Picture this: A $350 billion company loses patent protection on its blockbuster drug because someone couldn't be bothered to pay a $450 fee. Meanwhile, the Fulbright program—you know, America's flagship "we're the good guys" diplomacy effort—just had 11 of 12 board members rage-quit because politics got weird. Again.

But while adults are having meltdowns over paperwork and ideology, scientists are out here teaching eyeballs to regenerate like fish, accidentally discovering that COVID shots might cure HIV, and watching a couple literally quit their day jobs to cure a genetic death sentence.

So yeah, it's been a week. Let's dive in.

Table of Contents

The $450 mistake that cost Novo Nordisk billions (and why patients might thank them) news

Novo Nordisk forfeited patent protection for Ozempic in Canada after failing to pay a $450 maintenance fee - potentially the most expensive administrative oversight in pharmaceutical history. The diabetes drug giant hesitated over what amounts to pocket change for a company worth over $350 billion, missing the 2019 payment deadline for their semaglutide patent.

The financial results of this are pretty big. Canada represents the second-largest semaglutide market globally, worth $2.5 billion annually. Generic competitor Sandoz is now preparing to launch in early 2026, with expected price drops of 50-80%. Sandoz CEO Richard Saynor's reaction captured the industry's bewilderment: "I'm sure someone's lost their job, but never mind."

But what makes this particularly absurd? Novo's legal team actually requested a refund of the $250 fee in 2017, saying they needed "more time to see if they wanted to pay it." The internal discussions about whether to pay $450 (after late fees) likely cost more than the fee itself. And just so you know, under Canadian law, once a patent lapses, it cannot be revived - making this an irreversible mistake with billion-dollar consequences. And we can see that the patent has indeed expired.

The broader implications extend beyond corporate embarrassment. Americans seeking lower drug costs frequently cross into Canada, and this generic opening could accelerate medical tourism. The timing coincides with political pressure on drug pricing, potentially creating a case study in how patent mistakes can inadvertently improve patient access.

Read more from Science

Fulbright's mass exodus: When soft power meets hard politics news

Eleven of twelve Fulbright board members resigned en masse in June 2025, alleging unlawful Trump administration interference with the prestigious international exchange program. The unprecedented exodus followed accusations that the administration denied awards to a "substantial number" of already-selected scholars and subjected 1,200 foreign recipients to unauthorized ideological review.

The irony runs deep in the personnel decisions. Darren Beattie, previously fired from Trump's first administration for speaking at a white nationalist conference, now oversees programs designed to promote international understanding. The 1,200 contested applications reportedly sit "on Beattie's desk" awaiting review. Fields affected include biology, engineering, and even music - suggesting content-based rather than merit-based screening.

This represents the first mass resignation in the program's 79-year history, undermining what experts call America's "closest thing to pure soft power." With proposed budget cuts of 93% (from $741 million to $50 million), the Fulbright crisis exemplifies broader tensions between traditional diplomatic tools and the administration's "America First" approach.

The human cost affects real scholars with approved research projects studying everything from disease prevention to architectural preservation, suddenly finding their life plans upended by political considerations rather than academic merit.

Read more from the Financial Times and the Washington Post

Scientists trick eyeballs into thinking they're fish (and it works) research

Korean researchers achieved sustained retinal regeneration in mammals for the first time, offering unprecedented hope for millions with inherited blindness. The KAIST team discovered that blocking a single protein - PROX1 - allows the eye to essentially "unlock" its dormant ability to repair itself, similar to how fish and amphibians naturally regenerate damaged retinas.

The mechanism is elegantly simple. When retinal cells die, they release PROX1 protein that gets absorbed by support cells called Müller glia, effectively telling them to "stop working." The researchers developed an antibody that acts like a molecular cleanup crew, capturing this "stop work" signal before it reaches the repair cells. Once freed from this inhibition, Müller glia transform into regenerative specialists that can produce new photoreceptors.

Results in mouse models were significant: Animals with genetic retinitis pigmentosa showed sustained vision improvement for over six months, with some mice recovering normal visual acuity within one month of treatment. Unlike other approaches that work around vision loss, this therapy actually regenerates lost retinal tissue.

Clinical trials are planned for 2028 through spinout company Celliaz Inc. The approach could potentially treat multiple forms of inherited blindness regardless of the specific genetic mutation - a "one size fits many" solution that addresses the root problem rather than individual genetic variants.

Read the science published in Nature Communications, or read more KAIST

COVID vaccines accidentally taught us how to fight HIV research

COVID-19 mRNA vaccines inadvertently fueled a breakthrough in HIV research, revealing that the same technology could train immune systems to fight the virus that has eluded cure attempts for four decades. Scientists discovered that COVID vaccines activate specific immune pathways that "wake up" hidden HIV and help eliminate infected cells - without causing dangerous side effects.

The discovery emerged from studying HIV-positive individuals who received COVID-19 vaccinations. Researchers found that the vaccines activate the RIG-I/TLR-TNF-NFκB pathway, causing latent HIV to become transcriptionally active while simultaneously boosting HIV-specific killer T cells. This creates a "seek and destroy" effect targeting the hidden reservoirs that make HIV so difficult to cure.

Now scientist have shown a new method to ‘reveal’ the hiding virus by sending mRNA via lipid nanoparticles (LNPs), specifically a new kind of a LNP dubbed LNP X. This method is showing great promise but even the scientists responsible are showing healthy skepticism in translation as many methods from lab do not translate to the clinic.

However, political challenges also threaten progress. The Trump administration cancelled $258 million in HIV vaccine funding, including the CHAVD consortium, just as breakthrough results emerged. This represents a critical test of whether scientific momentum can survive political transitions in rare disease research.

STITCHR: The gene editor that thinks size doesn't matter (spoiler: it does) research

STITCHR gene editing technology shattered size barriers by enabling seamless insertion of DNA sequences up to 12.7 kilobases - roughly six times larger than current methods can handle reliably. Developed by Mass General Brigham researchers, this breakthrough could enable complete gene replacement rather than single-mutation correction.

The innovation repurposes "jumping genes" from nature. Scientists discovered they could reprogram retrotransposons - DNA sequences that naturally move around genomes - to deliver therapeutic cargo with GPS-like precision. Unlike traditional gene editing that relies on cellular repair mechanisms, STITCHR uses the body's existing molecular machinery to insert genes directly where needed.

Size matters tremendously in gene therapy. Many disease-causing genes exceed current delivery limits: the dystrophin gene (muscular dystrophy) spans 14 kilobases, while common viral vectors max out around 4.5kb. STITCHR's capacity could enable "one-and-done" therapies that replace entire genes regardless of which specific mutations patients carry.

The technology works entirely through RNA delivery, simplifying manufacturing and reducing safety concerns compared to DNA-based systems. Early demonstrations show successful insertion across multiple genomic locations with no residual "scars" - critical for therapeutic applications where precision matters.

You can find the research in Nature, or read more here

How to fight your genetic death sentence: Quit your job and cure yourself news & research

One of the most compelling patient-scientist stories in modern medicine reached a milestone when Eric Minikel and Sonia Vallabh completed enrollment in the first human trial for prion disease treatment. Their journey from law and urban planning to leading a research lab exemplifies how personal tragedy can drive a scientific breakthrough.

Their story began with a devastating discovery. When Sonia's mother died from fatal familial insomnia in 2010, genetic testing revealed Sonia had inherited the same mutation. Faced with a 90% chance of developing the same fatal disease, they quit their careers and transformed into biomedical researchers, earning PhDs and establishing their own laboratory at the Broad Institute.

Prion diseases represent one of medicine's greatest challenges - proteins that misfold and force other proteins to misfold in a chain reaction, causing rapid neurodegeneration. The couple's approach targets the root cause: reduce the raw material (prion protein) so there's less to misfold. Their antisense drug ION717 works like "molecular scissors with GPS," finding and destroying the genetic instructions that make prion protein.

The PrProfile trial completed enrollment on December 30, 2024, recruiting 56 patients across 16 international sites. The rapid enrollment (one patient every 4.3 days during active recruitment) demonstrated urgent community need and willingness to participate in groundbreaking research. Results expected in 2025-2026 will determine whether this approach can provide the first effective treatment for prion diseases.

Beyond personal stakes, their work establishes a model for patient-driven rare disease research, showing how love, determination, and scientific rigor can tackle seemingly impossible challenges. Whether their specific drug succeeds or not, they've already transformed the landscape for rare disease research and provided hope to families worldwide facing similar devastating diagnoses.

You can catch up more here

Look, Novo's $450 screwup is peak corporate comedy, but patients getting cheaper drugs? We'll take it. The Fulbright implosion is genuinely depressing. Turns out soft power is pretty fragile. However! Watching Eric and Sonia go from "we're gonna die" to "we're gonna cure this thing" in one decade? That's good stuff that inspires us.

The COVID-HIV connection has us cautiously excited. If a pandemic vaccine accidentally unlocked a 40-year mystery, what else are we missing? And honestly, the fish-eyeball thing is just cool. Science is weird and wonderful, even when everything else is falling apart.

What got you this week? The billion-dollar typo? The couple who literally changed careers to save their own lives? Hit reply! We read everything, and your takes always surprise us.

Share this with someone who appreciates good chaos. Until next week! Prateek & Jere

And if you’re still not convinced, no worries! Just unsubscribe here, you can always check back on us later

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