Metalyse 25 mg

1 vial contains 5,000 units (25 mg) tenecteplase.
The reconstituted solution contains 1,000 units (5 mg) tenecteplase per ml.
Potency of tenecteplase is expressed in units (U) by using a reference standard which is specific for tenecteplase and is not comparable with units used for other thrombolytic agents.
Excipients/Inactive Ingredients: Arginine, Phosphoric acid, Polysorbate 20.
Trace residue from manufacturing process: Gentamicin.

Pharmacotherapeutic group: Antithrombotic agents. ATC code: B01AD11.
Pharmacology: Pharmacodynamics: Mode of action: Tenecteplase is a recombinant fibrin-specific plasminogen activator that is derived from native t-PA by modifications at three sites of the protein structure. It binds to the fibrin component of the thrombus (blood clot) and selectively converts thrombus-bound plasminogen to plasmin, which degrades the fibrin matrix of the thrombus. Tenecteplase has higher fibrin specificity and greater resistance to inactivation by its endogenous inhibitor (PAI-1) compared to native t-PA.
Pharmacodynamics: After administration of tenecteplase dose dependent consumption of α2-antiplasmin (the fluid-phase inhibitor of plasmin) with consequent increase in the level of systemic plasmin generation have been observed. This observation is consistent with the intended effect of plasminogen activation. In comparative studies a less than 15% reduction in fibrinogen and a less than 25% reduction in plasminogen were observed in subjects treated with the maximum dose of tenecteplase (10,000 U, corresponding to 50 mg), whereas alteplase caused an approximately 50% decrease in fibrinogen and plasminogen levels. No clinically relevant antibody formation was detected at 30 days.
Clinical trials: AcT study: The Alteplase Compared to Tenecteplase (AcT) trial, was designed as a pragmatic, registry based, prospective, randomized, open label, controlled trial of intravenous tenecteplase vs. intravenous alteplase to provide evidence that tenecteplase is non-inferior to alteplase in patients with acute ischemic stroke within 4.5 h from last known well otherwise eligible for intravenous thrombolysis as per current guidelines. The trial achieved its primary outcome demonstrating a clinically relevant non inferiority with tenecteplase 0.25 mg/kg (max. 25 mg) vs alteplase 0.9 mg/kg (max. 90 mg): 296 (36.9%) of 802 patients in the tenecteplase group and 266 (34.8%) of 765 in the alteplase group had an mRS score of 0-1 at 90-120 days (unadjusted risk difference 2.1% [95% CI - 2.6 to 6.9], meeting the prespecified non-inferiority threshold of -5%).
Key safety outcomes were symptomatic intracerebral haemorrhage, orolingual angio-oedema, and extracranial bleeding requiring blood transfusion, all occurring within 24 h of thrombolytic administration, and 90-day all-cause mortality.
There were no meaningful differences in the rate of 24 h symptomatic intracerebral haemorrhage. Rates of imaging-defined intracranial haemorrhage (assessed blinded to symptom status and treatment allocation) showed no differences between the two groups, and the imaging-defined rates of type 2 parenchymal haematoma (i.e., haematoma occupying ≥30% of infarct with obvious mass effect) were similar to the observed rates of symptomatic intracerebral haemorrhage in the trial. There were no meaningful differences in the rate of 90-day mortality 90 days from treatment. Orolingual angioedema and peripheral bleeding requiring blood transfusion were rare and similar in both groups (see Table 1).

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EXTEND-IA TNK study: EXTEND-IA TNK was designed to assess whether tenecteplase is non-inferior to alteplase in achieving reperfusion at initial angiogram when administered within 4.5 h of ischaemic stroke onset in patients planned to undergo endovascular therapy.
Patients with ischaemic stroke who had occlusion of the internal carotid, basilar, or middle cerebral artery and who were eligible to undergo thrombectomy were randomised to receive tenecteplase 0.25 mg/kg or alteplase 0.9 mg/kg within 4.5 h after symptom onset. There were 101 patients in each treatment group. The primary outcome was reperfusion of greater than 50% of the involved ischaemic territory or an absence of retrievable thrombus at the time of the initial angiographic assessment. Noninferiority of tenecteplase was tested, followed by superiority. Secondary outcomes included the mRS score at 90 days.
The primary outcome occurred in 22% of the patients treated with tenecteplase vs 10% of those treated with alteplase (incidence difference, 12%; 95% CI 2, 21; incidence ratio, 2.2; 95% CI 1.1, 4.4; p=0.002 for non-inferiority; p=0.03 for superiority).
In an ordinal analysis of the modified Rankin scale score at 90 days, patients in the tenecteplase group had a median score of 2 (interquartile range, 0 to 3), which indicated significantly better function than the median score of 3 (interquartile range, 1 to 5) among patients in the alteplase group (common odds ratio, 1.7; 95% CI, 1.0 to 2.8; p=0.04). There was no significant difference in the incidence of recovery to independent function (modified Rankin scale score of 0 to 2 or no change from baseline function) at day 90, which occurred in 65 of 101 patients (64%) in the tenecteplase group and in 52 of 101 (51%) in the alteplase group (adjusted incidence ratio, 1.2; 95% CI, 1.0 to 1.5; p=0.06; adjusted odds ratio, 1.8; 95% CI, 1.0 to 3.4; p=0.06).
The proportion of mRS 0-1 at 90 days was 51% for the tenecteplase group and 43% for the alteplase group (p=0.23).
The sICH occurred in 1% of the patients in each group. There were 10 deaths (10%) in the tenecteplase group and 18 (18%) in the alteplase group, which was not significant in the pre-specified logistic-regression analysis. Most of the deaths were related to progression of major stroke (9 in tenecteplase group and 14 in alteplase group). Tenecteplase 0.25 mg/kg showed a similar safety profile compared to alteplase 0.9 mg/kg.
EXTEND-IA TNK Part 2 study: EXTEND-IA TNK Part 2 was designed to determine whether 0.4 mg/kg of tenecteplase safely improves reperfusion before endovascular thrombectomy vs 0.25 mg/kg of tenecteplase in patients with large vessel occlusion (LVO) ischaemic stroke.
Adult patients with ischaemic stroke due to occlusion of the intracranial internal carotid, basilar, or middle cerebral artery were included into the trial less than 4.5 h after symptom onset using standard iv thrombolysis eligibility criteria. Patients were randomly assigned (1:1) to receive the tenecteplase 0.25 mg/kg or 0.4 mg/kg. The primary outcome was reperfusion of greater than 50% of the involved ischaemic territory prior to thrombectomy, assessed by consensus of 2 blinded neuroradiologists.
The number of participants with more than 50% reperfusion of the previously occluded vascular territory was 29 of 150 (19.3%) in the 0.4 mg/kg group vs 29 of 150 (19.3%) in the 0.25 mg/kg group (unadjusted risk difference, 0.0% [95% CI -8.9%, 8.9%]; adjusted risk ratio (RR), 1.03 [95% CI 0.66, 1.61]; p=0.89). There were no significant differences in any of the 4 functional outcomes between the 0.4 mg/kg and 0.25 mg/kg groups nor in all-cause deaths (26 [17%] vs 22 [15%], unadjusted risk difference, 2.7% [95% CI -5.6%, 11.0%]).
The sICH occurred in 7 patients (4.7%) in the 0.40 mg/kg group and 2 patients (1.3%) in the 0.25 mg/kg group (unadjusted risk difference, 3.3% [95% CI, -0.5, 7.2]; risk ratio [RR], 3.50 [95% CI 0.74, 16.62]; p=0.12). There were 26 deaths (17%) in the 0.40 mg/kg tenecteplase group and 22 death (15%) in the 0.25 mg/kg tenecteplase group (adjusted RR, 1.27 [95% CI 0.77, 2.11]; p=0.35).
Real World Evidence: Several non-interventional studies compared tenecteplase (0.25 mg/kg) versus alteplase (0.9 mg/kg) in AIS with or without large vessel occlusion (LVO) within 4.5 hours after symptom onset. These observational studies reported adjusted (or propensity score matched) estimates, included in total >2,900 AIS patients (from studies with over 100 patients treated with tenecteplase), and reported a consistent similar or favourable safety and effectiveness profile of tenecteplase in comparison with intravenous alteplase. Endpoints measured included functional outcome (3-month mRS score), all-cause mortality, intracranial haemorrhage and symptomatic intracranial haemorrhage, rates of angioedema, door-to needle time, door-in-door out time, imaging-to-thrombolysis time, thrombolysis-to-puncture time, and onset-to-needle time.
Pharmacokinetics: Absorption and distribution: Tenecteplase is an intravenously administered, recombinant protein that activates plasminogen. Following i.v. bolus administration of 30 mg tenecteplase in patients with acute myocardial infarction, the initially estimated tenecteplase plasma concentration was 6.45±3.60 μg/mL (mean±SD). The distribution phase represents 31%±22% to 69%±15% (mean±SD) of the total AUC following the administration of doses ranges from 5 to 50 mg.
Data on tissue distribution were obtained in studies with radioactively labelled tenecteplase in rats. The main organ to which tenecteplase distributed was the liver. It is not known whether and to which extent tenecteplase binds to plasma proteins in humans. The mean residence time (MRT) in the body is approximately 1 h and the mean (±SD) volume of distribution at the steady-state (Vss) ranged from 6.3±2 L to 15±7 L.
Metabolism: Tenecteplase is cleared from the circulation by binding to specific receptors in the liver followed by catabolism to small peptides. Binding to hepatic receptors is, however, reduced compared to native t-PA, resulting in a prolonged half-life.
Elimination: After single intravenous bolus injection of tenecteplase in patients with acute myocardial infarction, tenecteplase antigen exhibits biphasic elimination from plasma. There is no dose dependence of tenecteplase clearance in the therapeutic dose range. The initial, dominant half-life is 24±5.5 (mean±SD) min, which is 5 times longer than native t-PA. The terminal half-life is 129±87 min, and plasma clearance is 119±49 ml/min.
Increasing body weight resulted in a moderate increase of tenecteplase clearance, and increasing age resulted in a slight decrease of clearance. Women exhibit in general lower clearance than men, but this can be explained by the generally lower body weight of women.
Linearity/Non-Linearity: The dose linearity analysis based on AUC suggested that tenecteplase exhibits non-linear pharmacokinetics in the dose range studied, i.e. 5 to 50 mg.
Special populations: Renal and hepatic impairment: Because elimination of tenecteplase is through the liver, it is not expected that renal dysfunction will affect the pharmacokinetics of METALYSE. This is also supported by animal data. However, the effect of renal and hepatic dysfunction on pharmacokinetics of tenecteplase in humans has not been specifically investigated.
Toxicology: Preclinical safety data: Intravenous single dose administration in rats, rabbits and dogs resulted only in dose-dependent and reversible alterations of the coagulation parameters with local haemorrhage at the injection site, which was regarded as a consequence of the pharmacodynamic effect of tenecteplase. Multiple-dose toxicity studies in rats and dogs confirmed these previously mentioned observations, but the study duration was limited to two weeks by antibody formation to the human protein tenecteplase, which resulted in anaphylaxis.
Safety pharmacology data in cynomolgus monkeys revealed reduction of blood pressure followed by transient changes of ECG but these occurred at exposures that were considerably higher than the clinical exposure.
With regard to the indication and the single dose administration in humans, reproductive toxicity testing was confined to the rabbit, as a sensitive species. Tenecteplase induced no teratogenicity. Repeated dose administration resulted in bleeding with secondary mortality of dams. In a few cases abortion and resorption of the foetus occurred. Effects were not seen after single dose administration of tenecteplase.
Mutagenicity and carcinogenicity are not expected for this class of recombinant proteins and genotoxicity and carcinogenicity testing were not necessary.
No local irritation of the blood vessel was observed after intravenous, intra-arterial or paravenous administration of the final formulation of tenecteplase.

Metalyse is indicated in adults for the thrombolytic treatment of acute ischaemic stroke (AIS) within 4.5 hours from last known well and after exclusion of intracranial haemorrhage.

Metalyse should be administered as early as possible and no later than 4.5 hours after last known well and after exclusion of intracranial haemorrhage by appropriate imaging techniques, see Precautions. The treatment effect is time-dependent; therefore, earlier treatment increases the probability of a favourable outcome.
Metalyse should be administered on the basis of body weight, with a maximum single dose of 5,000 units (25 mg) tenecteplase.
Benefit-risk of tenecteplase treatment should be carefully evaluated in patients weighing 50 kg or less due to limited availability of data.
The volume required to administer the correct total dose can be calculated from the following scheme (table 2): see Table 2.

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Adjunctive therapy: The safety and efficacy of this regimen with concomitant treatment with heparin or platelet aggregation inhibitors such as acetylsalicylic acid during the first 24 hours after treatment with Metalyse have not been investigated sufficiently. Therefore, administration of intravenous heparin or platelet aggregation inhibitors such as acetylsalicylic acid should be avoided in the first 24 hours after treatment with Metalyse due to an increased haemorrhagic risk.
If heparin is required for other indications the dose should not exceed 10,000 IU per day, administered subcutaneously.
Method of administration: The reconstituted solution should be administered intravenously and is for immediate use.
The required dose should be administered as a single intravenous bolus over 5 to 10 seconds.
Instructions for use/handling: Metalyse should be reconstituted by adding the appropriate volume of sterile water for injection to the vial containing the powder for solution for injection using a needle and a syringe (not provided in the package).
1. Remove the flip-off cap from the vial.
2. Fill a syringe with 5 ml of sterile water for injection and penetrate the vial stopper in the middle with the needle.
3. Add all the sterile water for injection into the vial by pushing the syringe plunger down slowly to avoid foaming.
4. Keep the syringe attached to the vial and reconstitute by swirling gently.
5. The reconstituted preparation is a colourless to pale yellow, clear solution. Only clear solution without particles should be used.
6. Directly before the solution is administered, invert the vial with the syringe still attached, so that the syringe is below the vial.
7. Transfer the appropriate volume of reconstituted solution of Metalyse into the syringe, based on the patient's weight (see Table 2).
8. A pre-existing intravenous line, which has been used for administration of 0.9% sodium chloride solution only, may be used for administration of Metalyse. Metalyse should not be mixed with other drugs, neither in the same vial nor the same venous line (not even with heparin).
9. Metalyse should be administered as a single dose to the patient, intravenously over 5 to 10 seconds. It should not be administered into a line containing dextrose as Metalyse is incompatible with dextrose solution.
10. The line should be flushed after Metalyse injection for proper delivery.
11. Any unused solution should be discarded.

Symptoms: In the event of overdose there may be an increased risk of bleeding.
Therapy: In case of severe prolonged bleeding substitution therapy may be considered.

Metalyse is contraindicated in patients with known hypersensitivity to the active substance tenecteplase, gentamicin (a trace residue from the manufacturing process) or to any of the excipients; situations associated with a risk of bleeding such as: significant bleeding disorder at present or within the past 6 months, known haemorrhagic diathesis; any history of central nervous system damage (i.e. neoplasm, aneurysm, intracranial or spinal surgery); severe uncontrolled arterial hypertension; prolonged or traumatic cardiopulmonary resuscitation (>2 minutes) within the past 2 weeks; severe hepatic dysfunction, including hepatic failure, cirrhosis, portal hypertension (oesophageal varices) and active hepatitis; active peptic ulceration; arterial aneurysm and known arterial/venous malformation; neoplasm with increased bleeding risk; acute pericarditis and/or subacute bacterial endocarditis; acute pancreatitis; acute ischaemic stroke without disabling neurological deficit; history or evidence or suspicion of intracranial haemorrhage including subarachnoid haemorrhage; patients with effective anticoagulation (e.g. INR >1.7) (see Bleeding under Precautions).

The appropriate presentation of tenecteplase product should be chosen carefully and in line with the indication. Metalyse 25 mg is intended for use in acute ischaemic stroke only.
Metalyse 8,000 U (40 mg) is intended for use in acute myocardial infarction only.
Metalyse should be prescribed by physicians experienced in the use of thrombolytic treatment and with the facilities to monitor that use. This does not preclude the pre-hospital use of Metalyse. As with other thrombolytics, it is recommended that when Metalyse is administered standard resuscitation equipment and medication be available in all circumstances.
Treatment must be performed with the involvement of physicians trained and experienced in neurological care. For the indication verification remote diagnostic measures may be considered as appropriate (see Thrombolytic treatment of acute ischaemic stroke under Dosage & Administration).
Traceability: In order to improve traceability of biological medicinal products, the trade name and the batch number of the administered product should be clearly recorded in the patient file.
Bleeding: The most common complication encountered during Metalyse therapy is bleeding. The concomitant use of other active substances affecting coagulation or platelet function (e.g.,heparin) may contribute to bleeding (see also Contraindications).
As fibrin is lysed during Metalyse therapy, bleeding from recent puncture sites may occur. Therefore, thrombolytic therapy requires careful attention to all possible bleeding sites (including those following catheter insertions, arterial and venous puncture, cutdown and needle puncture). The use of rigid catheters, intramuscular injections and non-essential handling of the patient should be avoided during treatment with Metalyse.
Should serious bleeding occur, in particular cerebral haemorrhage, concomitant heparin administration should be terminated immediately. Administration of protamine should be considered if heparin has been administered within 4 hours before the onset of bleeding. In the few patients who fail to respond to these conservative measures, judicious use of transfusion products may be indicated. Transfusion of cryoprecipitate, fresh frozen plasma, and platelets should be considered with clinical and laboratory reassessment after each administration. A target fibrinogen level of 1 g/L is desirable with cryoprecipitate infusion. Antifibrinolytic agents should also be considered.
The use of Metalyse therapy has to be carefully evaluated in order to balance the potential risks of bleeding with expected benefits under the following conditions: Low body weight <60 kg; Patients receiving oral anticoagulants treatment: The use of METALYSE may be considered when appropriate test(s) show no clinically relevant anticoagulant activity; Recent intramuscular injection or small recent traumas, such as biopsies, puncture of major vessels, cardiac massage for resuscitation.
Intracerebral haemorrhages represent the most frequent adverse event (up to approximately 19% of patients). However, this had not led to an increased overall morbidity or mortality.
The risk of intracranial haemorrhage in acute ischaemic stroke patients may be increased with the use of METALYSE.
This applies in particular in the following cases: all situations involving a high risk of haemorrhage including those listed in Contraindications; late time-to-treatment onset; patients pre-treated with acetylsalicylic acid (ASA) may have a greater risk of intracerebral haemorrhage, particularly if METALYSE treatment is delayed; compared to younger patients, patients of advanced age (over 80 years) may have a somewhat poorer outcome independent of treatment and may have an increased risk of intracerebral haemorrhage when thrombolysed. In general, the benefit-risk of thrombolysis in patients of advanced age remains positive. Thrombolysis in AIS patients should be evaluated on individual benefit-risk basis; treatment must not be initiated later than 4.5 hours after last known well because of unfavourable benefit/risk ratio mainly based on the following: positive treatment effects decrease over time; the mortality rate increases particularly in patients with prior ASA treatment; risk of symptomatic haemorrhage increases.
Hypersensitivity: Immune-mediated hypersensitivity reactions associated with the administration of METALYSE can be caused by the active substance tenecteplase, gentamicin (a trace residue from the manufacturing process) or any of the excipients (see also Contraindications).
No sustained antibody formation to the tenecteplase molecule has been observed after treatment. However, there is no experience with re-administration of METALYSE.
There is also a risk of hypersensitivity reactions mediated through a non-immunological mechanism.
Angio-oedema represents the most common hypersensitivity reaction reported with METALYSE. This risk may be enhanced in the indication acute ischaemic stroke and/or by concomitant treatment with ACE inhibitors.
Patients treated with METALYSE should be monitored for angio-oedema during and for up to 24h after administration.
If a severe hypersensitivity reaction (e.g. angio-oedema) occurs, appropriate treatment should be promptly initiated. This may include intubation.
Blood pressure monitoring: Systolic blood pressure (BP) >180 mmHg or diastolic BP >105 mmHg, or uncontrolled arterial hypertension, should be treated rapidly and aggressively in order to minimise delays to initiate thrombolysis.
BP monitoring up to 24 hours after tenecteplase treatment is necessary. Intravenous antihypertensive therapy is recommended if systolic BP >180 mmHg or diastolic BP >105 mmHg.
Special patient groups at reduced benefit-risk: The benefit/risk ratio of thrombolytic therapy is considered less favourable in patients who have had a prior stroke or in whom uncontrolled diabetes exists, although still positive in these patients.
The benefit/risk ratio of METALYSE administration should be thoroughly considered in AIS patients with the following conditions: rapidly improving symptoms; extensive infarctions (e.g. NIHSS >25); seizure at the onset of stroke; recent history of previous stroke or serious head or spinal trauma or major surgery (such as cardiac, thoracic, abdominal, or orthopaedic); elevated activated partial thromboplastin time (aPTT) at presentation; platelet count of less than 100,000/mm3; hypertension refractory to aggressive hyperacute antihypertensive treatment such that target blood pressure less than 180/105 mmHg cannot be achieved or maintained; blood glucose <2.7 mmol/L or >22.2 mmol/L.
In stroke patients the likelihood of a favourable outcome decreases with longer time from last known well to thrombolytic treatment, increasing age, increasing stroke severity and increased levels of blood glucose on admission while the likelihood of severe disability and death or symptomatic intracranial bleeding increases, independently of treatment.
Cerebral oedema: Reperfusion of the ischaemic area may induce cerebral oedema in the infarcted zone.
Effects on ability to drive and use machines: Not relevant.
Use in Children: Safety and efficacy data in children below 18 years of age are not available for METALYSE. Therefore, METALYSE is not recommended for use in children below 18 years of age.

Pregnancy: There is a limited amount of data from the use of METALYSE in pregnant women.
Nonclinical studies performed with tenecteplase have shown bleeding with secondary mortality of dams due to the known pharmacological activity of the drug and in a few cases abortion and resorption of the foetus occurred (effects only have been observed with repeated dose administration). Tenecteplase is not considered to be teratogenic (see Pharmacology: Toxicology: Preclinical safety data under Actions).
The benefit of treatment must be evaluated against the potential risks in case of during pregnancy.
Lactation: It is not known if tenecteplase is excreted into human milk.
Caution should be exercised when METALYSE is administered to a nursing woman and a decision must be made whether breastfeeding should be discontinued for the first 24 hours after administration of METALYSE.
Fertility: Clinical data as well as nonclinical studies on fertility are not available for Tenecteplase (METALYSE).

As with other thrombolytic agents, haemorrhage is the most common adverse reaction associated with the use of Metalyse. Haemorrhage at any site or body cavity can occur and may result in life-threatening situations, permanent disability or death.
The type of haemorrhage associated with thrombolytic therapy can be divided into two broad categories: superficial bleeding, normally from injection sites; internal bleeding at any site or body cavity.
With intracranial haemorrhage neurological symptoms such as somnolence, aphasia, hemiparesis, convulsion may be associated.
Except for the occurrence of ADR reperfusion arrhythmias in the indication acute myocardial infarction and the frequency of ADR intracranial haemorrhage in the indication acute ischaemic stroke, the safety profile of Metalyse in the indication acute ischaemic stroke and acute myocardial infarction is regarded similar based on the outcome demonstrated by published academic clinical randomised trials and Real World Evidence (RWE) data.
List of adverse reactions: Immune system disorders: anaphylactoid reaction including rash, urticaria, bronchospasm, laryngeal oedema.
Nervous system disorders: intracranial haemorrhage such as cerebral haemorrhage, cerebral haematoma, haemorrhagic stroke, haemorrhagic transformation stroke, intracranial haematoma, subarachnoid haemorrhage.
Eye disorders: eye haemorrhage.
Cardiac disorders: pericardial haemorrhage.
Vascular disorders: haemorrhage, embolism.
Respiratory, thoracic and mediastinal disorders: epistaxis, pulmonary haemorrhage.
Gastrointestinal disorders: gastrointestinal haemorrhage such as gastric haemorrhage, gastric ulcer haemorrhage, rectal haemorrhage, haematemesis, melaena, mouth haemorrhage; nausea; vomiting; retroperitoneal haemorrhage such as retroperitoneal haematoma.
Skin and subcutaneous tissue disorders: ecchymosis.
Renal and urinary disorders: urogenital haemorrhage such as haematuria, haemorrhage urinary tract.
General disorders and administration site conditions: injection site haemorrhage, puncture site haemorrhage.
Investigations: blood pressure decreased, body temperature increased.
Injury, poisoning and procedural complications: fat embolism, which may lead to corresponding consequences in the organs concerned.
Surgical and medical procedures: transfusion.

No formal interaction studies with METALYSE and medicinal products commonly administered in patients with acute ischaemic stroke have been performed.
Drugs affecting coagulation/platelet function: Medicinal products that affect coagulation or those that alter platelet function may increase the risk of bleeding, and should therefore be avoided in the first 24 hours after Metalyse treatment for acute ischaemic stroke, see also Contraindications.
ACE Inhibitors: Concomitant treatment with ACE inhibitors may enhance the risk of experiencing a hypersensitivity reaction (see Precautions).
Other medicinal products: Published academic randomised trials involving more than 2,000 patients treated with tenecteplase did not show any clinically relevant interactions with other medicinal products commonly used in patients with AIS.

Incompatibilities: METALYSE is incompatible with dextrose solution.

Do not store above 30°C. Keep the container in the outer carton in order to protect from light.
Shelf life: Unopened vials: 3 years.
Reconstituted solutions: The reconstituted solution has been demonstrated to be stable for 24 hours at 2-8°C and for 8 hours at 30°C.
From a microbiological point of view, the product should be used immediately after reconstitution. If not used immediately, in-use storage times and conditions prior to use are the responsibility of the user and would normally not be longer than 24 hours at 2-8°C or 8 hours at 30°C.

Anticoagulants, Antiplatelets & Fibrinolytics (Thrombolytics)

B01AD11 - tenecteplase ; Belongs to the class of enzymes. Used in the treatment of thrombosis.

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