Medically reviewed by Oliinyk Elizabeth Ivanovna, PharmD. Last updated on 2022-04-06
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For the treatment of Trichuris trichuria (whipworm), Enterobius vermicularis (pinworm or threadworm), Ascaris lumbricoides (roundworm), Ancylostoma duodenale (common hookworm), Necator americanus (American hookworm) in single or mixed gastrointestinal infestations.
There is no evidence that Adec Tablets are effective in the treatment of cysticercosis.
Adults and children over 2 years:
For the control of trichuriasis, ascariasis and hookworm infections, one tablet twice a day for three consecutive days.
For the control of enterobiasis a single tablet is administered. It is highly recommended that a second tablet is taken after two weeks, if re-infection is suspected.
Tablets may be chewed or swallowed whole. Crush the tablet before giving it to a young child. Always supervise a child while they are taking this medicine.
Method of Administration
Adec is contraindicated in pregnancy and in patients who have shown hypersensitivity to the product or any components.
Not recommended in the treatment of children under 2 years.
A case-control study of a single outbreak of Stevens-Johnson syndrome /toxic epidermal necrolysis (SJS/TEN) suggested a possible association with the concomitant use of metronidazole with mebendazole. Although there are no additional data on this potential interaction, concomitant use of mebendazole and metronidazole should be avoided.
Adec has no influence on the ability to drive and use machines.
Throughout this section adverse reactions are reported. Adverse reactions are adverse events that were considered to be reasonably associated with the use of Adec based on the comprehensive assessment of the available adverse event information. A causal relationship with Adec cannot be reliably established in individual cases. Further, because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in clinical practice.
The safety of Adec was evaluated in 6276 subjects who participated in 39 clinical trials for the treatment of single or mixed parasitic infestations of the gastrointestinal tract. In these 39 clinical trials, no adverse drug reactions (ADRs) occurred in >1% of Adec-treated subjects.
ADRs identified from clinical trials and post-marketing experience with Adec are included in Table 1. The displayed frequency categories use the following convention:
Very common (>1/10); Common (>1/100 to <1/10); Uncommon (>1/1000 to <1/100); Rare (>1/10,000 to <1/1000); Very rare (<1/10,000), Not known (cannot be estimated from the available data).
Table 1: Adverse Drug Reactions Reported in Clinical Trials and Post-marketing Experience for Adec
System Organ Class
Adverse Drug Reactions
(> 1/100 to < 1/10)
(> 1/1000 to < 1/100)
(>1/10,000 to <1/1000)
Blood and lymphatic system disorders
Immune system disorders
Hypersensitivity including anaphylactic reaction and anaphylactoid reactionb
Nervous system disorders
Abnormal liver function testsb
Skin and subcutaneous tissue disorders
Toxic epidermal necrolysisb;
a ADR frequency data derived from Clinical Trials or Epidemiological Studies
b ADRs not observed in clinical trials and frequency calculated using â€œRule of 3â€, as detailed in SmPC guideline 2009. 6276 patients exposed in clinical trials and epidemiological studies, divided by 3 (Frequency = 1/2092). Note: frequencies differ from those reported in the August 2009 CCDS, as these were not calculated using the formula detailed in the SmPC guideline 2009.
Reporting of suspected adverse reactions
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via:
Yellow Card Scheme
In patients treated at dosages substantially higher than recommended or for prolonged periods of time, the following adverse reactions have been reported rarely: alopecia, reversible liver function disturbances, hepatitis, agranulocytosis, neutropenia and glomerulonephritis. With the exception of agranulocytosis and glomerulonephritis, these also have been reported in patients who were treated with mebendazole at standard dosages.
Signs and symptoms
In the event of accidental overdosage, abdominal cramps, nausea, vomiting and diarrhoea may occur.
There is no specific antidote. Activated charcoal may be given if considered appropriate.
Pharmacotherapeutic group: anthelmintic for oral administration, benzimidazole derivatives; ATC code: P02CA01.
In vitro and in vivo work suggests that mebendazole blocks the uptake of glucose by adult and larval forms of helminths, in a selective and irreversible manner. Inhibition of glucose uptake appears to lead to endogenous depletion of glycogen stores within the helminth. Lack of glycogen leads to decreased formation of ATP and ultrastructural changes in the cells.
There is no evidence that Adec is effective in the treatment of cysticercosis.
Following oral administration, < 10% of the dose reaches the systemic circulation, due to incomplete absorption and to extensive pre-systemic metabolism (first-pass effect). Maximum plasma concentrations are generally seen 2 to 4 hours after administration. Dosing with a high fat meal leads to a modest increase in the bioavailability of mebendazole.
The plasma protein binding of mebendazole is 90 to 95%. The volume of distribution is 1 to 2 L/kg, indicating that mebendazole penetrates areas outside the vascular space. This is supported by data in patients on chronic mebendazole therapy (e.g., 40 mg/kg/day for 3-21 months) that show drug levels in tissue.
Orally administered mebendazole is extensively metabolised primarily by the liver. Plasma concentrations of its major metabolites (amino and hydroxylated amino forms of mebendazole) are substantially higher than those of mebendazole. Impaired hepatic function, impaired metabolism, or impaired biliary elimination may lead to higher plasma levels of mebendazole.
Mebendazole, the conjugated forms of mebendazole, and its metabolites likely undergo some degree of enterohepatic recirculation and are excreted in the urine and bile. The apparent elimination half-life after an oral dose ranges from 3 to 6 hours in most patients.
During chronic dosing (e.g., 40 mg/kg/day for 3-21 months), plasma concentrations of mebendazole and its major metabolites increase, resulting in approximately 3-fold higher exposure at steady-state compared to single dosing.
No relevant information additional to that contained elsewhere in the Summary of Product Characteristics.
No special requirements.
However, we will provide data for each active ingredient