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FDA approves first oral antiviral drug for COVID-19



FDA has received full approval to nirmatrelvir-ritonavir (Paxlovid) for the treatment of adult outpatients with mild to moderate COVID-19 who are at risk for severe illness, the agency said on Thursday.

“Today’s approval demonstrates that Paxlovid meets the agency’s stringent safety and efficacy standards and remains an important treatment option for people at high risk of progression to severe COVID-19, including those with pre-immune immunity,” Patricia Cavazzoni, MD. This is stated in a statement by the director of the FDA’s Center for Drug Evaluation and Research.

The approval of an antiviral drug to help prevent hospitalization and death in high-risk patients followed approval from the agency’s Antimicrobial Advisory Committee and was largely expected despite some concerns about relapse rates and multiple drug interactions. who received a warning about a boxed drug his label another news bulletin for health care providers.

“Prescribers should review all medications a patient is taking to evaluate potential drug interactions and determine if other medications the patient may be taking require dose adjustment, interruption, and/or additional monitoring,” the FDA said in a statement. . “Prescribers should consider the benefits of treatment with Paxlovid in reducing hospitalization and mortality, as well as the ability to appropriately manage the risk of potential drug interactions for the individual patient.”

Nirmatrelvir-ritonavir was a critical component of President Biden’s “test cure” strategy during the pandemic. Given that the antiviral is indicated for use within 5 days of symptom onset, the program aimed to get it quickly into the hands of positive patients, and even allowed pharmacists to prescribe the drug directly to patients.

Millions of people with COVID-19, including Biden, have already taken the drug since its Emergency Use Authorization (EUA) in late 2021, and numerous studies have confirmed the drug’s benefit in high-risk groups, while studies in lower-risk groups generally do not show practically no benefit.

In its notice of approval, the agency stated that previous packages distributed under the EUA will remain available for use. High-risk children aged 12 years and older will also continue to be eligible under the EUA, although approval does not extend to this group.

The agency also indicated that nirmatrelvir-ritonavir is not intended for use as a prophylactic therapy either before or after exposure to COVID (i.e., patients must be symptomatic and have a confirmed case before use).

Primary support for approval came from the final results of the EPIC-HR study, which demonstrated an 86% reduction in the risk of hospitalization or death at 28 days compared with placebo. Patients included in the study included unvaccinated adults aged 18 years and older with disease(s) that put them at high risk of severe disease, or adults aged 60 years and older with or without chronic disease.

Of the 1966 patients in the final analysis without SARS-CoV-2 antibodies at baseline, 0.9% of those receiving nirmatrelvir-ritonavir and 6.5% of those receiving placebo were hospitalized due to COVID-19 or died within 28 days. Some benefit against hospitalization or death was also seen in this trial among people with prior immunity to the virus that causes COVID-19 (0.2% versus 1.7%, respectively).

And in the negative EPIC-SR study, which included vaccinated patients with at least one risk factor for progression, there was a nonsignificant reduction in the risk of hospitalization and death in the nirmatrelvir-ritonavir group.

Data from these trials showed that cases of COVID-19 relapse occurred in a similar proportion of patients treated with nirmatrelvir-ritonavir and placebo, leading the agency to conclude that there was “no clear association” with the available evidence.

In addition, the FDA listed taste disturbance and diarrhea as the most common side effects of treatment.

  • Ian Ingram is the Managing Editor of MedPage Today and helps cover the site’s cancer coverage.


Neuralink: Elon Musk’s brain chip company says US has received approval for human research



Billionaire implant company Neuralink wants to help people regain vision and mobility.

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“Love and Death” Season 2



The following contains spoilers for love and death season 1

HBO love death concludes in the courtroom. Candy Montgomery (Elizabeth Olsen) details the events of her murder rampage by Getty Gore, which included an ax brought into the living room by Gore, a fight, and a trigger — “shhh” — that drove Candy into such a frenzy that she repeatedly stabbed Mountain. Psychotic break described in another testimony by Dr. Fred Faison as a dissociative event whose description was apparently bought by the jury and deemed sufficient for the defense to find Candy not guilty.

Candy Montgomery’s real-life case developed in a similar fashion when lawyer Don Crowder enlisted Dr. Candy’s support. Fred Faison, a psychologist and hypnotist, testifies in Candy’s defense. Through hypnosis, Faison reportedly helped Candy uncover moments of emotional trauma from the age of 4 when her mother really “shhh” Candy. At the booth, Candy said that Gore had also used the phrase and that Candy had “pissed off”.

The jury found Candy not guilty, apparently influenced by both testimony. (You can read about the real trial in 1984. Texas Monthly articles”Love and Death on Silicon Prairie Part 2: The Killing of Betty Gore“, itself taken from the book Proof of Love: A True Story of Suburban Passion and Death by John Bloom and Jim Atkinson.)

But while the lawsuit could end the events of the case and the source material for the HBO series, will it be the end of the show?

Want love death get season 2?

There have been no announcements for a second season yet. HBO himself only mentioned love death as a “limited series”, meaning it will most likely only run for one season.

If the series had continued the storyline, it would have done so without much source material. The lives of its protagonists were not widely publicized after the trial. Any future drama is likely to be fabricated.

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Joshua St. Clair is Associate Editor of Men’s Health.

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Now we know how Botox penetrates neurons and paralyzes muscles.



Botulism or Clostridium botulinum bacterium 3d illustration

Illustration of Clostridium botulinum, a bacteria that produces botulinum neurotoxin.


We finally know how Botox gets into the neurons. The discovery could help develop an antidote for the molecule’s neurotoxic effects, which can lead to paralysis or even death.

Botox uses a type of botulinum neurotoxin, a highly toxic substance produced by bacteria. The toxin disrupts communication between neurons, resulting in muscle paralysis. In small therapeutic doses, it can ease muscle spasms, cure migraines, or more commonly, reduce wrinkles. However, in high doses, this molecule causes botulism, a potentially fatal disease that does not require large amounts of treatment.

Frederic Meunier from the University of Queensland in Australia and colleagues analyzed how botulinum neurotoxin type A enters neurons using a technique called single molecule imaging. This allowed them to capture the movement of molecules labeled with a fluorescent dye.

The researchers placed the toxin in a dish of rat neurons. They tuned one camera to a neurotoxin and the other to receptors in neuronal membranes, also labeled with different colors of dyes.

Previously, only two receptors, called polysialoganglioside (PSG) and synaptic vesicle glycoprotein 2 (SV2), were thought to be key for toxin entry into cells. But when they tracked SV2’s response to the toxin, they saw that it moved in tandem with another receptor known as synaptotagmin 1 (Syt1).

“Basically we started thinking, ‘Oh, this is weird,'” Meunier says. The researchers genetically modified rat neurons to prevent Syt1 from binding to SV2 and repeated the experiment. If you suppress the binding between these two receptors, the toxin can no longer enter the cell, Meunier says.

The same was true when they genetically modified neurons to lack PSG, indicating that all three receptors are required for botulinum neurotoxin type A to enter cells. Future drugs that block the binding of the three receptors could prevent neurons from being infected by the toxin, Meunier said.

“By understanding more about the mechanism of cell entry, we are one step closer to preventing cell entry and preventing botulism,” says Sabine Pellett at the University of Wisconsin-Madison.


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