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Drug metabolism is the metabolic breakdown of drugs by living organisms, usually through specialized enzymatic systems. More generally, xenobiotic metabolism (from the Greek xenos "stranger" and biotic "related to living beings") is the set of metabolic pathways that modify the chemical structure of xenobiotics, which are compounds foreign to an organism's normal biochemistry, such as any drug ...
After phase II reactions, the xenobiotic conjugates may be further metabolised. A common example is the processing of glutathione conjugates to acetylcysteine (mercapturic acid) conjugates. [7] Here, the γ-glutamate and glycine residues in the glutathione molecule are removed by Gamma-glutamyl transpeptidase and dipeptidases.
One example is the N-glucuronidation of an aromatic amine, 4-aminobiphenyl, by UGT1A4 or UGT1A9 from human, rat, or mouse liver. [ 2 ] The substances resulting from glucuronidation are known as glucuronides (or glucuronosides) and are typically much more water - soluble than the non-glucuronic acid-containing substances from which they were ...
Metabolism (/ m ə ˈ t æ b ə l ɪ z ə m /, from Greek: μεταβολή metabolē, "change") is the set of life-sustaining chemical reactions in organisms.The three main functions of metabolism are: the conversion of the energy in food to energy available to run cellular processes; the conversion of food to building blocks of proteins, lipids, nucleic acids, and some carbohydrates; and the ...
Others include a phase that combines distribution, metabolism and excretion into a disposition phase. Other authors include the drug's toxicological aspect in what is known as ADME-Tox or ADMET . The two phases of metabolism and excretion can be grouped together under the title elimination .
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An example of a drug where first-pass metabolism is a complication and disadvantage is in the antiviral drug remdesivir. Remdesivir cannot be administered orally because the entire dose would be trapped in the liver with little achieving systemic circulation or reaching target organs and cells (for example, cells infected with SARS-CoV-2).
Phase 3 Slows the dimerization rate of vitamin A AVP-786 (d6-dextromethorphan) Phase 3 Reduce formation of toxic metabolite by CYP2D6 VX-561 (formerly CTP-656) (d9-ivacaftor) Phase 2 Reduce rate of tert-Bu group oxidation and in vivo clearance by CYP3A4 VX-984 (Novel cancer agent) Phase 1 Reduce aldehyde oxidase-driven metabolism