A drug used for more than a decade to treat cancer can cure Kovid-19

According to a new study, a drug that has been used for more than a decade to treat cancer can cure people with Kovid-19.

The drug, called pralatractate, is a chemotherapy drug that was originally developed to treat lymphomas – tumors that originate in the glands.

Chinese researchers found pralatreset outperform Remedisvir, the leading anti-viral drug currently used to treat Kovid-19 patients.

Pralatrexate was approved by the US Food and Drug Administration in 2009 for patients with terminal illness despite its toxicity.

Adverse effects of Pralatract include fatigue, nausea and mucus – inflammation and ulceration of the mucous membrane lining the digestive system.

However, reintroducing pralatreset in a way that eliminates its side effects, according to researchers, shows much greater potential.

Colorized electron micrograph of an apoptotic cell (pink) infected with SARS-COV-2 virus particles (green) isolated from a patient sample. Pralatract, a chemotherapy drug originally developed to treat lymphoma, could potentially be reproduced for the treatment of Kovid-19.

The researchers say that at the Shenzhen Institute of Advanced Technology in China, Dr. The researchers, led by Happing Zhang, say that identifying effective drugs that can treat Kovid-19, especially approved drugs, can be tested.

‘Our study showed that pralatreset is potentially capable of inhibiting SARS-COV-2 replication with stronger inhibitory activity than remedisvir in similar experimental conditions.’

After the global outbreak of Kovid-19, researchers were inspired by the idea of ​​remodeling existing drugs that were originally developed to treat many conditions.

Remedisvir was initially developed for the treatment of hepatitis C and then reconstructed as a potential Ebola treatment, the similarity in the structures of these viruses is due to SARS-CoV-2, the virus that binds to Kovid-19. Because of this, experts hoped that it might be able to help.  Fight the current epidemic

Remedisvir was initially developed for the treatment of hepatitis C and then reconstructed as a potential Ebola treatment, the similarity in the structures of these viruses is due to SARS-CoV-2, the virus that binds to Kovid-19. Because of this, experts hoped that it might be able to help. Fight the current epidemic

Remodevir’s private international service in the US Bohot Almost in June

Today, Boris Johnson was informed of a shortage of anti-coronavirus drugs in July after Donald Trump bought almost the entire global supply of remediesvir.

The US president was accused of ‘reducing’ the global coronavirus fight by splashing cash on one of only two drugs approved for treatment of Kovid-19 at the time.

UK Trade Minister Nadim Zahavi was among those who criticized his decision to let the rest of the world compete for the drug, originally designed to treat Ebola, but in recovery time for coronovirus patients Proven to accelerate.

But Downing Street and the Department of Health later played down the importance of the move, insisting that Britain had enough reserves to treat everyone who needed it.

The Prime Minister’s official spokesman said on 1 July: ‘The UK currently has a substantial stock of Remedisvir’.

And the Health Department said it had secured supplies in advance and had enough to treat every patient in the NHS who needed it.

The US Department of Health and Human Services (HSS) previously revealed that it had acquired more than 500,000 treatment courses of Remedisvir for US hospitals.

This represents the entire global supply for July and 90 percent of the shares for August and September, leading to a shortage of autumn.

Discussing the deal – which US health chiefs boasted was’ amazing ‘- Mr Zahavi told Sky News:’ It’s better to work together to underestimate each other, so we’ll continue that feeling .

Artificial intelligence can help identify how different drugs interact with SARS-CoV-2, which causes the virus Kovid-19.

To help in the virtual investigation of existing drugs, Zhang and his colleagues combined several computational techniques that simulate drug – virus interactions.

They used this hybrid approach to screen 1,906 existing drugs for their ability to inhibit the replication of SARS-COV-2 by targeting a viral protein called RNA-dependent RNA polymerase (RDRP).

RdRP is an essential protein encoded in the genome of all RNA-containing viruses, such as SARS-CoV-2.

The novel screening approach identified four promising drugs, which were then tested against SARS-CoV-2 in laboratory experiments.

Two of the drugs, pralatrexate and azithromycin, successfully prevent replication of the virus.

Further laboratory experiments have shown that Predelectract inhibits viral replication more strongly than Remedisvir, suggesting that the former may be remodeled for Kovid.

However, this chemotherapy drug may indicate significant side effects and, as it is used for people with terminal lymphoma, immediate use is not guaranteed for Kovid-19 patients.

Despite this, the findings support the use of a new screening strategy to identify drugs, according to the team.

“We have demonstrated the value of our novel hybrid approach that combines intensive-learning technologies with more traditional simulations of molecular dynamics,” Dr. Zhang said.

Researchers, who have published their work in PLOS Computational Biology, are now developing additional computational methods for constructing novel molecular structures that can be developed into new drugs to treat Kovid-19.

The study follows some general doubts about the efficiency of remedisavir, which was initially developed to treat hepatitis C and then repurchased as a potential Ebola treatment.

Remedisvir was tested in the early stages of this year’s pandemic, following disappointing results that treated Ebola in 2014.

There is no consensus on whether it is effective, although clinical trials show mixed results.

The NHS has approved it for use on Kovid-19 patients, in the hope that it may help, but is already being forced to ration the drug, which costs £ 2,400 ($ 3,120 per course) ) is.

In November, the World Health Organization (WHO) said that doctors should not treat patients with coronovirus based on how ill they are.

Authorities at the time said that ‘there is no evidence’ that it increases people’s chances of surviving the disease or prevents them from falling ill in sufficient amounts. ‘

He also warned that there is a potential for significant harm when using experimental Ebola medication as it may damage the kidneys and liver in some patients.

In December, however, a team of British experts told Nature Communications that Remedisvir ‘Kovid-19 treatment’ could be a very effective treatment for some patients.

It had helped cure a 31-year-old patient who suffered a rare reaction to the disease due to a genetic disorder called XLA, which prevented him from making antibodies to fight infection.

The study’s author, Dr. James Theventiran told the MRC Toxicology Unit at the University of Cambridge, “There have been separate studies to support or interrogate the effectiveness of Remedisvir, but nothing conducted during the first wave of infection may be optimal. ”.

What is Remedivir and does this coronavorous work?

Remedisvir, an anti-viral drug first designed to try and treat Ebola, has been used on Kovid-19 patients since the early days of the outbreak.

In response to the preliminary results of a notable study released in late April, the FDA issued an Emergency Use Authority for the drug on 1 May.

It was also given a green-light at the same time for use on the NHS in Britain.

There are claims of miraculous recovery, improved lifesaving barriers, and minor illness, but other studies have found that hospitalized patients with Kovid-19 do not make a difference.

Remedswear produced encouraging results earlier this year when it showed promise to both prevent and treat MER – another coronavirus – in macaque monkeys.

The drug helps prevent replication of viruses such as coronovirus and Ebola alike.

It is not entirely clear how the drug accomplishes this feat, but it prevents the genetic material of the virus, RNA, from being able to copy itself.

This, in turn, prevents the virus from being able to spread further inside the patient’s body.


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