Emidas Ls
Emidas Ls Uses, Dosage, Side Effects, Food Interaction and all others data.
The mechanism of action of betahistine is known partially. Betahistine has a very strong affinity as an antagonist for histamine H3 receptors and a weak affinity as an agonist for histamine H1 receptors. The active ingredient is a specific histamine agonist with virtually no H2-activity.
Betahistine has two modes of action. Primarily, it has a direct stimulating (agonistic) effect on H1 receptors located on blood vessels in the inner ear. It appears to act on the precapillary sphincter in the stria vascularis of the inner ear, thus reducing the pressure in the endolymphatic space.
In addition, betahistine has a powerful antagonistic effects at H3 receptors, and increases the levels of neurotransmitters released from the nerve endings. The increased amounts of histamine released from histaminergic nerve endings stimulates H1 receptors, thus augmenting the direct agonistic effects of betahistine on these receptors. This explains the potent vasodilatory effects of betahistine in the inner ear. This explains the efficacy of betahistine in the treatment of vertigo.
Through its actions on the histamine receptors, betahistine provides relief from vertigo associated with Ménière's disease.
Ginkgo biloba extract contains a group of terpene lactones (notably, ginkgolides and diterpenes) and ginkgo flavone glycosides (notably, ginkgetin, bilobetin, and sciadopitysin) that have antioxidant and vasoactive properties. Most of the studies that investigate the effect of ginkgo biloba use the standardized extract of Ginkgo biloba (EGb) 761 (EGb761), which was developed by a German pharmaceutical company in 1964. EGb761 contains 6% terpene lactones and 24% flavonoid glycosides. Flavonoids include quercetin, rutin, kaempferol, and isorhamnetin. Lactones include ginkgolide A, ginkgolide B, ginkgolide C, bilobalide, and ginkgotoxin, a lactone that is structurally related to pyridoxine. Ginkgo biloba is an herbal plant that is now cultivated worldwide. It is originally native to China, and ginkgo biloba extract has been used in traditional Chinese medicine for centuries.
After its nootropic properties were discovered, ginkgo biloba has gained attention as a therapeutic ingredient for memory and concentration enhancement in cognitive impairment and neurogenerative diseases, such as dementia. Ginkgo biloba was investigated in preliminary studies for a variety of therapeutic purposes such as improving cardiovascular health, sexual dysfunction, psychiatric disorders, skin disorders, and glaucoma. Ginkgo biloba is found in a number of homeopathic and over-the-counter herbal products and dietary supplements, but it has no approved therapeutic indications by regulatory bodies, such as the FDA, EMA, and Health Canada. Ginkgo folium, the leaf extract of Ginkgo biloba, is considered an anti-dementia drug by the World Health Organization.
Ginkgo biloba is a herbal ingredient with demonstrated antioxidant, vasoactive, antiapoptotic, anti-inflammatory, antiplatelet, and fibrinolytic properties. Ginkgo biloba has been investigated for use in a variety of medical conditions, but the most extensively studied area is in the context of cognitive impairment and neurodegenerative disorders. Ginkgo biloba was examined as a potential nootropic agent or cognitive enhancer but research findings supporting the therapeutic efficacy of ginkgo biloba extract (EGb) in dementia remain controversial. Some clinical studies of dementia that were up to one year long showed that EGb improves the cognitive performance and social functioning of patients. However, other studies did not support its clinical benefit for patients with cognitive impairment and dementia. Numerous meta-analysis studies showed insufficient evidence of the effectiveness of EGb in reducing both all-cause dementia incidence and Alzheimer's disease-associated dementia incidence in elderly patients with normal cognition or with mild cognitive impairment. Additionally, there is no up-to-date evidence that demonstrates the benefit of the long-term use of standardized EGb in reducing the risk of progression to Alzheimer's disease. A 2012 meta-analysis did not support the use of EGb in enhancing cognitive function in healthy adults.
Piracetam's mechanism of action is not fully understood. The drug influences neuronal and vascular functions and influences cognitive function without acting as a sedative or stimulant. Piracetam is a positive allosteric modulator of the AMPA receptor. It is hypothesized to act on ion channels or ion carriers, thus leading to increased neuron excitability. GABA brain metabolism and GABA receptors are not affected by piracetam
It has been found to increase blood flow and oxygen consumption in parts of the brain, but this may be a side effect of increased brain activity rather than a primary effect or mechanism of action for the drug.
Piracetam improves the function of the neurotransmitter acetylcholine via muscarinic cholinergic (ACh) receptors, which are implicated in memory processes. Furthermore, piracetam may have an effect on NMDA glutamate receptors, which are involved with learning and memory processes. Piracetam is thought to increase cell membrane permeability. Piracetam may exert its global effect on brain neurotransmission via modulation of ion channels (i.e., Na+, K+). It has been found to increase oxygen consumption in the brain, apparently in connection to ATP metabolism, and increases the activity of adenylate kinase in rat brains. Piracetam, while in the brain, appears to increase the synthesis of cytochrome b5, which is a part of the electron transport mechanism in mitochondria. But in the brain, it also increases the permeability of the mitochondria of some intermediaries of the Krebs cycle.
Piracetam is known to mediate various pharmacodynamic actions:
Neuronal effects:
Piracetam modulates the cholinergic, serotonergic, noradrenergic, and glutamatergic neurotransmission although the drug does not display high affinity to any of the associated receptors (Ki >10μM). Instead, piracetam increases the density of postsynaptic receptors and/or restore the function of these receptors through stabilizing the membrane fluidity . In the forebrain of aging mice, the density of NMDA receptors was increased by approximately 20% following 14 days of piracetam treatment. Based on the findings of various animal and human studies, the cognitive processses including learning, memory, attention and consciousness were enhanced from piracetam therapy without inducing sedation and psychostimulant effects . Piracetam mediate neuroprotective effects against hypoxia-induced damage, intoxication, and electroconvulsive therapy .
Vinpocetine increases cerebral metabolism; it increases glucose and O2 consumption; improves cerebral hypoxia tolerance; shifts glucose metabolism to the energetically more favourable aerobic pathway, but it increases the anaerobic pathway as well; it elevates the ATP concentration and the ATP/AMP ratio in the brain, and elevates the cerebral norepinephrine, dopamine and serotonin levels.
Vinpocetine considerably improves cerebral microcirculation by inhibiting platelet aggregation, reducing the pathologically increased blood viscosity, and increases erythrocyte deformability. It also promotes O2 transport into the tissues by reducing the O2 affinity of erythrocytes.
It selectively and intensely increases cerebral blood flow and the share of the brain in cardiac output, it reduces cerebral vascular resistance without affecting systemic circulation (blood pressure, heart rate, cardiac output, total peripheral resistance). It does not elicit steal phenomenon; on the contrary, it primarily improves the blood supply of the injured and ischaemic area while it remains unchanged in the intact areas (inverse steal effect). It further increases blood flow which is already increased as a result of hypoxia.
| Trade Name | Emidas Ls |
| Generic | Betahistine + Ginkgo Biloba + Piracetam + Vinpocetine |
| Type | Tablet |
| Therapeutic Class | |
| Manufacturer | Med Manor Organics Pvt Ltd |
| Available Country | India |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Betahistine Mesilate dilates precapiilary sphincters, increasing the blood flow in the inner ear. It controls the permeability of capillaries in the inner ear, thereby removes endolymphatic hydrops. It also improves cerebral circulation, increasing blood flow in the internal carotid artery. Thus, Betahistine Mesylate is clinically useful for the relief of vertigo and dizziness.
Ginkgo biloba is a herbal supplement found in over-the-counter or unapproved homeopathic products for various health conditions, such as cognitive, neurodegenerative, cardiovascular, and reproductive health disorders.
Ginkgo biloba does not currently have any approved therapeutic indications, and there is insufficient evidence to support its unapproved use. It is available in over-the-counter herbal products mostly for oral use, to improve memory and cognitive problems.
Cerebral vascular accidents and cerebral insufficiencies: Ischaemic or even haemorrhagic acute accidents, chronic manifestations of the above accidents or of cerebral atherosclerosis.
Mental retardation in children: Ease of resuming individual contact, sociability and learning, improved intellectual performances and school results.
Behaviour and psychotic problems in old age: Memory deficits, particularly with regard to fixation and evocation asthenia adaption disorders, disturbed psychomotor reactions. Patients suffering from myoclonus of cortical origin.
All forms of acute and chronic cerebral circulatory insufficiency: TIA (Transient Ischaemic Attack), reversible ischaemic neurological deficiency, progressive stroke, completed stroke, post-apoplectic conditions, multiinfarct dementia, cerebral arteriosclerosis, post-traumatic, hypertensive encephalopathy etc.
For the reduction of psychic or neurological symptoms of cerebral insufficiency (e.g., memory disturbances, dizziness, headache, aphasia, apraxia, locomotor disorders etc.).
Ophthalmology: It can be used for the treatment of vascular disorders of the choroid and retina due to arteriosclerosis, vasospasm, macular degeneration, arterial or venous thrombosis or embolism, and glaucoma secondary to the above mentioned disorders.
Otology: For the treatment of impaired hearing of vascular or toxic (iatrogenic) origin, presbyacusis, Meniere’s disease, cochleovestibular neuritis, tinnitus and dizziness of labyrinth origin.
For the treatment of vasovegetative symptoms of climacteric syndrome.For the treatment of vasovegetative symptoms of climacteric syndrome.
Emidas Ls is also used to associated treatment for these conditions: Menière's DiseaseCognitive Dysfunctions, Cognitive Function, DepressionAlcohol Dependency, Alcohol Withdrawl, Cognitive Deficits caused by Injuries, Craniocerebral, Cognitive Dysfunctions, Cognitive Impairments, Comatose caused by Blood Vessel (Vascular) Dysfunction, Comatose caused by CNS Toxicity, Comatose caused by Traumas, Learning Disorders, Myoclonus, Sickle Cell Disease (SCD), Giddiness caused by Injuries, CraniocerebralCerebrovascular stenosis, Neurological Disorders
How Emidas Ls works
Vertigo is a disturbing sensation of movement caused by dysfunction of the labyrinth (inner ear), vestibular nerve, cerebellum, brainstem, or Central Nervous System (CNS). Vestibular forms of vertigo are often accompanied by auditory dysfunctions such as hyperacusis, hearing loss, and tinnitus. In most cases, adaptive mechanisms of the CNS lead to functional recovery after episodes of vertigo, however, syndromes such as Ménière's disease tend to cause the recurrence of vertigo symptoms. This significantly impacts the quality of life and the ability to carry out daily activities.
H1-receptor activity
The mechanism of action of betahistine is multifactorial. Ménière's disease is thought to result from a disruption of endolymphatic fluid homeostasis in the ear. Betahistine mainly acts as a histamine H1-receptor agonist. The stimulation of H1-receptors in the inner ear causes a vasodilatory effect leading to increased permeability of blood vessels and a reduction in endolymphatic pressure; this action prevents the rupture of the labyrinth, which can contribute to the hearing loss associated with Ménière's disease. Betahistine is also purported to act by reducing the asymmetrical functioning of sensory vestibular organs and increasing vestibulocochlear blood flow, relieving symptoms of vertigo.
H3-receptor activity
In addition to the above mechanisms, betahistine also acts as a histamine H3-receptor antagonist, increasing the turnover of histamine from postsynaptic histaminergic nerve receptors, subsequently leading to an increase in H1-agonist activity. H3-receptor antagonism elevates levels of neurotransmitters including serotonin in the brainstem, inhibiting the activity of vestibular nuclei, thus restoring proper balance and decreasing vertigo symptoms.
Two key active ingredients in ginkgo biloba are terpene lactones (notably ginkgolides and diterpenes) and ginkgo flavone glycosides (notably ginkgetin, bilobetin, and sciadopitysin), which are present at varying concentrations. Ginkgo biloba extract EGb 761 is the standardized extract of ginkgo biloba used in studies, which contains 6% terpenoids and 24% flavonoid glycosides. Animal studies have shown that ginkgo biloba works on several neurotransmitter pathways and brain structures. Flavones were shown to inhibit lipid peroxidation; inhibit the uptake of serotonin, dopamine, and norepinephrine; and inhibit platelet aggregation. Terpene lactones may also act as potent antagonists of the platelet-activating factor and may possess anti-ischemic and fibrinolytic effects. They were also shown to downregulate adrenal peripheral benzodiazepine receptors and increase adrenocorticotropic hormone levels. Ginkgo biloba also reversibly inhibits monoamine oxidase A; and modestly inhibits anticholinesterase activity, leading to enhanced cholinergic transmission in the brain.
Several studies suggest that ginkgo biloba exerts neuroprotective effects by reducing free radical production in the prefrontal cortex, which may explain its improvement on short-term memory. Ginkgo biloba extract acts as a free radical scavenger, protecting neurons from oxidative damage and apoptosis related to aging, cerebral ischemia, and neurodegenerative disorders. Ginkgo biloba also inhibits amyloid-β neurotoxicity and protects against hypoxic challenges and increased oxidative stress. One study showed that bilobalide, a terpene lactone, delays the onset of hypoxic glycolysis. Ginkgo biloba has the potential to regulate metabolism, stabilize the membrane, and promote vasodilation. In the arterial endothelium, EGb stimulated the release of endogenous relaxing factors, such as endothelium-derived relaxing factor and prostacyclin. In the inflammatory environment that causes tissue damage, EGb promoted nitric oxide production, leading to enhanced peripheral and cerebral blood flow.
Piracetam interacts with the polar heads in the phospholipids membrane and the resulting mobile drug-lipid complexes are thought to reorganize the lipids and influence membrane function and fluidity . Such interaction has been reported in a study that investigated the effects of neuronal outgrowth induced by beta amyloid peptides; while amyloid peptides cause lipid disorganization within the cell membranes leading to neuronal death, piracetam demonstrated to decrease the destabilizing effects of amyloid peptide . The authors suggest that piracetam induces a positive curvature of the membrane by occupying the polar groups in the phospholipids to counteract the negative curvature induced by amyloid peptides , which in turn would decrease the likelihood of membrane fusion . This mechanism of action is thought to improve membrane stability, allowing the membrane and transmembrane proteins to maintain and recover the three-dimensional structure or folding for normal function such as membrane transport, chemical secretion, and receptor binding and stimulation .
Through restored membrane fluidity, piracetam promotes restored neurotransmission such as glutamatergic and cholinergic systems, enhances neuroplasticity and mediates neuroprotective and anticonvulsant effects at the neuronal level . It is also demonstrated that piracetam also improves the fluidity of platelet membranes. At the vascular level, piracetam decreases adhesion of erythrocytes to cell wall and reduces vasospasm which in turn improves microcirculation including cerebral and renal blood flow .
Dosage
Emidas Ls dosage
Usually for adults, administer orally 6 mg to 12 mg three times per day after meals. The dose may be adjusted according to the age of patient and severity of symptoms.
Oral: Adults:
- In cerebro-cortical insufficiency disorders, usual dose is one tablet (800 mg) 3 times a day.
- In myoclonic seizures, a dose of 7.2 gm daily, increasing by 4.8 gm per day every 3 to 4 days up to maximum of 20 gm daily, given in 2 or 3 divided doses.
Oral: Children:
The daily dosage depends on the weight of the child, 50 mg/kg of body weight in 3 divided doses. Once the desired results has been obtained, reduce the initial dose by half.
Parenteral formulations: When parenteral administration is needed (e.g. swallowing difficulties, unconsciousness) Piracetam can be administered intravenously.When treating severe symptoms, 12 g daily may need to be administered as an intravenous infusion.
Vinpocetine is taken 15-30 mg daily in 3 divided doseswith meals. The maintenance dose is 15 mg three times daily over long periods.
Piracetam is compatible (physico-chemical compatibility) with the perfusions of:
- Glucose 5%, 10%, 20%
- Fructose 5%, 10%, 20%
- Sodium chloride 0.9%
- Dextran 40 (10% in a 0.9% NaCl solution)
- Ringer Mannitol 20%
- HES solution (Hydroxy Ethyl Starch) 6% and 10%
The stability of these solutions has been demonstrated up to 24 hours.
Side Effects
Nausea or vomiting may rarely occur. Hypersensitivity reactions, such as skin rash, may rarely occur.
The side effects reported include nervousness, agitation, irritability, anxiety and sleep disturbances. The incidence of these during clinical trials was (≤ 5%) and they were more often noted in the older patients taking > 2.4 gm daily. In the majority of cases, a dose reduction sufficed to make these symptoms disappear. Some patients may complain of fatigue or drowsiness, gastrointestinal problems, e.g. nausea, vomiting, diarrhoea and stomachache have also been reported but their incidence during clinical trials was ≤ 2%. Other symptoms e.g. vertigo, headache, trembling and sexual stimulation have occasionally been reported.
Vinpocetine is well tolerated. In some cases transient fall of blood pressure and tachycardia may occur.
Toxicity
Symptoms of an overdose with betahistine (< 640 mg) include dry mouth, nausea, dyspepsia, abdominal pain, and somnolence. Serious complications such as convulsions, pulmonary or cardiac effects may occur with higher doses (> 640 mg), especially during intentional overdoses and combination with other drugs. In the case of an overdose with betahistine, provide supportive therapy, and contact the local poison control center for further management.
Oral LD50 of standardized extract in mice is 7730 mg/kg, which corresponds to 2300 mg/kg of active ingredients, 1900 mg/kg of flavone glycosides, and 464 mg/kg of terpene lactones. Intravenous LD50 is 1100 mg/kg.
No case of overdose has been reported so far. Cyanogenic glycosides found in raw ginkgo seeds are potentially toxic compounds; thus, contact or ingestion of ginkgo seeds can lead to serious reactions such as allergic skin reaction, including acute generalized exanthematous pustulosis, and convulsions. Ginkgo toxicity can manifest as bleeding, seizure, and serotonin syndrome. As there is no known antidote for ginkgo toxicity, treatment includes discontinuation of ginkgo and symptomatic and supportive care. Seizures may be attributed to ginkgotoxin, which can cause seizures at high doses.
The cases of overdose with piracetam is rare. The highest reported overdose with piracetam was oral intake of 75g which was associated with diarrhea and abdominal pain; the signs were most likely related to the extreme high dose of sorbitol contained in the used formulation. In cases of acute, significant overdosage, stomach emptying by gastric lavage or induced emesis is recommended as there are no known antidotes for piracetam . Management for an overdose will most likely be symptomatic treatment and may include hemodialysis, where the extraction efficacy of the dialyser is 50 to 60% for the drug .
Oral LD50 in a mouse acute toxicity study was 2000 mg/kg .
Precaution
Patients with a history of digestive ulcer or an active digestive ulcer, Patients with bronchial asthma, Patients with pheochromocytoma.
Because Vinpocetine can reduce the ability of blood to clot, those individuals with a tendency to bleed should avoid Vinpocetine.
Interaction
In a single case, confusion, irritability and sleep disorders were reported in concomitant use with thyroid extract. At present, no interaction has been observed with the following anti-epileptic drugs, clonazepam, carbamazepine, phenyton, phenobarbitone and sodium valporate, based on a small number of studies.
Slight changes in prothrombin time have been noted in those adding Vinpocetine to Warfarin dosing. The changes appear minimal. There are no other interactions reported so far. Therefore, it can be applied in combinations.
Volume of Distribution
In a pharmacokinetic study of rats, betahistine was found to be distributed throughout the body. Human data for betahistine's volume of distribution is not readily available.
No data available.
Vd is approximately 0.6L/kg. Piracetam may cross the blood-brain barrier as it was measured in the cerebrospinal fluid following intravenous administration . Piracetam diffuses to all tissues except adipose tissues, crosses placental barrier and penetrates the membranes of isolated red blood cells .
Elimination Route
When given orally, betahistine is rapidly and almost completely absorbed from the gastrointestinal tract. In the fasted state, Cmax is achieved within 1 hour of administration; in the fed state, Cmax is delayed, but the total drug absorption is similar. Food, therefore, has little effect on the absorption of betahistine.
Studies assessed the pharmacokinetic parameters of terpene lactones, the main component of ginkgo biloba. Following oral administration of ginkgo biloba solution, the mean absolute bioavailability was 80% for ginkgolide A, 88% for ginkgolide B and 79% for biloalide. In an early rat study, about 60% of radiolabeled EGb 761 was absorbed with a Tmax of 1.5 hours. The highest amount of radioactivity was measured in the stomach and small intestine.
In another study, after a single oral dose of 120 mg EGb 761 in healthy volunteers, Cmax was 22.22 ± 4.57 ng/mL for ginkgolide A, 8.27 ± 1.82 ng/mL for ginkgolide B, and 54.42 ± 13.62 ng/mL for biloalide. AUC0-∞ was 121.35 ± 22.92 ng × h/mL for ginkgolide A, 59.88 ± 11.39 ng × h/mL for ginkgolide B, and 217.24 ± 44.07 ng × h/mL for biloalide. Tmax ranged from 1.17 to 1.54 hours for those three compounds.
Piracetam displays a linear and time-dependent pharmacokinetic properties with low intersubject variability over a large range of doses. Piracetam is rapidly and extensively absorbed following oral administration with the peak plasma concentration is reached within 1 hour after dosing in fasted subjects. Following a single oral dose of 3.2 g piracetam, the peak plasma concentration (Cmax) was 84 µg/mL. Intake of food may decrease the Cmax by 17% and increase the time to reach Cmax (Tmax) from 1 to 1.5 hours. Tmax in the cerebrospinal fluid is achieved approximately 5 hours post-administration .
The absolute bioavailability of piracetam oral formulations is close to 100% and the steady state plasma concentrations are achieved within 3 days of dosing .
Half Life
The half-life of betahistine is 3-4 hours.
Unpublished human data reports that after oral administration of 80 mg EGb 761, the half-life was four hours for ginkgolides A and six hours for ginkgolides B. The half-life of bilobalide was three hours after administration of 120 mg EGb 761 extract.
The plasma half life of piracetam is approximately 5 hours following oral or intravenous administration. The half life in the cerebrospinal fluid was 8.5 hours .
Clearance
No data available.
The apparent total body clearance is 80-90 mL/min .
Elimination Route
Betahistine is mainly excreted in the urine; with approximately 85-91% being detected in urine samples within 24 hours of administration.
At 72 hours following oral administration in rats, about 38% of the ginkgo biloba extract was excreted via expiration, 22% was excreted in urine, and 29% was excreted in feces. About 70% of ginkgolides A, 50% of ginkgolides B, and 30% of bilobalide were excreted unchanged in the urine.
Piracetam is predominantly excreted via renal elimination, where about 80-100% of the total dose is recovered in the urine. Approximately 90% of the dose of piracetam is excreted in the urine as unchanged drug .
Pregnancy & Breastfeeding use
Safety of Betahistine during pregnancy has not been established. This drug should be administered to pregnant patients or women suspected of being pregnant, only if the expected therapeutic benefit is thought to outweigh any possible risk.
Piracetam should not be prescribed during pregnancy or when breast feeding, except under exceptional circumstances. Piracetam is able to cross the placenta.
Pregnancy category- Not classified
Contraindication
Hypersensitivity to betahistine mesylate, pheochromocytoma, peptic ulcer, acute bronchial asthma.
Piracetam is contra-indicated in patients with severe renal insufficiency (creatinine clearance < 20 ml/min) and hepatic impairment. As the principal route of elimination for Piracetam is via the kidney, special care must be taken when treating patients known to suffer from renal insufficiency. Monitoring of renal function is recommended in such cases. The increase in half-life is directly related to the decrease in renal function and creatinine clearance. This is also true for the older patient in whom creatinine clearance is dependent on age. When the creatinine clearance is < 60 ml/min, or serum creatinine is >1.25 mg/100 ml, the dosage prescribed should be calculated as following:
CrCl 60-40 ml/min: Dosage should be 1/2 of normal dose
CrCl 40-20 ml/min: Dosage should be 1/4 of normal dose
Vinpocetine is contraindicated in pregnancy and lactation. Hypersensitivity to its components is also contraindicated.
Special Warning
Children: No formal pharmacokinetic study has been conducted in children.
Elderly: In the elderly, the half-life of piracetam is increased and the increase is related to the decrease in renal function in this population (see Section Dosage and Administration).
Renal impairment: Piracetam clearance is correlated to creatinine clearance. It is therefore recommended to adjust the daily dose of piracetam based on creatinine clearance in patients with renal impairment
Hepatic impairment: The influence of hepatic impairment on the pharmacokinetics of piracetam has not been evaluated. Because 80 to 100% of the dose is excreted in the urine as unchanged drug, hepatic impairment solely would not be expected to have a significant effect on piracetam elimination.
Acute Overdose
Piracetam appears to be devoid of toxicity even at very high doses and, therefore, the need for specific measures to be taken in case of an overdose is avoided. Drug Interactions: In a single case, confusion, irritability and sleep disorders were reported in concomitant use with thyroid extract. At present, no interaction has been observed with the following anti-epileptic drugs, clonazepam, carbamazepine, phenytoin, phenobarbitone and sodium valproate, based on a small number of studies.
Storage Condition
Store in cool and dry place. Protect from light & moisture.
Store in a cool and dry place at a temperature below 30˚C , Keep away from sunlight. Keep out of the reach of children.
Store in a cool and dry place, protected from light and moisture
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