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Tenecteplase

Tenecteplase is a recombinant tissue plasminogen activator (tPA) and thrombolytic agent engineered for rapid intravenous administration to dissolve blood clots in acute thrombotic conditions.^[1] It is a bioengineered variant of alteplase with enhanced fibrin specificity, resistance to plasminogen activator inhibitor-1 (PAI-1), and a prolonged half-life (initial phase 20–24 minutes; terminal phase 90–130 minutes), enabling single-bolus dosing over 5 seconds.^[1] Developed using recombinant DNA technology in Chinese hamster ovary cells, tenecteplase catalyzes the conversion of plasminogen to plasmin, preferentially targeting fibrin-bound clots to restore blood flow while minimizing systemic fibrinogen depletion.^[2] Approved by the U.S. Food and Drug Administration (FDA) in 2000 for the treatment of ST-elevation myocardial infarction (STEMI) to reduce mortality associated with acute myocardial infarction, tenecteplase is administered as a weight-based single intravenous bolus, with doses ranging from 30 mg for patients under 60 kg to a maximum of 50 mg for those 90 kg or greater.^[2] In March 2025, the FDA expanded its approval to include acute ischemic stroke (AIS) in adults, recommending initiation within 3 hours of symptom onset using a lower weight-tiered dose capped at 25 mg to improve outcomes in eligible patients.^[3] Off-label uses have included pulmonary embolism and central venous catheter occlusion, supported by its fibrinolytic efficacy and convenience over multi-infusion alternatives like alteplase.^[4] The primary adverse effect of tenecteplase is bleeding, occurring in up to 4.7% of cases as major hemorrhage, with risks of intracranial hemorrhage (approximately 0.9% in STEMI trials and 3.4% in AIS studies) heightened by factors such as advanced age, concurrent anticoagulant use, or recent surgery.^[2] Contraindications include active internal bleeding, recent stroke or intracranial trauma, uncontrolled hypertension, and known hypersensitivity to tPA agents.^[1] Other notable risks encompass thromboembolism, arrhythmias, and rare anaphylactic reactions, necessitating careful patient selection and monitoring during and after administration.^[4] Clinical trials, such as ASSENT-2 for STEMI and recent AcT and EXTEND-IA TNK for stroke, have demonstrated noninferiority or superiority to alteplase in efficacy, with advantages in ease of use and cost-effectiveness.^[4]

Clinical use

Indications

Tenecteplase is indicated for the reduction of mortality associated with acute ST-elevation myocardial infarction (STEMI) in adults.^[1] This primary indication stems from its role as a fibrin-specific thrombolytic agent administered as a single intravenous bolus to restore coronary blood flow in patients presenting with STEMI symptoms, particularly when immediate percutaneous coronary intervention (PCI) is not available.^[1] The approval was supported by the ASSENT-2 trial, a double-blind randomized study involving over 16,900 patients, which established non-inferiority to alteplase with 30-day all-cause mortality rates of 6.0% for tenecteplase versus 6.2% for alteplase.^[5] In March 2025, the U.S. Food and Drug Administration (FDA) approved tenecteplase as a secondary indication for the treatment of acute ischemic stroke (AIS) in adults, to be initiated within 3 hours of symptom onset for improving functional outcomes.^[6] This approval reflects evidence from multiple randomized trials demonstrating comparable efficacy to alteplase in achieving recanalization and better neurologic recovery in eligible patients, leveraging tenecteplase's rapid bolus administration for time-critical cerebrovascular emergencies.^[7] Its pharmacokinetics enable quick onset, aligning with the narrow therapeutic window for stroke intervention.^[1] Tenecteplase remains investigational for pulmonary embolism (PE), with ongoing research exploring its use in intermediate-risk cases to reduce hemodynamic decompensation, as evidenced by the PEITHO trial showing improved right ventricular function but increased bleeding risk compared to anticoagulation alone.^[8]

Administration and dosing

Tenecteplase is administered intravenously as a single bolus injection over 5 to 10 seconds, without the need for a subsequent infusion.^[1]^[9] For the treatment of acute ST-elevation myocardial infarction (STEMI), dosing is weight-based and capped at a maximum total dose of 50 mg, administered as soon as possible after the onset of symptoms. The recommended doses are as follows:

Patient Weight	Dose
Less than 60 kg	30 mg
60 kg to less than 70 kg	35 mg
70 kg to less than 80 kg	40 mg
80 kg to less than 90 kg	45 mg
90 kg or more	50 mg

^[1] For acute ischemic stroke, dosing is weight-based and capped at a maximum total dose of 25 mg, administered as a single intravenous bolus within 3 hours of symptom onset. The recommended doses are as follows:

Patient Weight	Dose
Less than 60 kg	15 mg
60 kg to less than 70 kg	17.5 mg
70 kg to less than 80 kg	20 mg
80 kg to less than 90 kg	22.5 mg
90 kg or more	25 mg

^[1] Tenecteplase is supplied as a lyophilized powder in a 50 mL vial containing 50 mg of the drug. Preparation involves reconstituting the powder with 10 mL of sterile water for injection to yield a concentration of 5 mg/mL; the vial should be gently swirled (not shaken) until dissolved, resulting in a colorless to pale yellow transparent solution. No further dilution is required, and the reconstituted solution should be used immediately or stored refrigerated at 2°C to 8°C for up to 8 hours. Prior to administration, any intravenous lines containing dextrose should be flushed with 0.9% sodium chloride to avoid precipitation.^[1]

Safety and tolerability

Contraindications

Tenecteplase, a fibrin-specific thrombolytic agent, carries significant risks of bleeding complications, necessitating careful evaluation of patient history and clinical status prior to administration. Contraindications are categorized as absolute (where use is prohibited due to high risk of life-threatening hemorrhage) or relative (where benefits may outweigh risks on a case-by-case basis). These are informed by major clinical guidelines and the drug's prescribing information, with variations depending on the indication—primarily ST-elevation myocardial infarction (STEMI) or acute ischemic stroke (AIS).^[10]^[7]^[11]

Absolute Contraindications

For STEMI (per 2025 ACC/AHA guidelines), absolute contraindications include active internal bleeding; history of intracranial hemorrhage at any time; known structural cerebral vascular lesion (e.g., arteriovenous malformation); known malignant intracranial neoplasm (primary or metastatic); ischemic stroke within 3 months (except acute ischemic stroke within 4.5 hours of symptom onset); suspected aortic dissection; active bleeding or bleeding diathesis (excluding menses); significant closed-head or facial trauma within 3 months; intracranial or intraspinal surgery within 2 months; and severe uncontrolled hypertension (systolic blood pressure >180 mm Hg or diastolic blood pressure >110 mm Hg).^[10]^[11] For AIS (per FDA labeling and AHA/ASA recommendations, with 2025 updates endorsing tenecteplase as an alternative to alteplase), absolute contraindications encompass active internal bleeding; active intracranial hemorrhage; intracranial or intraspinal surgery or trauma within 2 months; known bleeding diathesis; current severe uncontrolled hypertension (systolic >185 mm Hg or diastolic >110 mm Hg despite treatment); presence of intracranial conditions that may increase bleeding risk, such as neoplasm, arteriovenous malformation, or aneurysm; and history of ischemic stroke within 3 months (except the current stroke).^[7]^[12]^[11]

Relative Contraindications

Relative contraindications, applicable to both indications unless specified, include recent (within 2-4 weeks) major surgery or trauma; recent (within 10 days) puncture of a non-compressible blood vessel; traumatic or prolonged (>10 minutes) cardiopulmonary resuscitation; known bleeding risks such as active peptic ulcer, diabetic hemorrhagic retinopathy, or other ophthalmic conditions; history of ischemic stroke greater than 3 months prior; chronic severe poorly controlled hypertension; significant hypertension on presentation (systolic >180 mm Hg or diastolic >110 mm Hg); non-compressible vascular punctures; and oral anticoagulant therapy at therapeutic levels. For pregnancy, tenecteplase should be used only if the potential benefit justifies the potential risk to the fetus, as there are no adequate and well-controlled studies in pregnant women. These factors require individualized risk-benefit assessment.^[10]^[7]^[11]

Special Populations

Tenecteplase should be avoided in patients with severe hepatic impairment, as it increases bleeding risk due to impaired clotting factor synthesis. Concurrent use of anticoagulants (e.g., warfarin, direct oral anticoagulants) without reversal is cautioned against, given the heightened hemorrhage potential; if recent anticoagulant exposure is present, laboratory confirmation of normalized coagulation parameters is essential prior to administration. In patients with concurrent antiplatelet or anticoagulant therapy, the overall bleeding risk escalates, warranting guideline-directed reversal strategies where feasible.^[4]^[11]

Adverse effects

The most common adverse effects of tenecteplase are bleeding events, which occur due to its fibrinolytic activity and can range from minor to life-threatening. These include intracranial hemorrhage (ICH), with an incidence of 0.9% in the ASSENT-2 trial and up to 1.7% in patients aged 75 years or older; in AIS trials supporting 2025 approval, symptomatic ICH rates were approximately 3.4%. Gastrointestinal bleeding can occur as a form of major non-cerebral hemorrhage, and injection-site hemorrhage contributes to minor bleeding.^[1] In the ASSENT-2 trial involving over 16,900 patients with ST-elevation myocardial infarction, the rate of non-cerebral bleeding complications was 26.4% for tenecteplase compared to 29.0% for alteplase, while the rate of major bleeding (excluding ICH) was 4.7% vs 5.9%; stroke rates were similar at 1.8% versus 1.7%. Overall, tenecteplase demonstrated a lower need for blood transfusions (4.3% versus 5.5%).^[1] Serious risks, though less frequent, include hypersensitivity reactions such as anaphylaxis, which manifest as urticaria, hypotension, or bronchospasm and occur in less than 0.5% of cases.^[1] Thromboembolic events, including cholesterol embolization, have been reported post-administration, though their frequency is unknown and may relate to underlying disease rather than the drug itself.^[4] Arrhythmias, such as bradycardia during infusion or reperfusion-related ventricular irritability, can also arise and necessitate preparedness with anti-arrhythmic therapy.^[11] Management of adverse effects focuses on prompt intervention for bleeding, including immediate discontinuation of tenecteplase, heparin, and antiplatelet agents, followed by supportive measures like blood transfusions or protamine sulfate to reverse heparin effects.^[1] Reperfusion arrhythmias require monitoring and standard anti-arrhythmic treatment, while hypersensitivity reactions are managed with conventional therapies such as antihistamines or epinephrine.^[11] Long-term, tenecteplase does not appear to cause unique chronic effects beyond the general risks associated with thrombolytic therapy, such as potential antibody formation upon readministration, though data on sustained effects from single doses are limited.^[1]

Pharmacology

Mechanism of action

Tenecteplase is a recombinant fibrin-specific variant of the endogenous enzyme tissue plasminogen activator (tPA), engineered for enhanced thrombolytic properties.^[4] As a serine protease, it promotes fibrinolysis by preferentially binding to fibrin within thrombi, where it catalyzes the conversion of plasminogen to plasmin.^[4] Plasmin then hydrolyzes fibrin cross-links, solubilizing the clot matrix and restoring vascular patency without broadly activating systemic coagulation factors.^[13] The binding of tenecteplase to fibrin facilitates localized activation of fibrin-bound plasminogen, amplifying the proteolytic cascade at the thrombus site.^[14] This targeted interaction can be conceptually represented as:

\text{Tenecteplase} + \text{Fibrin-bound Plasminogen} \rightarrow \text{Plasmin} + \text{Fibrin degradation products}

The resulting plasmin degrades the fibrin scaffold, leading to thrombus dissolution while limiting exposure of free plasminogen in circulation.^[4] Tenecteplase achieves its fibrin specificity through targeted genetic modifications from wild-type tPA: asparagine substitution at threonine 103 (T103N) and glutamine at asparagine 117 (N117Q) in the kringle 1 domain, plus a tetra-alanine replacement of the KHRR sequence at residues 296–299 in the protease domain (KHRR296–299AAAA).^[14] These alterations yield a 14-fold higher fibrin specificity relative to alteplase, promoting selective plasminogen activation on clots and thereby reducing systemic fibrinogenolysis.^[14] The tetra-alanine substitution further confers 80-fold greater resistance to plasminogen activator inhibitor-1 (PAI-1), preserving enzymatic activity within the thrombus environment.^[14]

Pharmacokinetics

Tenecteplase is administered as a single intravenous bolus over 5 seconds, resulting in immediate bioavailability and peak plasma concentrations achieved within minutes following injection.^[15]^[16] The drug distributes primarily within the plasma volume, with an initial volume of distribution ranging from 4.2 to 6.3 L, which approximates plasma volume and reflects limited extravascular distribution.^[16] The steady-state volume of distribution is 6.1 to 9.9 L, consistent with the large molecular size of tenecteplase as a glycoprotein (~58 kDa), which restricts tissue penetration beyond the vascular compartment.^[16] Metabolism of tenecteplase occurs primarily through hepatic clearance mechanisms involving the low-density lipoprotein receptor-related protein (LRP), leading to rapid catabolism into peptides and amino acids without the formation of active metabolites.^[16]^[15] Elimination follows a biphasic pattern, with an initial half-life of 20 to 24 minutes and a terminal half-life of 90 to 130 minutes; the mean plasma clearance is 99 to 119 mL/min in patients with acute myocardial infarction.^[15]^[17] Clearance is independent of renal function due to predominant hepatic elimination, and while age may account for minor variability (approximately 11%), no dose adjustments are required for elderly patients or those with renal or hepatic impairment.^[16]^[18] Additionally, the high-affinity fibrin binding of tenecteplase extends its effective half-life at the clot site compared to plasma clearance.^[17]

Chemistry and development

Structure and properties

Tenecteplase is a recombinant 527-amino acid glycoprotein engineered as a single-chain variant of human tissue plasminogen activator (tPA), retaining key structural domains including the finger domain for fibrin binding, the kringle 1 domain for lysine binding, and the serine protease domain for catalytic activity.^[1] To enhance stability and fibrin specificity, three targeted mutations were introduced: threonine 103 to asparagine (T103N) and asparagine 117 to glutamine (N117Q) within the kringle 1 domain, along with a tetra-alanine substitution (positions 296–299, replacing the native KHRR sequence) in the protease domain. These modifications, achieved through recombinant DNA technology in Chinese hamster ovary cells, result in a protein primarily glycosylated at three N-linked sites.^[1] The calculated molar mass of tenecteplase is 58,742 Da.^[1] This mass accounts for the core polypeptide chain and its post-translational glycosylation, distinguishing it from the unglycosylated form. As a lyophilized sterile powder, tenecteplase appears white to pale yellow and is highly soluble in sterile water for injection, forming a colorless to pale yellow transparent solution at pH approximately 7.3 upon reconstitution at 5 mg/mL.^[1] The unreconstituted powder remains chemically and physically stable when stored at controlled room temperature (not exceeding 30°C) and protected from light.^[1] Commercially, tenecteplase is formulated without preservatives in 25 mg and 50 mg single-dose vials, accompanied by excipients including 522 mg L-arginine, approximately 160 mg phosphoric acid, and 4 mg polysorbate 20 to aid stability and solubility.^[1] The glycoprotein structure influences its pharmacokinetic behavior, such as extended circulation time relative to non-glycosylated variants.

History

Tenecteplase, also known as TNK-tPA, was developed by Genentech in the 1990s as a bioengineered variant of human tissue plasminogen activator (tPA) to overcome limitations of alteplase, such as its shorter plasma half-life and reduced fibrin specificity.^[15] The drug incorporates specific amino acid substitutions in the tPA molecule, resulting in a 527-amino acid glycoprotein produced via recombinant DNA technology in Chinese hamster ovary cells.^[15] This engineering marked tenecteplase as the first tPA variant with enhanced fibrin specificity, enabling single-bolus administration and improved thrombolytic profile.^[19] The pivotal Assessment of the Safety and Efficacy of a New Thrombolytic (ASSENT-2) trial, a double-blind randomized study conducted from 1998 to 1999 and published in 1999, enrolled 16,949 patients with acute ST-elevation myocardial infarction (STEMI) and established tenecteplase's noninferiority to front-loaded alteplase in reducing 30-day mortality, with comparable safety outcomes including rates of intracranial hemorrhage.^[20] These results supported tenecteplase's role as an effective thrombolytic for acute myocardial infarction (AMI). Regulatory milestones followed swiftly, with the U.S. Food and Drug Administration (FDA) granting approval on June 2, 2000, for tenecteplase (marketed as TNKase) to reduce mortality associated with AMI in adults.^[21] In Europe, the European Commission authorized marketing of tenecteplase (as Metalyse) on February 23, 2001, for thrombolytic treatment of AMI with persistent ST-segment elevation.^[22] In January 2024, the European Medicines Agency expanded approval of Metalyse for treatment of acute ischemic stroke within 4.5 hours of symptom onset.^[23] On March 3, 2025, the FDA expanded tenecteplase's indications to include treatment of acute ischemic stroke in adults, based on efficacy data from the EXTEND-IA TNK trials demonstrating superior reperfusion compared to alteplase.^[6]

Research

Stroke treatment

Tenecteplase has emerged as a promising thrombolytic agent for acute ischemic stroke (AIS), particularly in patients eligible for intravenous thrombolysis within 4.5 hours of symptom onset. Key randomized controlled trials have evaluated its efficacy compared to the standard alteplase. The EXTEND-IA TNK trial (2018), a phase 2 study of 202 patients with large-vessel occlusion undergoing endovascular thrombectomy, demonstrated superior reperfusion rates with tenecteplase (0.25 mg/kg bolus) versus alteplase (22% vs. 10% complete reperfusion on angiography before thrombectomy), alongside improved 90-day functional outcomes (modified Rankin Scale [mRS] score 0-1 in 40% vs. 29%). The NOR-TEST trial (2017), a phase 3 multicenter study of 1100 patients with mild to moderate AIS, established non-inferiority of tenecteplase (0.4 mg/kg bolus) to alteplase for the primary outcome of excellent functional recovery (mRS score 0-1 at 3 months: 64% vs. 63%), supporting its broader applicability. The AcT trial (2022), a phase 3 noninferiority study involving 1600 patients across 48 Canadian centers, confirmed tenecteplase (0.25 mg/kg) as noninferior to alteplase for 90-120 day functional outcomes (mRS score 0-1: 36.9% vs. 34.8%), with higher rates of early neurological improvement.^[24]^[25] Tenecteplase offers practical advantages over alteplase, including rapid single-bolus administration (5 seconds) compared to alteplase's 60-minute infusion, which facilitates quicker workflow in emergency settings and reduces the need for continuous monitoring. It also shows potential for enhanced lysis in large-vessel occlusions due to its higher fibrin specificity and resistance to plasminogen activator inhibitor-1, as evidenced by improved recanalization in trials like EXTEND-IA TNK. Current guidelines endorse tenecteplase as an alternative to alteplase for eligible AIS patients. The 2019 American Heart Association/American Stroke Association (AHA/ASA) guidelines recommend tenecteplase (0.25 mg/kg or 0.4 mg/kg) as a reasonable alternative to alteplase (Class IIb, Level B-R) for thrombolysis within 4.5 hours, particularly in settings where rapid administration is prioritized.^[26] Meta-analyses support its use in an extended time window of 4.5-24 hours for select patients with favorable imaging (e.g., small infarct core, mismatch on perfusion imaging), showing improved functional outcomes without increased harm compared to placebo or standard care. However, phase 3 trials like TIMELESS (2024) and TRACE-III (2024) did not meet their primary endpoints for benefit in the 4.5-24 hour window, though tenecteplase was safe, with potential subgroup benefits (e.g., M1 occlusions).^[27]^[28] Clinical outcomes with tenecteplase are comparable to alteplase, with similar 90-day mortality rates (approximately 5%) and symptomatic intracranial hemorrhage incidence (around 4-5%) across pooled trial data. Its single-bolus regimen enhances cost-effectiveness through simplified logistics and lower drug waste, as modeled in economic analyses of real-world U.S. and Canadian settings.^[29] In 2025, the U.S. Food and Drug Administration (FDA) approved tenecteplase for AIS treatment in adults, based primarily on the AcT trial results, enabling broader adoption and integration into standard protocols nationwide.

Other applications

Tenecteplase has been investigated for the treatment of pulmonary embolism, particularly in intermediate-risk cases, where phase III trials have demonstrated its efficacy in reducing hemodynamic decompensation through bolus administration, which shortens treatment time compared to infusion-based thrombolytics. The PEITHO trial, a multicenter randomized study involving 1,005 patients, showed that tenecteplase plus heparin significantly lowered the risk of hemodynamic collapse or death within seven days compared to heparin alone, although it was associated with a higher incidence of major extracranial bleeding.^[8] Follow-up phase 4 investigations, such as PEITHO-2, have explored strategies like early transition to oral anticoagulation after initial parenteral anticoagulation for 72 hours in intermediate-risk pulmonary embolism, supporting its role in streamlined acute management.^[30] In prehospital settings, tenecteplase's single-bolus pharmacokinetics make it suitable for emergency administration by paramedics, with phase 2 studies demonstrating feasibility for acute stroke thrombolysis outside hospital environments. The Australian TASTE trial (Tenecteplase versus Alteplase for Stroke Thrombolysis Evaluation in the Ambulance), initiated in 2019, is a phase 2 study evaluating tenecteplase on mobile stroke units; its protocol supports logistical advantages over alteplase, with ongoing assessment of early reperfusion and safety.^[31]^[32] Pediatric applications of tenecteplase remain investigational, with limited evidence from small observational cohorts in ST-elevation myocardial infarction (STEMI) and no regulatory approvals to date. Case series and retrospective data suggest potential utility in rare pediatric STEMI cases due to its fibrin specificity, but prospective trials are lacking, and dosing adjustments are extrapolated from adult studies. A 2025 safety surveillance report indicates tenecteplase may be safe in childhood arterial ischemic stroke based on initial data.^[33] Tenecteplase has shown noninferiority to alteplase in phase 3 trials like TRACE-2 (2023), a multicenter study of over 1,400 patients excluding those planned for thrombectomy, supporting its use for IV thrombolysis in functional recovery. For combination with mechanical thrombectomy, trials like EXTEND-IA TNK have demonstrated improved recanalization rates in eligible stroke cases undergoing thrombectomy, contributing to enhanced 90-day modified Rankin Scale scores.^[34] Challenges in applying tenecteplase to non-myocardial infarction settings include managing higher clot burdens, such as in pulmonary embolism or stroke-related thrombi, which may alter its lysis efficiency compared to coronary settings. Completed phase 3 trials like TRACE-2, TIMELESS, and TRACE-III as of 2024 have addressed extended windows and diverse conditions, with ongoing studies exploring further applications beyond approved uses.^[27]^[28]

References

[1]
[PDF] Reference ID: 5540622 - accessdata.fda.gov
Tenecteplase is a tissue plasminogen activator (tPA) produced by recombinant DNA technology using a mammalian cell line (Chinese Hamster Ovary cells).
[2]
Tenecteplase - StatPearls - NCBI Bookshelf
Jun 25, 2023 · Adverse effects of tenecteplase, including bleeding, anaphylaxis, thromboembolism, and arrhythmia, are similar to other thrombolytics. Bleeding ...
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TNKase (Tenecteplase) Package Insert - accessdata.fda.gov
Sep 26, 2003 · The most frequent adverse reaction associated with TNKase is bleeding (see WARNINGS). Should serious bleeding occur, concomitant heparin and ...
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FDA Roundup: March 4, 2025
Mar 4, 2025 · On Friday, the FDA approved TNKase (tenecteplase) to treat acute ischemic stroke (AIS) in adults. The most common adverse reaction is bleeding. ...
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Mar 3, 2025 · TNKase is also FDA-approved for the treatment of acute ST-elevation myocardial infarction (STEMI) in adults. About TNKase® (tenecteplase).
[7]
Food and Drug Administration Approval of Tenecteplase
May 23, 2025 · We think the evidence is clear that TNK, like tPA, should be offered to patients within 4.5 hours of stroke onset, if they meet other treatment ...
[8]
Fibrinolysis for Patients with Intermediate-Risk Pulmonary Embolism
Apr 10, 2014 · In a randomized, double-blind trial, we compared tenecteplase plus heparin with placebo plus heparin in normotensive patients with intermediate- ...
[9]
[PDF] Metalyse, INN-Tenecteplase - European Medicines Agency
The required dose should be administered as a single intravenous bolus over approximately. 10 seconds. For instructions on reconstitution of the medicinal ...
[10]
Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association | Stroke
Summary of each segment:
[11]
2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the ...
Absolute and Relative Contraindications for Fibrinolytic Therapy in STEMI. Absolute Contraindications. Any prior ICH. Known structural cerebral vascular ...
[12]
None
### Contraindications for TNKase (Tenecteplase)
[13]
Acute Ischemic Stroke Treatment | TNKase® (tenecteplase)
Indication. Acute Ischemic Stroke. TNKase (tenecteplase) is indicated for the treatment of acute ischemic stroke (AIS) in adults.
[14]
[PDF] TNKASE® (tenecteplase) for injection, for intravenous use
Jan 18, 2024 · TNKase is for intravenous (IV) administration only, administered as a single bolus over 5 seconds. Individualize dosage based on the patient's ...
[15]
Comparison of clot lysis activity and biochemical properties of ...
Feb 4, 2014 · ... mutations resulted in an extended half-life (18 vs. 4 min), higher fibrin specificity (14-fold) and increased resistance towards PAI-1 (80 ...
[16]
A faster-acting and more potent form of tissue plasminogen activator. | PNAS
### Summary of Tenecteplase (TNK-t-PA) Mutations and Effects
[17]
[PDF] TNKase® (Tenecteplase) - accessdata.fda.gov
Each vial will deliver 50 mg of. Tenecteplase. CLINICAL PHARMACOLOGY. General. Tenecteplase is a modified form of human tissue plasminogen activator (tPA) that ...
[18]
Pharmacokinetics and Pharmacodynamics of Tenecteplase in ...
Oct 14, 2012 · Tenecteplase exhibited biphasic (two-compartment) kinetics in 60 patients, and monophasic kinetics in 20 patients. It is likely that ...2. Pharmacokinetic Methods · 4.1 Pharmacokinetics In... · 4.2 Pharmacokinetics In...
[19]
Pharmacotherapy Update | Tenecteplase (TNKase): A Clinical Review
In the ASSENT-2 trial with nearly 17,000 patients enrolled, the rates of major and minor bleeding as well as blood transfusions were significantly lower with ...Missing: 26.4%
[20]
[PDF] Metalyse, INN-Tenecteplase
Because elimination of tenecteplase is through the liver, it is not expected that renal dysfunction will affect its the pharmacokinetics. This is also supported ...
[21]
Tenecteplase: Uses, Interactions, Mechanism of Action - DrugBank
Tenecteplase is a fibrin-specific tissue-plasminogen activator. It binds to fibrin rich clots and cleaves the Arg/Val bond in plasminogen to form plasmin.
[22]
Tenecteplase Thrombolysis for Acute Ischemic Stroke
Oct 13, 2020 · Tenecteplase is a fibrinolytic drug with higher fibrin specificity and longer half-life than the standard stroke thrombolytic, alteplase.
[23]
the ASSENT-2 double-blind randomised trial - PubMed
We did a double-blind, randomised, controlled trial to assess the efficacy and safety of tenecteplase compared with alteplase. Methods: In 1021 hospitals ...
[24]
Tenecteplase - Product Approval Information - Licensing Action
Tenecteplase is indicated for reduction of mortality associated with acute myocardial infarction (AMI). Under this authorization, you are approved to ...
[25]
Tenecteplase Boehringer Ingelheim Pharma GmbH Co. KG
Dec 5, 2005 · Overview. On 23 February 2001, the European Commission granted a marketing authorisation for Tenecteplase Boehringer Ingelheim Pharma KG ...
[26]
Tenecteplase versus Alteplase for Stroke Thrombolysis Evaluation ...
Treatment with tenecteplase on the MSU in Melbourne resulted in a superior rate of early reperfusion compared with alteplase, and no safety concerns were noted.
[27]
Tenecteplase for the Treatment of Pediatric Arterial Ischemic Stroke
Feb 11, 2025 · Our initial data suggest that TNK may be safe in childhood arterial ischemic stroke. Strategically designed prospective studies are needed.Missing: STEMI | Show results with:STEMI
[28]
Tenecteplase for Ischemic Stroke at 4.5 to 24 Hours without ...
Jun 14, 2024 · Tenecteplase is an effective thrombolytic agent for eligible patients with stroke who are treated within 4.5 hours after the onset of stroke.