Pathways

Abacavir is an oral antiviral drug used to treat HIV/AIDS. It is a nucleotide analog reverse transcriptase inhibitor that targets HIV infected cells in the body. When HIV infects a cell, the virus first binds and fuses with the cell, releasing its nucleocapsid containing its RNA and reverse transcriptase into the cytosol of the cell. The reverse transcriptase converts the viral RNA into viral DNA in the cytosol. The viral DNA goes to the nucleus through the nuclear pore complex where it undergoes the process of transcription. The new viral RNA formed from transcription is transported back to the cytosol through the nuclear pore complex and translation occurs to produce viral proteins. These viral proteins are assembled and new HIV viruses bud from the cell. Abacavir enters the cell via solute carrier family 22 member 1 and is converted into abacavir 5’-monophosphate by adenosine kinase. Adenosine deaminase-like protein then converts abacavir 5’-monophosphate into carbovir monophosphate. The carbovir monophosphate is metabolized to carbovir diphosphate via guanylate kinase. Finally, the catalyzation of carbovir diphosphate to carbovir triphosphate occurs. Carbovir triphosphate is an analog of deoxyguanosine-5'-triphosphate (dGTP). Carbovir triphosphate inhibits the activity of HIV-1 reverse transcriptase by competing with its substrate, dGTP and by incorporation into viral DNA. Carbovir triphosphate lacks the 3'-OH group which is needed to form the 5′ to 3′ phosphodiester linkage essential for DNA chain elongation, therefore, once carbovir triphosphate gets incorporated into DNA, this causes DNA chain termination, preventing the growth of viral DNA. Less viral proteins are therefore produced, and there is a reduction in new viruses being formed. Common side effects from taking abacavir include diarrhea, nausea, fatigue, headache, loss of appetite and hypersentitvity reactions (fever, skin rash, gastrointestinal and respiratory symptoms)

Abacavir is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Abacavir passes through the liver and is then excreted from the body mainly through the kidney.

Abciximab or Abcixifiban is a platelet aggregation inhibitor drug sold under the name ReoPro. It is administered intravenously, and can act to decrease platelet aggregation for up to two days after administration. Abciximab is an antigen binding fragment that targets glycoprotein IIb/IIIa receptors on the outer membrane of platelets. In the vein, Abciximab causes a conformational change in the integrins on the surface of activated platelets. This prevents the binding of fibrinogen to these integrins, which in turn prevents the platelets from being held together by these fibrinogen fibres. The conformational change also prevents the binding of von Willebrand factor to the platelets, which also prevents aggregation and adhesion.

Abciximab or Abcixifiban is a platelet aggregation inhibitor drug sold under the name ReoPro. It is administered intravenously, and can act to decrease platelet aggregation for up to two days after administration. Abciximab is an antigen binding fragment that targets glycoprotein IIb/IIIa receptors on the outer membrane of platelets. In the vein, Abciximab causes a conformational change in the integrins on the surface of activated platelets. This prevents the binding of fibrinogen to these integrins, which in turn prevents the platelets from being held together by these fibrinogen fibres. The conformational change also prevents the binding of von Willebrand factor to the platelets, which also prevents aggregation and adhesion.

Abciximab or Abcixifiban is a platelet aggregation inhibitor drug sold under the name ReoPro. It is administered intravenously, and can act to decrease platelet aggregation for up to two days after administration. Abciximab is an antigen binding fragment that targets glycoprotein IIb/IIIa receptors on the outer membrane of platelets. In the vein, Abciximab causes a conformational change in the integrins on the surface of activated platelets. This prevents the binding of fibrinogen to these integrins, which in turn prevents the platelets from being held together by these fibrinogen fibres. The conformational change also prevents the binding of von Willebrand factor to the platelets, which also prevents aggregation and adhesion.

Abciximab (also known as c7E3 Fab) is integrin (integrin alpha-IIb and integrin beta-3) receptor antagonist. Binding of abciximab to integrin receptor will block any large molecule to attach on the receptor, which will lead to block any associated signal transduction pathways.