Analysis of how Bikeren Pronol Tablets (Bituvi) inhibits HIV virus replication and its pharmacological mechanism

Biktarvy is a compound oral drug used for the treatment of HIV infection. It consists of Bictegravi (Bictegravi r), propanosivir fumarate (Emtricitabine) and tenofovir disoproxil fumarate (Tenofovir alafenamide, TAF). Its antiHIV effect is based on a multi-target mechanism that synergistically inhibits viral replication. As an integrase inhibitor, bictegravir can block the integration of viral DNA produced by reverse transcription of HIV into the host cell genome, thus preventing the generation of new viruses. It is the core point of action of the entire compound drug.

Prenosivir fumarate is a nucleoside reverse transcriptase inhibitor (NRTI) whose structure is similar to the natural nucleotides required for viral replication. During the viral reverse transcription process, prenocivir will be misused by viral reverse transcriptase and incorporated into the viral DNA chain, causing chain termination, thereby preventing the HIVRNA from being reversely transcribed into DNADNA, providing protection for host cells from infection. This effect complements that of bictegravir, enhancing the ability to block all aspects of the HIV replication cycle.

Tenofovir disoproxil fumarate (TAF) is also a nucleoside reverse transcriptase inhibitor. Its advantage is that it can achieve high intracellular activity at low doses while reducing toxicity to the kidneys and bones. TAF is converted into the active form tenofovir diphosphate after entering the body, binds to the viral reverse transcriptase and is incorporated into the viral DNA chain, producing a chain termination effect. Combined with prenocivir, these two NRTIs can form a double blockade, significantly reducing the efficiency of virus replication in host cells.

Through the multi-target synergy of biktegravir, prenocivir and TAF, Biktarvy can not only quickly reduce the viral load in the blood, but also delay the development of drug resistance and maintain long-term viral suppression. In clinical use, a significant decrease in viral load can usually be observed within a few weeks after taking the drug, but long-term medication is still the key to maintaining efficacy. Patients should strictly follow the doctor's instructions during use and avoid missing doses or stopping the medication on their own to maintain continued viral suppression and reduce the risk of AIDS progression.

Reference materials:https://www.drugs.com/