Drugs that have been used for more than a decade to treat cancer could cure Covid-19

A drug that has been used for more than a decade to treat cancer could cure people with Covid-19, according to a new study.

The drug, called pralatrexate, is a chemotherapy drug that was originally developed to treat lymphomas – tumors that come from the glands.

Chinese researchers found that pralatrexate performs better than remdesivir, which is currently the leading antiviral drug used to treat Covid-19 patients.

Pralatrexate was approved by the U.S. Food and Drug Administration in 2009 for patients with borderline disease despite its toxicity.

Adverse effects of pralatrexate include muscle weakness, nausea and mucositis – swelling and ulceration of the mucous membranes that line the digestive tract.

However, reproducing pralatrexate in a way that eliminates its side effects reveals a lot of potential, according to researchers.

Color scanning electron analysis of apoptotic (pink) cells severely infected with SARS-COV-2 virus particles (green), isolated from a patient sample. pralatrexate, a chemotherapy drug originally developed to treat lymphoma, could be relapsed to treat Covid-19

‘Identifying effective drugs that can treat Covid-19 is important and urgent, especially the approved drugs that can be tested immediately in clinical trials,’ says the study’s authors, led by Dr. Haiping Zhang at Shenzhen Institute of Advanced Technology, China.

‘Our study found that pralatrexate is able to strongly inhibit SARS-CoV-2 reproduction with stronger inhibitory activity than remdesivir within the same experimental conditions.’

In the aftermath of the global revolution of Covid-19, researchers were inspired by the idea of ​​replacing existing drugs developed to treat other conditions.

Remdesivir was first developed to treat hepatitis C and then reintroduced as a potential Ebola treatment, Due to the similarity in the structures of these viruses to SARS-CoV-2, the virus that causes Covid-19, experts hoped it could help.  fight the routine pandemic

Remdesivir was first developed to treat hepatitis C and then reintroduced as a potential Ebola treatment, Due to the similarity in the structures of these viruses to SARS-CoV-2, the virus cause Covid-19, experts hoped it could help. fight the routine pandemic

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Boris Johnson in July had to allay fears about a shortage of anti – coronavirus drugs today after Donald Trump bought almost the entire global supply of remdesivir.

The U.S. president has been accused of disrupting the global coronavirus fight by spraying the money on one of only two drugs approved to treat Covid-19 at the time.

UK business minister Nadhim Zahawi was among those who criticized his decision to force the rest of the world to compete for the drug, which was originally designed to treat Ebola but tested to accelerate recovery time for coronavirus patients.

But then Downing Street and the Department of Health then played the essence of the move, claiming that the UK has enough stock for everyone who needs to be treated.

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

And the Department of Health said they had received provision in advance and had enough for all NHS patients who need treatment.

The U.S. Department of Health and Human Services (HSS) had earlier revealed that it had received more than 500,000 courses of remdesivir treatment for American hospitals.

It represents total global supply for July and 90 percent of stocks for August and September, leading to fears of a shortage of harvest.

Commenting on the deal – which US health chiefs boasted was’ amazing ‘- Mr Zahawi told Sky News:’ It’s much better to work together than to work to weaken each other, and so we will continue in that spirit. ‘

Artificial intelligence can help identify such drugs by simulating how different drugs would interact with SARS-CoV-2, the virus that causes Covid-19.

To aid in meaningful screening of existing drugs, Zhang and colleagues developed several computational methods similar to drug virus interactions.

They used this hybrid method to screen 1,906 existing drugs for their ability to inhibit the reproduction of SARS-CoV-2 by targeting a viral protein called RNA polymerase RNA which is dependent on RNA (RdRP).

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

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

Two of the drugs, pralatrexate and azithromycin, successfully inhibited the reproduction of the virus.

Further laboratory tests showed that pralatrexate inhibited viral reproduction more strongly than remdesivir, suggesting that the latter could be replicated for Covid.

However, this chemotherapy drug can induce serious side effects and, since it is used for people with terminal lymphoma, immediate use is not guaranteed for Covid-19 patients.

Nevertheless, the findings support the use of the new screening strategy to identify drugs that may have been tweaked, according to the team.

‘We have demonstrated the value of our novel hybrid approach that combines deep learning technologies with more traditional simulations of molecular dynamics,’ said Dr Zhang.

The researchers, who have published their work in PLOS Computational Biology are now developing additional computational techniques to generate new molecular structures that could be upgraded to new drugs to Covid -19 handle.

The study follows some common complaints about the effectiveness of remdesivir, which was first developed to treat hepatitis C and then reinstated as a potential Ebola treatment.

Following the disappointing results of Ebola treatment in 2014, remdesivir was tested at an early stage of this year’s pandemic.

There is no consensus on whether it is effective, however, with clinical trials showing mixed results.

The NHS has approved its use on Covid-19 patients in the hope that it will help, but they are already taking them to the drug’s ration, which costs £ 2,400 per course ($ 3,120).

In November, the World Health Organization (WHO) said doctors should not treat coronavirus patients with remdesivir no matter how ill they are.

Officials at the time said there was’ no evidence ‘that it strengthens people’s chances of surviving the disease or prevents them from becoming ill enough to require mechanical ventilation’.

They also warned that there is a ‘potential for significant harm’ when using the experimental Ebola drug as it may cause kidney and liver damage in some patients.

In December, however, a team of British experts at Nature Communications reported that remdesivir could be a highly effective Covid-19 treatment ‘for some patients’.

He had helped treat a 31-year-old patient who suffered a poor response to the disease, due to a genetic disorder called XLA, which prevented him from making antibodies to fight infection.

‘There have been various studies that support or question the effectiveness of remdesivir, but some of those conducted during the first wave of diseases may not be the best for assessing its properties. antiviral, ‘said study author Dr James Thaventhiran of the MRC Toxicology Unit at Cambridge University. .

WHAT DOES IT COVER AND DOES IT WORK INCLUDE CORONAVIRUS?

Remdesivir, an antiviral drug originally developed to try to treat Ebola, was used experimentally on Covid-19 patients from the early days of the revolution.

The FDA issued an emergency use permit for the drug on May 1, in response to the preliminary results of a special study released in late April.

It has also been given the green light for simultaneous use on the NHS in Britain.

There are claims about miraculous recovery, better survival odds and shorter illness, but other studies have found that it makes no difference to hospitalized patients with Covid-19.

Remdesivir delivered encouraging results earlier this year when it showed promise for both prevention and treatment of MERS – another coronavirus – in macaque monkeys.

The drug appears to help stop the reproduction of both viruses such as coronavirus and Ebola.

It is not entirely clear how the drug performs this function, but it appears to prevent the virus’ genetic material, RNA, from being able to replicate itself.

That in turn stops the virus from being able to multiply further inside the patient’s body.

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