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Image illustrates DNA, RNA, and protein synthesis. The first two are nucleic acids. A nucleic acid inhibitor is a type of antibacterial that acts by inhibiting the production of nucleic acids. There are two major classes: DNA inhibitors and RNA inhibitors. [1] The antifungal flucytosine acts in a similar manner.
[23] [24] It was developed by the synthesis and broad spectrum antiviral activity of 2,3-dihydroxypropyladenine. [24] Tenofovir DF was the first nucleotide reverse-transcriptase inhibitor approved by the FDA for the treatment of HIV-1 infection in October 2001. [18] [23]
Dihydropteroate synthase inhibitors are drugs that inhibit the action of dihydropteroate synthase. They include sulfonamides, dapsone, and para-aminosalicylic acid. [1] Tetrahydrofolate synthesis pathway. In bacteria, antibacterial sulfonamides act as competitive inhibitors of the enzyme dihydropteroate synthase, DHPS.
Many are primarily DHFR inhibitors, but raltitrexed is an inhibitor of thymidylate synthase, and pemetrexed inhibits both and a third enzyme. Antifolates act specifically during DNA and RNA synthesis, and thus are cytotoxic during the S-phase of the cell cycle.
As a nucleoside inhibitor, the guanosine analog prodrug is used to stop viral RNA synthesis and viral mRNA capping by incorporating into RNA and pairing to uracil or cytosine. Branaplam is currently in phase I/II clinical trial for the treatment of Spinal Muscular Atrophy (SMA). This molecule is from a class of pyridazine small molecules and ...
Leflunomide is an immunomodulatory drug that achieves its effects by inhibiting the mitochondrial enzyme dihydroorotate dehydrogenase (DHODH), which plays a key role in the de novo synthesis of uridine monophosphate (rUMP), which is required for the synthesis of DNA and RNA.
The antibacterial activity of rifamycins relies on the inhibition of bacterial DNA-dependent RNA synthesis. [8] This is due to the high affinity of rifamycins for the prokaryotic RNA polymerase. The selectivity of the rifamycins depends on the fact that they have a very poor affinity for the analogous mammalian enzyme.
The viral DNA is then integrated into the host chromosomal DNA, which then allows host cellular processes, such as transcription and translation, to reproduce the virus. RTIs block reverse transcriptase's enzymatic function and prevent completion of synthesis of the double-stranded viral DNA, thus preventing HIV from multiplying. [citation needed]
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