four cholinesterase inhibitors have been approved by the United States Food and Drug Administration, three of which are routinely used for the symptomatic treatment of mild-to-moderate AD. Strategies will be reviewed with regard to cognitive, functional, and behavioral domains. Providing a different treatment option for patients with AD, memantine is a low-to-moderate affinity, uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist that has been approved for the treatment of moderate-to-severe AD. The clinical efficacy and tolerability of memantine monotherapy and combination therapy in patients with AD will be presented. Finally, the role of nonpharmacologic intervention will be discussed.