Motusol Max 2.32% w/w Gel 30g – Targeted Pain Relief of Joints & Muscles in Acute strains & sprains

Product Information

Diclofenac preferentially distributes and persists in inflamed tissue. It is found in concentrations up to 20 times higher than in plasma. After applying the gel on the skin you can use a permeable (non-occlusive) bandage but allow the gel to dry on the skin for a few minutes. Do not use an airtight occlusive dressing.

Motusol Max 2.32% w/w Gel 30g - Boots

Pharmacotherapeutic group: Topical products for joint and muscular pain; Anti-inflammatory preparations, non-steroids for topical use If you are exposed to direct sunlight or artificial sun there is a risk of skin reactions. You should avoid sunlight or artificial sun during treatment and for two weeks after stopping treatment. on open injuries, inflammations or infections of the skin as well as on eczema or mucous membranes, Tell your doctor or pharmacist if you are taking, have recently taken or might take/use any other medicines. In intended, cutaneous use of Motusol Max no interactions have become known so far.

year toxicity study, a dose-dependent increase in the incidence of thrombosis of the heart was observed in diclofenac-treated rats.

Motusol Max 2.32% w/w Gel 50g – Targeted Pain Relief of

Also contains:carbomer, cocoyl caprylocaprate, macrogol cetostearyl ether, liquid paraffin, diethylamine, isopropyl alcohol, propylene glycol (E1520), fragrance (containing Adults and adolescents aged 14 years and over: Apply 3-4 times a day to the affected area of skin. Do not use for longer than 7 days. If the symptoms worsen or do not improve after 3-5 days, consult a doctor. The maximum daily dose is 8g of gel.Inhibition of prostaglandin synthesis may adversely affect the pregnancy and/or the embryo/fetal development. Data from epidemiological studies suggest an increased risk of miscarriage and of cardiac malformation and gastroschisis after use of a prostaglandin synthesis inhibitor in early pregnancy. The absolute risk for cardiovascular malformation was increased from less than 1%, up to approximately 1.5 %. The risk is believed to increase with dose and duration of therapy. In animals, administration of a prostaglandin synthesis inhibitor has been shown to result in increased pre-and post-implantation loss and embryofetal lethality. In addition, increased incidences of various malformations, including cardiovascular, have been reported in animals given a prostaglandin synthesis inhibitor during the organogenetic period.