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Mestinon uses




See full prescribing information for complete boxed warning.



Mestinon is indicated for pretreatment against the lethal effects of Soman nerve agent poisoning. Pyridostigmine is intended for use in conjunction with protective garments, including a mask. At the first sign of nerve agent poisoning, pyridostigmine should be stopped, and atropine and pralidoxime therapy started immediately.

The evidence for the effectiveness of pyridostigmine as pretreatment against Soman-induced toxicity was derived from animal studies alone [see Nonclinical Toxicology (13.2)]. FOR MILITARY MEDICAL USE ONLY

Mestinon is a reversible cholinesterase inhibitor indicated for pretreatment against the lethal effects of soman nerve agent poisoning. (1)

Mestinon is for use in conjunction with



PRIMARY PROTECTION AGAINST EXPOSURE TO CHEMICAL NERVE AGENTS IS THE WEARING OF PROTECTIVE GARMENTS INCLUDING MASKS, HOODS AND OVERGARMENTS DESIGNED SPECIFICALLY FOR THIS USE.INDIVIDUALS MUST NOT RELY SOLELY UPON PRETREATMENT WITH PYRIDOSTIGMINE, AND THE ANTIDOTES ATROPINE AND PRALIDOXIME (2-PAM) TO PROVIDE COMPLETE PROTECTION FROM POISONING BY THE CHEMICAL NERVE AGENT SOMAN.PYRIDOSTIGMINE MUST NOT BE TAKEN AFTER EXPOSURE TO SOMAN. IF PYRIDOSTIGMINE IS TAKEN IMMEDIATELY BEFORE EXPOSURE (E.G., WHEN THE GAS ATTACK ALARM IS GIVEN) OR AT THE SAME TIME AS POISONING BY SOMAN, IT IS NOT EXPECTED TO BE EFFECTIVE, AND MAY EXACERBATE THE EFFECTS OF A SUB-LETHAL EXPOSURE TO SOMAN [See Clinical Pharmacology (12.2)].The dose of pyridostigmine is one 30 mg tablet every 8 hours, started at least several hours prior to exposure to Soman. At the first sign of nerve agent poisoning, pyridostigmine should be discontinued and treatment with atropine and pralidoxime should be instituted immediately. There is no known advantage to taking pyridostigmine just prior to or concurrent with Soman exposure. According to the mechanism of action of pyridostigmine described below [See Clinical Pharmacology (12.2)], pyridostigmine should be effective when it is given sufficiently in advance of Soman poisoning to provide a pool of protected enzyme. Therefore, it is expected that pyridostigmine will not be effective if administered just prior to or during exposure to Soman. The benefits and risks of use beyond 14 consecutive days have not been definitively established, therefore, continued use beyond 14 consecutive days should be evaluated in the context of the likelihood of exposure to Soman nerve agent.



Mestinon Tablets, USP, 30 mg, are round, white and imprinted with the letters "PBT"



5.1 Stopping Pyridostigmine and Using Atropine and 2-PAM in the Event of Soman Exposure

See Dosage and Administration (2) and Boxed Caution statement (at beginning of Full Prescribing Information).

Pyridostigmine pretreatment offers no benefit against the nerve agent Soman unless the nerve agent antidotes atropine and pralidoxime (2-PAM) are administered once symptoms of poisoning appear. Pyridostigmine should be discontinued at the first sign of nerve agent poisoning since it may exacerbate the effects of a sub-lethal exposure to Soman.

5.2 Individuals at Increased Risk of Anticholinergic Adverse Reactions

Pyridostigmine should be used with caution in persons with bronchial asthma, chronic obstructive pulmonary disease, bradycardia, cardiac arrhythmias, and, for example, in people being treated for hypertension or glaucoma with beta adrenergic receptor blockers.

5.3 Use in Bromide-Sensitive Individuals

Caution should be taken when administering Mestinon to individuals with known bromide sensitivity. The risks and benefits of administration must be weighed against the potential for rash or other adverse reactions in these individuals. [See Adverse Reactions ]

5.4 Action in Case of Serious Adverse Reactions

If personnel experience serious adverse reactions such as difficult breathing, severe dizziness, or loss of consciousness as a result of ingestion of Mestinon, they should be advised to temporarily discontinue use of product and seek immediate medical attention. Serious adverse events should be reported to their commander and responsible medical officer.



The most common adverse reactions are diarrhea, abdominal pain, dysmenorrhea, and twitch.

The adverse reactions to Mestinon are typically of two varieties, muscarinic and nicotinic. Muscarinic adverse reactions include abdominal cramps, bloating, flatulence, diarrhea, emesis, increased peristalsis, nausea, hypersalivation, urinary incontinence, increased bronchial secretion, diaphoresis, miosis, and lacrimation. Nicotinic adverse reactions are comprised chiefly of muscle cramps, fasciculations, and weakness. Pyridostigmine is a quaternary ammonium compound and does not readily cross the blood-brain barrier. Compared to the peripheral effects of Mestinon, central nervous system manifestations are less frequent and less serious, primarily consisting of headache and vertigo, with minor and clinically insignificant changes in heart rate, blood pressure, and respiratory function. Extremely high doses may produce CNS symptoms of agitation, restlessness, confusion, visual hallucinations, and paranoid delusions. Electrolyte abnormalities, possibly resulting from high serum bromide concentrations, also have been reported. Death may result from cardiac arrest or respiratory paralysis and pulmonary edema. As with any compound containing bromide, a skin rash may be observed in an occasional patient, which usually subsides promptly upon discontinuance of the medication.

Most common adverse reactions ( ≥ 3% ) are diarrhea, abdominal pain, dysmenorrhea, and twitch. (6)

6.1 Clinical Studies Experience

In a controlled study of 90 healthy volunteers comparing pyridostigmine 30 mg every 8 hours to placebo for 21 days, the following incidence of adverse reactions was reported.



N = 60



N = 30

Abdominal Pain70
Dry Skin20
Urinary Frequency20
Neck pain20

Other less common adverse reactions seen during controlled and uncontrolled clinical trials for pyridostigmine include the following:

During safety studies at the recommended dosage, there were two reports of loss of consciousness, one of which also included urinary and fecal incontinence, stiffness of the upper torso and arms, post-syncopal skin pallor, post-syncopal confusion, and post-syncopal weakness (suggesting a seizure event).


7.1 Mefloquine

A potential interaction between the antimalarial drug mefloquine and Mestinon exists through a possible additive effect on the gastrointestinal tract. The most common complaint about both drugs is loose bowels. It has been reported that simple additive effects on the atrial rate occur when mefloquine and Mestinon are combined.

7.2 Other Anticholinesterase Drugs

Because anticholinesterase drugs are often used in the treatment of glaucoma, the use of Mestinon in such situations may have an additive effect that may cause or exacerbate problems with night vision.

7.3 Narcotics

The bradycardia associated with the use of narcotics may exacerbate pyridostigmine-induced bradycardia.

7.4 Drugs that Interfere with Neuromuscular Transmission

Particular caution should be observed in the administration of depolarizing neuromuscular blocking agents during surgery since the degree of neuromuscular blockade that ensues may be enhanced by previously administered Mestinon. Doses of non-depolarizing neuromuscular blocking agents (e.g., pancuronium bromide) may need to be increased in patients previously administered pyridostigmine. Atropine antagonizes the muscarinic effects of pyridostigmine, and this interaction is utilized to counteract the muscarinic symptoms of pyridostigmine toxicity. Anticholinesterase agents are sometimes effective in reversing neuromuscular block induced by aminoglycoside antibiotics. However, aminoglycoside antibiotics, local and some general anesthetics, antiarrhythmic agents, and other drugs that interfere with neuromuscular transmission should be used cautiously, if at all.

7.5 Drugs Converted to Pantothenic Acid (e.g., Dexpanthenol)

Theoretically, drugs such as dexpanthenol, which are converted to pantothenic acid in vivo, may have additive effects with pyridostigmine by increasing production of acetylcholine.


8.1 Pregnancy

Pregnancy Category B

Pyridostigmine produced no teratogenic effects in rats given up to 30 mg/kg/day and in rabbits given up to 45 mg/kg/day orally during the period of organogenesis. These doses are 3 and 10 times, respectively, the recommended human dose of 90 mg on a mg/m2 basis. In rats, a slight degree of delayed skeletal ossification was seen at 30 mg/kg, a dose which caused maternal toxicity, and a slight increase in the incidence of hydronephrosis was seen at all dose levels (lowest dose tested was 3 mg/kg). In rabbits, a slight increase in the incidence of hydronephrosis was seen at 45 mg/kg, a dose which caused maternal toxicity, and increased incidences of blood vessel variations were seen at all doses (lowest dose tested was 5 mg/kg). There are no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed.

8.3 Nursing Mothers

It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk caution should be exercised when pyridostigmine is administered to a nursing woman.

8.4 Pediatric Use

Safety and effectiveness in pediatric patients have not been established.

8.5 Geriatric Use

Clinical studies of pyridostigmine did not contain sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. In general, dose selection for an elderly patient should be cautious, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.

In the elderly the elimination half-life, volume of distribution (central and steady state) were comparable with the young (21-51 years of age). However, the systemic plasma clearance was significantly lower in the elderly compared to the young (6.7 ± 2.2 vs. 9.5 ± 2.7 ml/min/kg).This drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal function.

8.6 Persons with Renal Impairment

This drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Caution should be observed, and dosage be selected carefully, when administering Mestinon to patients with impaired renal function. In anephric patients, a 3-fold increase in the elimination half-life and a 75% decrease in systemic clearance was observed [see Clinical Pharmacology (12.3)] It may be useful to monitor renal function.

8.7 Persons with Hepatic Impairment

No information is available on the pharmacokinetics of pyridostigmine in hepatic impaired patients.


9.2 Abuse

Although the abuse potential of pyridostigmine has not been specifically assessed, no abuse of, tolerance to, withdrawal from, or drug-seeking behavior was observed in patients who received pyridostigmine in clinical trials. Cholinesterase inhibitors are not believed to be associated with drug abuse.


As is true of all cholinergic drugs, overdosage of Mestinon may result in cholinergic crisis, a state characterized by increasing muscle weakness that, through involvement of the muscles of respiration, may lead to death. Overdosage with pyridostigmine must be differentiated from the acute manifestations of nerve agent poisoning which may also be characterized by a cholinergic crisis. Atropine should be used to treat pyridostigmine overdosage.

In the treatment of pyridostigmine overdosage, maintaining adequate respiration is of primary importance. Tracheostomy, bronchial aspiration, and postural drainage may be required to maintain an adequate airway; respiration can be assisted mechanically if required. Supplemental oxygen may be necessary. Pyridostigmine should be discontinued immediately and 1-4 mg of atropine sulfate administered i.v. Additional doses of atropine may be given every 5-30 minutes as needed to control muscarinic symptoms. Atropine overdosage should be avoided, as tenacious secretions and bronchial plugs may result. It should be kept in mind that unlike muscarinic effects, the skeletal muscle effects and consequent respiratory paralysis (nicotinic effects) which can occur following pyridostigmine overdosage are not alleviated by atropine.


Mestinon is an orally active, reversible cholinesterase inhibitor. Its chemical name is: 3-hydroxy-1-methylpyridinium bromide dimethylcarbamate.

CAS registration number is 101-26-8.Pyridostigmine bromide has a molecular formula of C9H13BrN202, a molecular weight of 261.12, and the following molecular structure:Pyridostigmine bromide tablets, USP contain 30 mg Mestinon for oral administration. The inactive ingredients included in the tablet formula are: lactose anhydrous, colloidal silicon dioxide, and stearic acid. Chemical Structure


12.1 Mechanism of Action

Pyridostigmine is a reversible cholinesterase inhibitor.

12.2 Pharmacodynamics

The mechanism of Soman induced death is reasonably well-understood; death is believed to result primarily from respiratory failure due to irreversible inhibition of the enzyme acetylcholinesterase and the consequent increase in the level of the neurotransmitter acetylcholine 1) at nicotinic receptors at the neuromuscular junction, resulting in pathological stimulation and ultimate failure of the muscles of respiration, 2) at muscarinic receptors in secretory glands and smooth muscle, resulting in excessive respiratory secretions and bronchoconstriction, and 3) at cholinergic receptors in the brain, resulting in central respiratory depression.

The effect of pyridostigmine is presumed to result from its reversible inhibition of a critical number of acetylcholinesterase active sites in the peripheral nervous system, protecting them from irreversible inhibition by Soman. When the pyridostigmine-induced inhibition of the enzyme is subsequently reversed, there is a small residual amount of enzyme activity that is adequate to sustain life (provided atropine and 2-PAM are subsequently administered). An implication of this presumed mechanism is that it is not helpful to give pyridostigmine either just before or during exposure to Soman.

12.3 Pharmacokinetics

Mestinon is poorly absorbed from the gastrointestinal tract with an absolute bioavailability of 10-20%. Following a single oral dose of 30 mg Mestinon in the fasting state, the TMAX was 2.2 ± 1.0 hours. The pharmacokinetics of Mestinon is linear over the dose range of 30-60 mg. Following multiple doses of pyridostigmine (30 mg every 8 hours for 21 days), the average steady-state trough concentration of pyridostigmine was about ¼ of the peak concentration after a single dose.

The volume of distribution was about 19 ± 12 liters, indicating that pyridostigmine distributes into tissues. No information on protein binding of pyridostigmine is available. Pyridostigmine undergoes hydrolysis by cholinesterases and is metabolized in the liver. It is excreted in the urine both as unchanged drug and its metabolites. The systemic clearance of Mestinon is 830 mL/min and the elimination half-life of Mestinon is approximately 3 hours.

Renal Impairment

In anephric patients (n=4), the elimination half-life increased 3 fold and the systemic clearance decreased by 75% [see Use in Specific Populations (8.6)].

Hepatic Impairment

No information is available on the pharmacokinetics of pyridostigmine in hepatic impaired patients.


The clearance of Mestinon is not influenced by gender.


In a pyridostigmine study in the elderly (71-85 years), the elimination half-life of pyridostigmine was similar to the half-life in the young (21-51 years). However, the systemic plasma clearance was 30% lower in the elderly.


13.1 Carcinogenesis, Mutagenesis, Impairment of Fertility


No long-term studies to evaluate carcinogenicity have been performed in animals.


Pyridostigmine was mutagenic and clastogenic in an in vitro mammalian gene mutation assay in mouse lymphoma cells, in the presence of metabolic activation only. Pyridostigmine was not mutagenic in an in vitro bacterial reverse mutation assay and in an in vitro mammalian gene mutation assay in Chinese hamster ovary cells, and was not clastogenic in an in vitro assay in Chinese hamster ovary cells or in an in vivo mouse micronucleus assay.

Impairment of Fertility

Pyridostigmine did not impair fertility in male and female rats given oral doses of up to 45 mg/kg/day (5 times the recommended human daily dose of 90 mg on a mg/m2 basis) beginning at 10 (males) or 2 (females) weeks prior to mating.

13.2 Animal Toxicology and/or Pharmacology

Evidence of the effectiveness of pyridostigmine as a pre-treatment for Soman poisoning was obtained from studies in animals alone, because it is clearly unethical to perform such studies in humans. While the results of these animal studies cannot be extrapolated to humans with certainty, the extrapolation is supported by the reasonably well understood pathophysiologic mechanisms of the toxicity of Soman and the mechanism of the protective effect of pyridostigmine pretreatment, as examined in various animal species. In addition, the results of these animal studies establish that pyridostigmine is reasonably likely to produce clinical benefit in humans. The section below explains the current understanding of the mechanism of Soman toxicity and the beneficial effect of pyridostigmine pretreatment, as well as the basis for extrapolating the animal findings to humans.

Pyridostigmine pretreatment has been shown in animals to decrease the lethality of the nerve agent Soman, provided atropine and pralidoxime (2-PAM) are administered immediately after exposure to Soman. Rhesus monkeys were given oral doses of pyridostigmine every 8 hours for a total of 6 doses, and were challenged with Soman given intramuscularly 5 hours after the last pyridostigmine dose. Two dosage groups of pyridostigmine were used: a low dose group given 1.2 mg/kg for all 6 doses, and a high dose group given 1.2 and 1.8 mg/kg for the first and second doses, respectively, and 2.4 mg/kg for the final 4 doses. These animals were also given atropine and 2-PAM after exposure to Soman. An untreated control group, and a group given atropine and 2-PAM (but not pyridostigmine), were also used. The primary endpoint in this study was a decrease in the lethality of Soman expressed as an increase in the LD 50 (the dose of Soman that killed 50 % of the animals). The atropine/2-PAM control group showed a small but statistically significant 1.6 fold increase in the Soman LD 50 compared to the untreated control group. The groups given pyridostigmine as well as atropine and 2-PAM showed increases in the Soman LD 50 of at least 40 fold compared to the untreated control group and at least 25 fold compared to the atropine/2-PAM group. The two dose levels of pyridostigmine showed similar effectiveness. Additional studies in rhesus monkeys and guinea pigs also showed effectiveness of pyridostigmine (in the presence of post-Soman administration of atropine and 2-PAM). The magnitude of effect in guinea pigs was smaller than that in monkeys (Soman LD 50 increased 4-7 fold compared to untreated control and 2-4 fold compared to atropine/2-PAM alone). Pyridostigmine produced only small and inconsistent effects in studies in rats, mice and rabbits. It is thought that the effect of pyridostigmine in rats and mice is masked by high blood levels of the enzyme carboxylesterase, which eliminates Soman from blood and makes those species highly resistant to Soman. In a study in which rats were given an inhibitor of carboxylesterase, pretreatment with pyridostigmine plus atropine increased the LD 50 of Soman 8.5 fold compared to untreated controls. Humans have little or no carboxylesterase in blood. Animal studies have shown that pyridostigmine pretreatment was effective only when animals were given atropine and 2-PAM after exposure to Soman.


Evidence of the effectiveness of pyridostigmine as a pretreatment for Soman poisoning was obtained from studies in animals alone, because it is clearly unethical to perform such studies in humans.


Mestinon tablets, USP, 30 mg, are round, white tablets imprinted with the letters "PBT".

Immediate Container: Twenty-one (21) tablets individually sealed in a blister or strip package which is supplied in a protective sleeve. NDC: 46594-750-01NSN 6505-01-178-7903The NSN refers to the actual unit that is ordered from supply (if someone orders 1 of this stock number they will get one Mylar bag as a unit of issue (or one package of 10 blister packs). The exterior carton lists the NSN and the description of the product that the NSN applies to and lists 10 PG (packages) as the quantity within the carton.


Store refrigerated between 2 and 8°C (36-46°F). Protect from light. Do not dispense the content of unit packages (10 blister packs) and shipping containers (10 packages of 10 each blister packs) after removal from refrigeration for more than a total of 3 months. Do not use after the 10 year expiration date provided on the package. Military personnel should be advised to discard the contents of the individual unit packages of pyridostigmine 3 months after issue.


Mestinon Tablets, USP, are supplied with a Patient Information Sheet.

Personnel should be instructed to read the Patient Information Sheet before using Mestinon Tablets. The following information and advice should be discussed with personnel when PB is issued.

17.1 Indication and Conditions of Use

See Dosage and Administration (2).

17.2 Dosage and Administration

See Dosage and Administration (2).

Personnel should contact their unit medical officer if adverse reactions from PB continue and limit duty performance.

17.3 Contraindications and Precautions

Mestinon must not be taken by persons with

See Contraindications (4).Personnel should be instructed to inform their doctor or medic before taking PB if they:See Warnings and Precautions (5.2).

17.4 Side Effects

This list of adverse reactions is not complete.

See Adverse Reactions (6).Most side effects are mild and will disappear without treatment. Mestinon has been safely used and has been FDA approved for over 40 years in the U.S. to treat a disease called myasthenia gravis (MG). Human studies of PB at doses intended for military use have found PB to be generally safe. Personnel should contact their unit medical officer if side effects from PB continue and limit duty performance.

17.5 Collection of Information

DOD may collect information on the use of PB to help decide how best to protect deployed forces in the future. Information that identifies individual persons will remain confidential. However, the FDA may review any data collected by DOD for the purpose of evaluating PB.

17.6 Questions and Requests for Information

Questions about personnel rights and welfare should be directed to the unit medical officer, or e-mailed to

Personnel can receive information about PB from unit medical officers or medics. Questions about PB can also be e-mailed directly to the U.S. Army Medical Research and Materiel Command at address

Distributed by:

Defense Supply Center, Philadelphia

Medical Directorate

700 Robbins Ave

Philadelphia, PA 19111


Office of The Surgeon General

U.S. Army Medical Materiel Development Activity


1430 Veterans Drive

Fort Detrick, MD 21702-5012

Mestinon pharmaceutical active ingredients containing related brand and generic drugs:

Active ingredient is the part of the drug or medicine which is biologically active. This portion of the drug is responsible for the main action of the drug which is intended to cure or reduce the symptom or disease. The other portions of the drug which are inactive are called excipients; there role is to act as vehicle or binder. In contrast to active ingredient, the inactive ingredient's role is not significant in the cure or treatment of the disease. There can be one or more active ingredients in a drug.

Mestinon available forms, composition, doses:

Form of the medicine is the form in which the medicine is marketed in the market, for example, a medicine X can be in the form of capsule or the form of chewable tablet or the form of tablet. Sometimes same medicine can be available as injection form. Each medicine cannot be in all forms but can be marketed in 1, 2, or 3 forms which the pharmaceutical company decided based on various background research results.
Composition is the list of ingredients which combinedly form a medicine. Both active ingredients and inactive ingredients form the composition. The active ingredient gives the desired therapeutic effect whereas the inactive ingredient helps in making the medicine stable.
Doses are various strengths of the medicine like 10mg, 20mg, 30mg and so on. Each medicine comes in various doses which is decided by the manufacturer, that is, pharmaceutical company. The dose is decided on the severity of the symptom or disease.

Mestinon destination | category:

Destination is defined as the organism to which the drug or medicine is targeted. For most of the drugs what we discuss, human is the drug destination.
Drug category can be defined as major classification of the drug. For example, an antihistaminic or an antipyretic or anti anginal or pain killer, anti-inflammatory or so.

Mestinon Anatomical Therapeutic Chemical codes:

A medicine is classified depending on the organ or system it acts [Anatomical], based on what result it gives on what disease, symptom [Therapeutical], based on chemical composition [Chemical]. It is called as ATC code. The code is based on Active ingredients of the medicine. A medicine can have different codes as sometimes it acts on different organs for different indications. Same way, different brands with same active ingredients and same indications can have same ATC code.

Mestinon pharmaceutical companies:

Pharmaceutical companies are drug manufacturing companies that help in complete development of the drug from the background research to formation, clinical trials, release of the drug into the market and marketing of the drug.
Researchers are the persons who are responsible for the scientific research and is responsible for all the background clinical trials that resulted in the development of the drug.



  1. Dailymed."PYRIDOSTIGMINE BROMIDE TABLET [VALEANT CANADA LIMITED]". (accessed August 28, 2018).
  2. "pyridostigmine". (accessed August 28, 2018).
  3. "pyridostigmine". (accessed August 28, 2018).

Frequently asked Questions

Can i drive or operate heavy machine after consuming Mestinon?

Depending on the reaction of the Mestinon after taken, if you are feeling dizziness, drowsiness or any weakness as a reaction on your body, Then consider Mestinon not safe to drive or operate heavy machine after consumption. Meaning that, do not drive or operate heavy duty machines after taking the capsule if the capsule has a strange reaction on your body like dizziness, drowsiness. As prescribed by a pharmacist, it is dangerous to take alcohol while taking medicines as it exposed patients to drowsiness and health risk. Please take note of such effect most especially when taking Primosa capsule. It's advisable to consult your doctor on time for a proper recommendation and medical consultations.

Is Mestinon addictive or habit forming?

Medicines are not designed with the mind of creating an addiction or abuse on the health of the users. Addictive Medicine is categorically called Controlled substances by the government. For instance, Schedule H or X in India and schedule II-V in the US are controlled substances.

Please consult the medicine instruction manual on how to use and ensure it is not a controlled substance.In conclusion, self medication is a killer to your health. Consult your doctor for a proper prescription, recommendation, and guidiance.


Review conducted a study on Mestinon, and the result of the survey is set out below. It is noteworthy that the product of the survey is based on the perception and impressions of the visitors of the website as well as the views of Mestinon consumers. We, as a result of this, advice that you do not base your therapeutic or medical decisions on this result, but rather consult your certified medical experts for their recommendations.

Visitor reports

Visitor reported useful

No survey data has been collected yet

Visitor reported side effects

No survey data has been collected yet

Visitor reported price estimates

No survey data has been collected yet

Visitor reported frequency of use

No survey data has been collected yet

Six visitors reported doses

What is the dose of Mestinon drug you are taking?
According to the survey conducted among website users, the maximum number of people are using the following dose 6-10mg. Few medications come in only one or two doses. Few are specific for adult dose and child dose. The dose of the medicine given to the patient depends on the severity of the symptom/disease. There can be dose adjustments made by the doctor, based on the progression of the disease. Follow-up is important.

One visitor reported time for results

What is the time duration Mestinon drug must be taken for it to be effective or for it to reduce the symptoms?
Most chronic conditions need at least some time so the dose and the drug action gets adjusted to the body to get the desired effect. The stastistics say website users needed 3 month to notice the result from using Mestinon drug. The time needed to show improvement in health condition after using the medicine Mestinon need not be same for all the users. It varies based on other factors.
3 month1

One visitor reported administration

The drugs are administered in various routes, like oral or injection form. They are administered before food or after food. How are you taking Mestinon drug, before food or after food?
Click here to find out how other users of our website are taking it. For any doubts or queries on how and when the medicine is administered, contact your health care provider immediately.
With a meal1

Two visitors reported age

> 601

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The information was verified by Dr. Rachana Salvi, MD Pharmacology

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