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| | tenecteplase Basic information |
| Product Name: | tenecteplase | | Synonyms: | tenecteplase;Tnkase;Plasminogen activator (human tissue-type), 103-L-asparagine-117-L-glutamine-296-L-alanine-297-L-alanine-298-L-alanine-299-alanine-;Tnk-tpa;Unii-wgd229o42w;Plasminogen activator(human tissue-type),103-L-asparagine-117-L-glutamine-296-L-alanine-297-L-alanine-298-L-alanine-299-L-alanine-;Research Grade Tenecteplase (DHB88401);Research Grade Tenecteplase | | CAS: | 191588-94-0 | | MF: | | | MW: | 0 | | EINECS: | | | Product Categories: | | | Mol File: | Mol File | ![tenecteplase Structure]() |
| | tenecteplase Chemical Properties |
| form | Liquid | | color | Colorless to light yellow |
| | tenecteplase Usage And Synthesis |
| Uses | Treatment of acute thrombotic disorders. | | General Description | Tenecteplase is a tPA produced by recombinant CHO cells.The molecule is a 527-amino acid glycoprotein developed byintroducing the following modifications to the cDNA construct:Thr103 to Asp, Asp117 to Gln, both within the kringle-1domain, and a tetra-alanine substitution at amino acids 296 to299 in the protease domain. The drug is a sterile, lyophilizedpowder recommended for single IV bolus administration afterreconstitution with sterile water. Tenecteplase should be administeredimmediately after reconstitution. | | Mechanism of action | Tenecteplase is composed of 527 amino acids with 17 disulfide bridges. It differs structurally from
anteplase by three point mutations. The mutations were bioengineered to occur at
amino acid 103, where threonine (T) is replaced by asparagine; at amino acid 117, where
asparagine (N) is replaced by glutamine; and at amino acids 296 to 299, where lysine (K)-histidinearginine-arginine are replaced with four alanines. Thus, the name TNK is derived from the
mutations. The replacement of these amino acids along with their attached carbohydrate side chains
results in a prolonged half-life (~17 minutes) and allows a single bolus application. These
point-mutation changes also change the binding of tenecteplase to plasminogen activator inhibitor-1
(PAI-1) by 80-fold, thus improving activity. A physiological enzyme, PAI-1 inhibits fibrinolysis.
Finally, tenecteplase shows a 15-fold higher fibrin specificity. The drug is still eliminated via hepatic
mechanisms. | | Clinical Use | Thrombolytic:
Acute myocardial infarction | | Drug interactions | Potentially hazardous interactions with other drugs
Drugs that affect coagulation or platelet function:
increased risk of bleeding. | | Metabolism | Tenecteplase is cleared from circulation by binding to
specific receptors in the liver followed by catabolism to
small peptides. |
| | tenecteplase Preparation Products And Raw materials |
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