Browsing Pathways

Methadyl Acetate (also known as Acetylmethadol) is analgesic that can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of methadyl acetate will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Hyperpolarization of neuron is caused by inactivation of calcium channels and activation of potassium channels via facilitated by G-protein.

3-Methyl-thiofentanyl is a fentanyl analog and an opioid analgesic that works by inducing central nervous system (CNS) depression. 3-Methylthiofentanyl binds to the mu, delta, and kappa opioid receptors. These ultimately lead to decreased pain sensation as well as a number of side effects, such as euphoria, sedation, depressed breathing. In neurons, 3-methyl-thiofentanyl binds to mu opioid receptors, stimulating the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as GABA is inhibited. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability. 3-Methyl-thiofentanyl acts at A delta and C pain fibres in the dorsal horn of the spinal cord. By decreasing neurotransmitter action there is less pain transmittance into the spinal cord. This leads to less pain perception.

Abacavir (also known as Ziagen or Epzicom) is an antiviral agent that is used for treating HIV/AID. Cellular enzyme converts abacavir to its activate metabolite, carbovir triphosphate, for inhibiting HIV-1 reverse transcriptase (RT) by competing with dGTP, which is the natural substrate of RT. Without HIV-1 reverse transcriptase, complementary DNA (cDNA) could not be generated; therefore, viral DNA couldn't be completed.

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)

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.