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AIDS is caused by hiv virus (HIV), which attacks the most important CD4T lymphocytes that destroy the body's immune system, causing loss of immune function, which in turn is prone to infection with various diseases, with a high death rate.
a joint assessment by the CDC and WHO, there are currently about 1.25 million people living with HIV in the country, and about 80,000 new infections are expected each year.
existing combined antiretroviral therapy (cART) has significantly improved the life expectancy and quality of life of people living with HIV after treatment, reducing the further spread of HIV.
, however, cART requires daily medication, is expensive, has side effects, and has a high mutation rate of HIV-1 (type 1 HIV) that can lead to resistance to antiretroviral drugs.
, there is an urgent need to develop new mechanisms of action and inexpensive therapeutic drugs.
Recently, researchers from the University of Utah and the National Institutes of Health published the latest research results on AIDS treatment drugs in PNAS, which developed a long-acting drug CTP31, which has shown strong inhibitory effects on a variety of pregenital HIV isolates, and has been shown to be effective in suppressing HIV-embedded virus AD8 (SHIVAD8) replication infection in rhesus monkeys, in addition, CPT31 monotherapy can prevent virus rebound after cART is deactivated.
makes CPT31 a new candidate for HIV prevention and treatment.
Cholesterol-PIE12-trijudome (CPT31) is a D peptide (which is not biodegradable and stable in the body) that targets key parts of the HIV fusion mechanism, namely the highly conservative gp41 N peptide pocket area, thereby inhibiting its damage to CD4T.
To test the inhibition effect of CPT31, the researchers first tested the inhibition of CPT31 on 118 HIV particles from CAVD (AIDS Vaccine Cooperative Organization) and found that CPT31 completely inhibited the 118 HIV-1 prosthetic virus particles.
further tests using 60 separation strains with primary replication capability, it was found that 96% of the separation strains could be inhibited by low concentrations of CPT31.
shows that CPT31 has a broad-spectrum anti-HIV-1 effect.
the inhibition effect of CPT31 on HIV-1 isolated strains, the researchers constructed a model of RHSA HIV infection with SHIVAD8-EO virus and tried to assess CPT31's ability to block viral infection in primates.
shiVAD8-EO after injecting four rhesus monkeys with CPT31.
the rhesus monkey plasma was continuously tested for virus sequence after the outbreak, and it was found that it had not been infected with the virus for 21 weeks.
CPT31 low-dose treatment and virus inoculation of rhesus monkeys for a second course of treatment, and found that CPT31 again inhibited the infection of the virus.
after the third treatment and inoculation, the virus was detected in the plasma of three rhesus monkeys, and sequencing revealed that it was not a drug-resistant variant, but rather a result of insufficient doses of CPT31.
data show that CPT31 therapy can effectively prevent SHIVAD8-EO virus infection in rhesus monkeys.
CPT31 can prevent rhesus monkeys from contracting the virus at the same time, the researchers of rhesus monkeys inoculated with low dose shiVAD8-EO after the establishment of the chronic virus infection CPT31 single drug treatment, found that short-term after treatment in its plasma virus load dropped rapidly, indicating that CPT31 can also effectively inhibit the replication of viruses in the body.
Although the virus rebounded later, but by the plasma virus RNA testing, found that during the treatment of CPT31 appeared anti-CPT31 virus variants, that is, the virus transmitted in rhesus monkeys are carrying Q577R CPT31 resistance replacement, some of the new L543Q changes.
an infectious assessment of these virus variants, the researchers found that the replication time of the AD8-577R SHIV variant was delayed by one to two days compared to the wild variant, while the AD8-577R/543Q SHIV variant was delayed by one day.
that the replacement of amino acids that cause CPT31 resistance has no significant effect on SHIVAD8-EO's in-body replication capability.
addition, the researchers found that CPT31 monotherapy, in addition to controlling virus replication in MONKEY-8-EO infected macaques, could also prevent virus rebound after routine cART therapy is deactivated.
After the first inhibition of SHIVAD8-EO replication through cART, CPT31 single-drug treatment can control the virus rebound of rhesus monkeys In short, researchers have developed a drug CPT31 that gives AIDS patients new hope, which can effectively prevent HIV infection, but also effectively inhibit the level of virus in AIDS patients, but also has long-lasting, economic advantages, is expected to become a complementary treatment or new treatment options for cART.
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