POM: Prescription only medicine
This information is intended for use by health professionals
|Transdermal patches||Rivastigmine in vivo release rates per 24 h|
|Alzest 4.6 mg/24 h||4.6 mg|
|Alzest 9.5 mg/24 h||9.5 mg|
|Rivastigmine 13.3 mg/24 h*||13.3 mg|
Initial doseTreatment is started with 4.6 mg/24 h.
Maintenance doseAfter a minimum of four weeks of treatment and if well tolerated according to the treating physician, the dose of 4.6 mg/24 h should be increased to 9.5 mg/24 h, the daily recommended effective dose, which should be continued for as long as the patient continues to demonstrate therapeutic benefit.
Dose escalation9.5 mg/24 h is the recommended daily effective dose which should be continued for as long as the patient continues to demonstrate therapeutic benefit. If well tolerated and only after a minimum of six months of treatment at 9.5 mg/24 h, the treating physician may consider increasing the dose to 13.3 mg/24 h in patients who have demonstrated a meaningful cognitive deterioration (e.g. decrease in the MMSE) and/or functional decline (based on physician judgement) while on the recommended daily effective dose of 9.5 mg/24 h (see section 5.1).The clinical benefit of rivastigmine should be reassessed on a regular basis. Discontinuation should also be considered when evidence of a therapeutic effect at the optimal dose is no longer present. Treatment should be temporarily interrupted if gastrointestinal adverse reactions are observed until these adverse reactions resolve. Transdermal patch treatment can be resumed at the same dose if treatment is not interrupted for more than three days. Otherwise treatment should be re-initiated with 4.6 mg/24 h.
Switching from capsules or oral solution to transdermal patchesBased on comparable exposure between oral and transdermal rivastigmine (see section 5.2), patients treated with rivastigmine capsules or oral solution can be switched to Alzest transdermal patches as follows:• A patient on a dose of 3 mg/day oral rivastigmine can be switched to 4.6 mg/24 h transdermal patches. • A patient on a dose of 6 mg/day oral rivastigmine can be switched to 4.6 mg/24 h transdermal patches.• A patient on a stable and well tolerated dose of 9 mg/day oral rivastigmine can be switched to 9.5 mg/24 h transdermal patches. If the oral dose of 9 mg/day has not been stable and well tolerated, a switch to 4.6 mg/24 h transdermal patches is recommended. • A patient on a dose of 12 mg/day oral rivastigmine can be switched to 9.5 mg/24 h transdermal patches.After switching to 4.6 mg/24 h transdermal patches, provided these are well tolerated after a minimum of four weeks of treatment, the dose of 4.6 mg/24 h should be increased to 9.5 mg/24 h, which is the recommended effective dose. It is recommended to apply the first transdermal patch on the day following the last oral dose.Special populations • Paediatric population: There is no relevant use of rivastigmine in the paediatric population in the treatment of Alzheimer's disease. • Patients with body weight below 50 kg: Particular caution should be exercised in titrating patients with body weight below 50 kg above the recommended effective dose of 9.5 mg/24 h (see section 4.4). They may experience more adverse reactions and may be more likely to discontinue due to adverse reactions. • Hepatic impairment: Due to increased exposure in mild to moderate hepatic impairment as observed with the oral formulation, dosing recommendations to titrate according to individual tolerability should be closely followed. Patients with clinically significant hepatic impairment may experience more dose-dependent adverse reactions. Patients with severe hepatic impairment have not been studied. Particular caution should be exercised in titrating these patients (see sections 4.4 and 5.2). • Renal impairment: No dose adjustment is necessary for patients with renal impairment (see section 5.2).
Method of administrationTransdermal patches should be applied once a day to clean, dry, hairless, intact healthy skin on the upper or lower back, upper arm or chest, in a place which will not be rubbed by tight clothing. It is not recommended to apply the transdermal patch to the thigh or to the abdomen due to decreased bioavailability of rivastigmine observed when the transdermal patch is applied to these areas of the body. The transdermal patch should not be applied to skin that is red, irritated or cut. Reapplication to the exact same skin location within 14 days should be avoided to minimise the potential risk of skin irritation.
Patients and caregivers should be instructed on important administration instructions:• The previous day's patch must be removed before applying a new one every day (see section 4.9). • The patch should be replaced by a new one after 24 hours. Only one patch should be worn at a time (see section 4.9). • The patch should be pressed down firmly for at least 30 seconds using the palm of the hand until the edges stick well. • If the patch falls off, a new one should be applied for the rest of the day, then it should be replaced at the same time as usual the next day. • The patch can be used in everyday situations, including bathing and during hot weather. • The patch should not be exposed to any external heat sources (e.g. excessive sunlight, saunas, solarium) for long periods of time. • The patch should not be cut into pieces.
Misuse of the medicinal product and dosing errors resulting in overdoseMisuse of the medicinal product and dosing errors with rivastigmine transdermal patch have resulted in serious adverse reactions; some cases have required hospitalisation, and rarely led to death (see section 4.9). Most cases of misuse of the medicinal product and dosing errors have involved not removing the old patch when putting on a new one and the use of multiple patches at the same time. Patients and their caregivers must be instructed on important administration instructions for rivastigmine transdermal patch (see section 4.2).
Gastrointestinal disordersGastrointestinal disorders such as nausea, vomiting and diarrhoea are dose-related, and may occur when initiating treatment and/or increasing the dose (see section 4.8). These adverse reactions occur more commonly in women. Patients who show signs or symptoms of dehydration resulting from prolonged vomiting or diarrhoea can be managed with intravenous fluids and dose reduction or discontinuation if recognised and treated promptly. Dehydration can be associated with serious outcomes.
Weight lossPatients with Alzheimer's disease may lose weight whilst taking cholinesterase inhibitors, including rivastigmine. The patient's weight should be monitored during therapy with rivastigmine transdermal patches.
BradycardiaRivastigmine may cause bradycardia which constitutes a risk factor in the occurrence of torsade de pointes, predominantly in patients with risk factors. Caution is advised in patients at higher risk of developing torsade de pointes; for example, those with uncompensated heart failure, recent myocardial infarction, bradyarrhythmias, a predisposition to hypokalaemia or hypomagnesaemia, or concomitant use with medicinal products known to induce QT prolongation and/or torsade de pointes (see sections 4.5 and 4.8).
Other adverse reactionsCare must be taken when prescribing Alzest transdermal patches:• to patients with sick sinus syndrome or conduction defects (sino-atrial block, atrio-ventricular block) (see section 4.8);• to patients with active gastric or duodenal ulcers or patients predisposed to these conditions because rivastigmine may cause increased gastric secretions (see section 4.8);• to patients predisposed to urinary obstruction and seizures because cholinomimetics may induce or exacerbate these diseases;• to patients with a history of asthma or obstructive pulmonary disease.
Skin application site reactionsSkin application site reactions may occur with rivastigmine patch and are usually mild or moderate in intensity. Patients and caregivers should be instructed accordingly.These reactions are not in themselves an indication of sensitisation. However, use of rivastigmine patch may lead to allergic contact dermatitis.Allergic contact dermatitis should be suspected if application site reactions spread beyond the patch size, if there is evidence of a more intense local reaction (e.g. increasing erythema, oedema, papules, vesicles) and if symptoms do not significantly improve within 48 hours after patch removal. In these cases, treatment should be discontinued (see section 4.3).Patients who develop application site reactions suggestive of allergic contact dermatitis to rivastigmine patch and who still require rivastigmine treatment should only be switched to oral rivastigmine after negative allergy testing and under close medical supervision. It is possible that some patients sensitised to rivastigmine by exposure to rivastigmine patch may not be able to take rivastigmine in any form. There have been rare post-marketing reports of patients experiencing allergic dermatitis (disseminated) when administered rivastigmine irrespective of the route of administration (oral, transdermal). In these cases, treatment should be discontinued (see section 4.3).
Other warnings and precautionsRivastigmine may exacerbate or induce extrapyramidal symptoms.Contact with the eyes should be avoided after handling Alzest transdermal patches (see section 5.3). Hands should be washed with soap and water after removing the patch. In case of contact with eyes or if the eyes become red after handling the patch, rinse immediately with plenty of water and seek medical advice if symptoms do not resolve.
Special populations• Patients with body weight below 50 kg may experience more adverse reactions and may be more likely to discontinue due to adverse reactions (see section 4.2). Carefully titrate and monitor these patients for adverse reactions (e.g. excessive nausea or vomiting) and consider reducing the maintenance dose to the 4.6 mg/24 h transdermal patch if such adverse reactions develop.• Hepatic impairment: Patients with clinically significant hepatic impairment may experience more adverse reactions. Dosing recommendations to titrate according to individual tolerability must be closely followed. Patients with severe hepatic impairment have not been studied. Particular caution must be exercised in titrating these patients (see sections 4.2 and 5.2).
PregnancyIn pregnant animals, rivastigmine and /or metabolites crossed the placenta. It is not known if this occurs in humans. No clinical data on exposed pregnancies are available. In peri/postnatal studies in rats, an increased gestation time was observed. Rivastigmine should not be used during pregnancy unless clearly necessary.
Breast feedingIn animals, rivastigmine is excreted in milk. It is not known if rivastigmine is excreted into human milk. Therefore, women on rivastigmine should not breast-feed.
FertilityNo adverse effects of rivastigmine were observed on fertility or reproductive performance in rats (see section 5.3). Effects of rivastigmine on human fertility are not known.
Summary of the safety profileApplication site skin reactions (usually mild to moderate application site erythema), are the most frequent adverse reactions observed with the use of rivastigmine transdermal patch. The next most common adverse reactions are gastrointestinal in nature including nausea and vomiting.Adverse reactions in Table 1 are listed according to MedDRA system organ class and frequency category. Frequency categories are defined using the following convention: very common (≥1/10); common (≥1/100 to <1/10); uncommon (≥1/1,000 to <1/100); rare (≥1/10,000 to <1/1,000); very rare (<1/10,000); not known (cannot be estimated from the available data).
Tabulated list of adverse reactionsTable 1 displays the adverse reactions reported in 1,670 patients with Alzheimer's dementia treated in randomised, double-blind, placebo and active-controlled clinical studies with rivastigmine transdermal patches for a duration of 24-48 weeks and from post-marketing data.
|Infections and infestations|
|Common||Urinary tract infection|
|Metabolism and nutrition disorders|
|Common||Anorexia, decreased appetite|
|Common||Anxiety, depression, delirium, agitation|
|Not known||Hallucinations, restlessness, nightmares|
|Nervous system disorders|
|Common||Headache, syncope, dizziness|
|Very rare||Extrapyramidal symptoms|
|Not known||Worsening of Parkinson's disease, seizure, tremor, somnolence|
|Not known||Atrioventricular block, atrial fibrillation, tachycardia, sick sinus syndrome|
|Common||Nausea, vomiting, diarrhoea, dyspepsia, abdominal pain|
|Not known||Hepatitis, elevated liver function tests|
|Skin and subcutaneous tissue disorders|
|Not known||Pruritus, erythema, urticaria, vesicles, allergic dermatitis (disseminated)|
|Renal and urinary disorders|
|General disorders and administration site conditions|
|Common||Application site skin reactions (e.g. application site erythema*, application site pruritus*, application site oedema*, application site dermatitis, application site irritation), asthenic conditions (e.g. fatigue, asthenia), pyrexia, weight decreased|
Description of selected adverse reactionsWhen doses higher than 13.3 mg/24 h were used in the above-mentioned placebo-controlled study, insomnia and cardiac failure were observed more frequently than with 13.3 mg/24 h or placebo, suggesting a dose effect relationship. However, these events did not occur at a higher frequency with rivastigmine 13.3 mg/24 h transdermal patches than with placebo.The following adverse reactions have only been observed with rivastigmine capsules and oral solution and not in clinical studies with rivastigmine transdermal patches: malaise, confusion, sweating increased (common); duodenal ulcers, angina pectoris (rare); gastrointestinal haemorrhage (very rare); and some cases of severe vomiting were associated with oesophageal rupture (not known).
Skin irritationIn double-blind controlled clinical trials, application site reactions were mostly mild to moderate in severity. The incidence of application site skin reactions leading to discontinuation was ≤2.3% in patients treated with Rivastigmine transdermal patches. The incidence of application site skin reactions leading to discontinuation was higher in the Asian population with 4.9% and 8.4% in the Chinese and Japanese population respectively. In two 24-week double-blind, placebo-controlled clinical trials, skin reactions were measured at each visit using a skin irritation rating scale. When observed in patients treated with Rivastigmine transdermal patches, skin irritation was mostly slight or mild in severity. It was rated as severe in ≤2.2% of patients in these studies and in ≤3.7% of patients treated with Rivastigmine transdermal patches in a Japanese study.
Reporting of suspected adverse reactionsReporting 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 the Yellow Card Scheme, website: www.mhra.gov.uk/yellowcard.
SymptomsMost cases of accidental overdose of oral rivastigmine have not been associated with any clinical signs or symptoms and almost all of the patients concerned continued rivastigmine treatment 24 hours after the overdose. Cholinergic toxicity has been reported with muscarinic symptoms that are observed with moderate poisonings such as miosis, flushing, digestive disorders including abdominal pain, nausea, vomiting and diarrhoea, bradycardia, bronchospasm and increased bronchial secretions, hyperhidrosis, involuntary urination and/or defecation, lacrimation, hypotension and salivary hypersecretion. In more severe cases nicotinic effects might develop such as muscular weakness, fasciculations, seizures and respiratory arrest with possible fatal outcome. Additionally there have been post-marketing cases of dizziness, tremor, headache, somnolence, confusional state, hypertension, hallucinations and malaise. Overdose with rivastigmine transdermal patch resulting from misuse/dosing errors (application of multiple patches at a time) has been reported in the post-marketing setting and rarely in clinical trials.
ManagementAs rivastigmine has a plasma half-life of about 3.4 hours and a duration of acetylcholinesterase inhibition of about 9 hours, it is recommended that in cases of asymptomatic overdose all Alzest transdermal patches should be removed immediately and no further transdermal patch should be applied for the next 24 hours. In overdose accompanied by severe nausea and vomiting, the use of antiemetics should be considered. Symptomatic treatment for other adverse reactions should be given as necessary. In massive overdose, atropine can be used. An initial dose of 0.03 mg/kg intravenous atropine sulphate is recommended, with subsequent doses based on clinical response. Use of scopolamine as an antidote is not recommended.
Clinical studies in Alzheimer's dementiaThe efficacy of rivastigmine transdermal patches in patients with Alzheimer's dementia has been demonstrated in a 24-week double-blind, placebo-controlled core study and its open-label extension phase and in a 48-week double blind comparator study.
24-week placebo-controlled studyPatients involved in the placebo-controlled study had an MMSE (Mini-Mental State Examination) score of 1020. Efficacy was established by the use of independent, domain-specific assessment tools which were applied at regular intervals during the 24-week treatment period. These include the ADAS-Cog (Alzheimer's Disease Assessment Scale Cognitive subscale, a performance-based measure of cognition) and the ADCS-CGIC (Alzheimer's Disease Cooperative Study Clinician's Global Impression of Change, a comprehensive global assessment of the patient by the physician incorporating caregiver input), and the ADCS-ADL (Alzheimer's Disease Cooperative Study Activities of Daily Living, a caregiver-rated assessment of the activities of daily living including personal hygiene, feeding, dressing, household chores such as shopping, retention of ability to orient oneself to surroundings as well as involvement in activities related to finances). The 24-week results for the three assessment tools are summarised in Table 2.
|ITT-LOCF population||Rivastigmine transdermal patches 9.5 mg/24 h N = 251||Rivastigmine capsules 12 mg/day N = 256||Placebo N = 282|
|Mean baseline ± SD||27.0 ± 10.3||27.9 ± 9.4||28.6 ± 9.9|
|Mean change at week 24 ± SD||-0.6 ± 6.4||-0.6 ± 6.2||1.0 ± 6.8|
|p-value versus placebo||0.005*1||0.003*1|
|Mean score ± SD||3.9 ± 1.20||3.9 ± 1.25||4.2 ± 1.26|
|p-value versus placebo||0.010*2||0.009*2|
|Mean baseline ± SD||50.1 ± 16.3||49.3 ± 15.8||49.2 ± 16.0|
|Mean change at week 24 ± SD||-0.1 ± 9.1||-0.5 ± 9.5||-2.3 ± 9.4|
|p-value versus placebo||0.013*1||0.039*1|
|Patients with clinically significant response (%)|
|ITT-LOCF population||Rivastigmine transdermal patches 9.5 mg/24 h N = 251||Rivastigmine capsules 12 mg/day N = 256||Placebo N = 282|
|At least 4 points improvement on ADAS-Cog with no worsening on ADCS-CGIC and ADCS-ADL p-value versus placebo||17.4 0.037*||19.0 0.004*||10.5|
48-week active comparator controlled studyPatients involved in the active comparator controlled study had an initial baseline MMSE score of 10-24. The study was designed to compare the efficacy of the 13.3 mg/24 h transdermal patch against the 9.5 mg/24 h transdermal patch during a 48-week double-blind treatment phase in Alzheimer's disease patients who demonstrated functional and cognitive decline after an initial 24-48 week open-label treatment phase while on a maintenance dose of 9.5 mg/24 h transdermal patch. Functional decline was assessed by the investigator and cognitive decline was defined as a decrease in the MMSE score of >2 points from the previous visit or a decrease of >3 points from baseline. Efficacy was established by the use of ADAS-Cog (Alzheimer's Disease Assessment Scale Cognitive subscale, a performance-based measure of cognition) and the ADCS-IADL (Alzheimer's Disease Cooperative Study Instrumental Activities of Daily Living) assessing instrumental activities which include maintaining finances, meal preparation, shopping, ability to orient oneself to surroundings, ability to be left unattended. The 48-week results for the two assessment tools are summarised in Table 4.
|Population/Visit||Rivastigmine 15 cm2 N = 265||Rivastigmine 10 cm2 N = 271||Rivastigmine 15 cm2||Riva-stigmine 10 cm2|
|CI confidence interval. DLSM difference in least square means. LOCF Last Observation Carried Forward. ADAS-cog scores: A negative difference in DLSM indicates greater improvement in rivastigmine 15 cm2 as compared to rivastigmine 10 cm2. ADCS-IADL scores: A positive difference in DLSM indicates greater improvement in rivastigmine 15 cm2 as compared to rivastigmine 10 cm2. N is the number of patients with an assessment at baseline (last assessment in the initial open-label phase) and with at least 1 post-baseline assessment (for the LOCF). The DLSM, 95% CI, and p-value are based on an ANCOVA (analysis of covariance) model adjusted for country and baseline ADAS-cog score. * p<0.05 Source: Study D2340-Table 11-6 and Table 11-7|
AbsorptionAbsorption of rivastigmine from rivastigmine transdermal patches is slow. After the first dose, detectable plasma concentrations are observed after a lag time of 0.5-1 hour. Cmax is reached after 10-16 hours. After the peak, plasma concentrations slowly decrease over the remainder of the 24-hour period of application. With multiple dosing (such as at steady state), after the previous transdermal patch is replaced with a new one, plasma concentrations initially decrease slowly for about 40 minutes on average, until absorption from the newly applied transdermal patch becomes faster than elimination, and plasma levels begin to rise again to reach a new peak at approximately 8 hours. At steady state, trough levels are approximately 50% of peak levels, in contrast to oral administration, with which concentrations fall off to virtually zero between doses. Although less pronounced than with the oral formulation, exposure to rivastigmine (Cmax and AUC) increased over-proportionally by a factor of 2.6 and 4.9 when escalating from 4.6 mg/24 h to 9.5 mg/24 h and to 13.3 mg/24 h, respectively. The fluctuation index (FI), a measure of the relative difference between peak and trough concentrations ((Cmax-Cmin)/Cavg), was 0.58 for rivastigmine 4.6 mg/24 h transdermal patches, 0.77 for rivastigmine 9.5 mg/24 h transdermal patches and 0.72 for rivastigmine 13.3 mg/24 h transdermal patches, thus demonstrating a much smaller fluctuation between trough and peak concentrations than for the oral formulation (FI = 3.96 (6 mg/day) and 4.15 (12 mg/day)).The dose of rivastigmine released from the transdermal patch over 24 hours (mg/24 h) cannot be directly equated to the amount (mg) of rivastigmine contained in a capsule with respect to plasma concentration produced over 24 hours.The single-dose inter-subject variability in rivastigmine pharmacokinetic parameters (normalised to dose/kg bodyweight) was 43% (Cmax) and 49% (AUC0-24h) after transdermal administration versus 74% and 103%, respectively, after the oral form. The inter-patient variability in a steady-state study in Alzheimer's dementia was at most 45% (Cmax) and 43% (AUC0-24h) after use of the transdermal patch, and 71% and 73%, respectively, after administration of the oral form.A relationship between active substance exposure at steady state (rivastigmine and metabolite NAP226-90) and bodyweight was observed in Alzheimer's dementia patients. Compared to a patient with a body weight of 65 kg, the rivastigmine steady-state concentrations in a patient with a body weight of 35 kg would be approximately doubled, while for a patient with a body weight of 100 kg the concentrations would be approximately halved. The effect of bodyweight on active substance exposure suggests special attention to patients with very low body weight during up-titration (see section 4.4).Exposure (AUC∞) to rivastigmine (and metabolite NAP266-90) was highest when the transdermal patch was applied to the upper back, chest, or upper arm and approximately 2030% lower when applied to the abdomen or thigh.There was no relevant accumulation of rivastigmine or the metabolite NAP226-90 in plasma in patients with Alzheimer's disease, except that plasma levels were higher on the second day of transdermal patch therapy than on the first.
DistributionRivastigmine is weakly bound to plasma proteins (approximately 40%). It readily crosses the blood-brain barrier and has an apparent volume of distribution in the range of 1.8-2.7 l/kg.
BiotransformationRivastigmine is rapidly and extensively metabolised with an apparent elimination half-life in plasma of approximately 3.4 hours after removal of the transdermal patch. Elimination was absorption rate limited (flip-flop kinetics), which explains the longer t½ after transdermal patch (3.4 h) versus oral or intravenous administrations (1.4 to 1.7 h). Metabolism is primarily via cholinesterase-mediated hydrolysis to the metabolite NAP226-90. In vitro, this metabolite shows minimal inhibition of acetylcholinesterase (<10%). Based on in vitro studies, no pharmacokinetic interaction is expected with medicinal products metabolised by the following cytochrome isoenzymes: CYP1A2, CYP2D6, CYP3A4/5, CYP2E1, CYP2C9, CYP2C8, CYP2C19, or CYP2B6. Based on evidence from animal studies, the major cytochrome P450 isoenzymes are minimally involved in rivastigmine metabolism. Total plasma clearance of rivastigmine was approximately 130 litres/h after a 0.2 mg intravenous dose and decreased to 70 litres/h after a 2.7 mg intravenous dose, which is consistent with the non-linear, over-proportional pharmacokinetics of rivastigmine due to saturation of its elimination.The metabolite-to-parent AUC∞ ratio was around 0.7 after transdermal patch administration versus 3.5 after oral administration, indicating that much less metabolism occurred after dermal compared to oral treatment. Less NAP226-90 is formed following application of the transdermal patch, presumably because of the lack of presystemic (hepatic first pass) metabolism, in contrast to oral administration.
EliminationUnchanged rivastigmine is found in trace amounts in the urine; renal excretion of the metabolites is the major route of elimination after transdermal patch administration. Following administration of oral 14C-rivastigmine, renal elimination was rapid and essentially complete (>90%) within 24 hours. Less than 1% of the administered dose is excreted in the faeces.A Population pharmacokinetic analysis showed that nicotine use increases the oral clearance of rivastigmine by 23% in patients with Alzheimer's disease (n=75 smokers and 549 non-smokers) following rivastigmine oral capsule doses for up to 12 mg/day.
Older peopleAge had no impact on the exposure to rivastigmine in Alzheimer's disease patients treated with rivastigmine transdermal patches.
Hepatic impairmentNo study was conducted with rivastigmine transdermal patches in subjects with hepatic impairment. After oral administration, the Cmax of rivastigmine was approximately 60% higher and the AUC of rivastigmine was more than twice as high in subjects with mild to moderate hepatic impairment than in healthy subjects.Following a single 3 mg or 6 mg oral dose, the mean oral clearance of rivastigmine was approximately 46-63% lower in patients with mild to moderate hepatic impairment (n=10, Child-Pugh score 5-12, biopsy proven) than in healthy subjects (n=10).
Renal impairmentNo study was conducted with rivastigmine transdermal patches in subjects with renal impairment. Based on population analysis, creatinine clearance did not show any clear effect on steady state concentrations of rivastigmine or its metabolite. No dose adjustment is necessary in patients with renal impairment (see section 4.2).
Matrix:- poly [(2-ethylhexyl)acrylate, vinylacetate] - medium molecular weight polyisobutene- high molecular weight polyisobutene - silica, colloidal anhydrous - paraffin, light liquid
Backing liner:- polyethylene/thermoplastic resin/aluminium coated polyester film
Release liner:- polyester film, fluoropolymer-coatedOrange printing ink
6 Riverview Road, Beverley, Hull, HU17 0LD
+44 (0)1482 860228
+44 (0)1748 828873
+44 (0)1482 389858