Abciximab: Difference between revisions

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==Mechanism of Action==
==Mechanism of Action==


Abciximab is a chimeric human-murine monoclonal antibody Fab fragment which inhibits [[platelet aggregation]] by binding to the glycoprotein IIb/IIIa receptors on platelets. It prevents [[fibrinogen]] and [[von Willebrand factor]] from binding to the receptor in a dose-dependent manner. Abciximab may also bind to the [[vitronectin]] receptor and to the [[Mac-1]] receptor on activated [[monocytes]].<ref name="Faulds-1994">{{Cite journal  | last1 = Faulds | first1 = D. | last2 = Sorkin | first2 = EM. | title = Abciximab (c7E3 Fab). A review of its pharmacology and therapeutic potential in ischaemic heart disease. | journal = Drugs | volume = 48 | issue = 4 | pages = 583-98 | month = Oct | year = 1994 | doi =  | PMID = 7528131 }}</ref>
Abciximab is a chimeric human-murine monoclonal antibody F<sub>ab</sub> fragment which inhibits [[platelet aggregation]] by binding to the glycoprotein IIb/IIIa receptors on platelets. It prevents [[fibrinogen]] and [[von Willebrand factor]] from binding to the receptor in a dose-dependent manner. Abciximab may also bind to the [[vitronectin]] receptor and to the [[Mac-1]] receptor on activated [[monocytes]].<ref name="Faulds-1994">{{Cite journal  | last1 = Faulds | first1 = D. | last2 = Sorkin | first2 = EM. | title = Abciximab (c7E3 Fab). A review of its pharmacology and therapeutic potential in ischaemic heart disease. | journal = Drugs | volume = 48 | issue = 4 | pages = 583-98 | month = Oct | year = 1994 | doi =  | PMID = 7528131 }}</ref>


==References==
==References==

Revision as of 23:48, 29 January 2014

Template:Abciximab Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sheng Shi, M.D. [2], Pratik Bahekar, MBBS [3]

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Overview

Abciximab (previously known as c7E3 Fab), a glycoprotein IIb/IIIa receptor antagonist manufactured by Janssen Biologics BV and distributed by Eli Lilly under the trade name ReoPro, is a platelet aggregation inhibitor mainly used during and after coronary artery procedures like angioplasty to prevent platelets from sticking together and causing thrombus formation within the coronary artery. It is a glycoprotein IIb/IIIa inhibitor.[1]

While abciximab has a short plasma half-life, due to its strong affinity for its receptor on the platelets, it may occupy some receptors for weeks. In practice, platelet aggregation gradually returns to normal about 96 to 120 hours after discontinuation of the drug. Abciximab is made from the Fab fragments of an immunoglobulin that targets the glycoprotein IIb/IIIa receptor on the platelet membrane.[2]

Category

Antiplatelet, Glycoprotein IIb/IIIa Receptor Antagonist

US Brand Names

ReoPro®

FDA Package Insert

Indications and Usage | Dosage and Administration | Contraindications | Warnings and Precautions | Adverse Reactions | Overdosage | Description | Clinical Pharmacology | Clinical Studies | How Supplied/Storage and Handling | Labels and Packages

Mechanism of Action

Abciximab is a chimeric human-murine monoclonal antibody Fab fragment which inhibits platelet aggregation by binding to the glycoprotein IIb/IIIa receptors on platelets. It prevents fibrinogen and von Willebrand factor from binding to the receptor in a dose-dependent manner. Abciximab may also bind to the vitronectin receptor and to the Mac-1 receptor on activated monocytes.[3]

References

  1. "Abciximab". Drugs.com. Archived from the original on |archive-url= requires |archive-date= (help). Retrieved 13 March 2010.
  2. "International Nonproprietary Names for Pharmaceutiical Substances" (PDF). WHO Drug Information. 7 (4). 1993.
  3. Faulds, D.; Sorkin, EM. (1994). "Abciximab (c7E3 Fab). A review of its pharmacology and therapeutic potential in ischaemic heart disease". Drugs. 48 (4): 583–98. PMID 7528131. Unknown parameter |month= ignored (help)