drug discovery

Nitrile Gloves, Not Ribbons

Posted on by Elise Johnson

Every October, the noise starts up again: it’s breast cancer’s turn for awareness. I brace for it a little every year. What bothers me isn’t the concept, it’s watching companies race to out-pink each other.

A pink ribbon on a shirt or a car can foster a certain amount of solidarity, but at the corporate level, the awareness noise is genuinely inescapable: a building lit up pink for the night, a pink yogurt lid, or a player running out onto the field in pink cleats. Many companies have run some version of the same campaign, and what actually happens to the profit from pink merchandise varies wildly: modest percentages, hard caps on total donations, or numbers that only recently moved after enough people asked questions.

In addition to the question of money is the question of effect: what does a company’s participation do? If the goal actually is awareness, I’ve never understood who remains unaware. It tends to generate goodwill instead, and the sometimes cynical among us might call that marketing, whether or not that’s the intent.

Here’s a sentence that’s true to me, one most people have their own version of: my sister had breast cancer. One in eight women in the U.S. will hear that diagnosis in her lifetime (though women aren’t the only ones who get it). So we are aware. We have been aware for a long time.

At one point, however, we actually needed awareness, in the literal sense of the word. When the American Cancer Society started its breast cancer awareness campaign in 1985, breast cancer was a disease people didn’t discuss in polite company, self-exams weren’t routine, and mammograms weren’t the norm they are now. Getting people to talk about it, check themselves, and get screened was a real, specific goal, and awareness did its job at the time. Last year marked the campaign’s fortieth anniversary, a point at which even the American Cancer Society’s own retrospective pointedly admitted: awareness alone isn’t enough anymore.

October runs on that word, awareness, as if noticing something were the same as solving it. As if on November 1st, we can dust off our hands, congratulate ourselves, and move on to the next color of the month. But breast cancer research doesn’t run on that calendar. Real, promising work has been happening. Learning about it might not change anything either, not directly, but it’s one step closer to what the American Cancer Society itself is now calling “Turning Awareness Into Action.”

More Than a Pretty Face

This starts, perhaps unexpectedly, with the axolotl, a foot-long Mexican salamander known for its perpetual smile and the feathery gills that fan out from its head like a spray of coral. The most common pet-store variety is also, conveniently for this piece, pale pink. It has become plastered across backpacks, folders, plush toys, and t-shirts. My nine-year-old niece and her friends are obsessed with them.

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Can GLP-1 RAs Help Me Live Longer? Well…

Posted on by Michele Arduengo, PhD
scientist working in a research lab

GLP-1 Receptor Agonists (GLP-RAs) have transformed the treatment of diabetes and obesity and are an important advance in the successful treatment of these and maybe other chronic diseases. These medicines were originally developed to treat diabetes, with Ozempic, a semaglutide, released in 2016. In 2023 these drugs became known more generally because of their off-target effect of stimulating weight loss (1).

GLP-1 stands for “glucagon-like peptide 1”, a peptide hormone that is released from cells in the small intestine in the presence of nutrients. One of its functions is to mediate the secretion of insulin in response to these nutrients by activating the GLP-1 receptor in the pancreas.

What are some of the off-target effects of GLP-1RAs on aging that researchers are uncovering?

Several research studies of GLP-1 RAs have indicated that not only do they have the positive effects of regulating blood glucose and weight, but they have also shown benefits that include reduction of heart, liver and kidney diseases. A study published in Nature in 2026 by Feng and colleagues (2) now presents evidence that these drugs may even affect aging in a mouse model, attenuating age effects and maintaining cognition. The results are promising. The scientists looked at several recognized hallmarks of aging, including stem cell attrition, inflammation, protein folding and stability issues, and genomic stability. For both hematopoietic stem cells (HSCs) and neural stem cells (NSCs), the authors found that treatment with semaglutide increased the regenerative capacity of the respective tissues. Furthermore, they found that in semaglutide treatment increased expression of mitochondria-related genes and the oxidative-stress response genes, increased ATP content, and reduced levels of reactive oxygen species.

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A New Human Neuron Model for Tau-Targeted Drug Screening

Posted on by Johanna Lee

Every neuron relies on a protein called tau to keep its internal skeleton, the microtubule network, working properly. In a group of brain diseases known as “tauopathies,” tau stops doing its job. It misfolds, clumps together, and eventually contributes to the neuron loss that causes memory changes and shifts in behavior. Scientists studying these diseases have long wanted to watch this process unfold from its earliest moments in living human neurons. However, this has been surprisingly difficult.

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AI Identifies the Target. Someone Still Has to Validate It.

Posted on by Elise Johnson

Did you see the movie where Spider-Man files his taxes? Or the one where Wonder Woman sits on hold with her insurance company while her pasta water boils over? Or where Captain America finds blight on his tomato plants and drives to the county extension office where he spends fifty minutes with a seventy-four-year-old master gardener named Marlys then leaves with a handwritten note covering his soil composition, his watering schedule, and what Marlys calls “the mulching situation”?

No. Because the ordinary day-to-day doesn’t stand a chance next to the saving of the world.

We spend most of our lives in the ordinary. Not because we’re failing to reach the extraordinary, but because the ordinary is what holds everything together while we get there. It’s not the backdrop but the foundation. It’s what the story depends on, whether or not it gets any credit.

Drug Discovery Has a Storytelling Problem

Drug discovery runs almost entirely on ordinary days, punctuated by the moments that make the news: a new target gets identified, a compound shows promise, a trial produces results. Those moments get the headlines, press releases and keynote slots. What doesn’t get the same attention is the years of work behind those moments: the assays, the failed experiments, the redesigns, the slow accumulation of evidence that either holds up or doesn’t. That work has always been the majority of drug discovery.

Some of the most important work in drug discovery ends in a result nobody publishes, but a dead end isn’t a failure of the program. It’s the program working. The researcher who rules something out has learned something true. That knowledge travels forward even when it doesn’t make the headline because it can redirect the next hypothesis, narrow the next experiment or just quietly move things along. That work moves research forward without anyone announcing it.

The Shiniest Thing in the Room

Artificial intelligence is drug discovery’s latest extraordinary announcement, and the fanfare is legitimate. Most of the druggable proteome has never been touched. Of approximately 4,500 human proteins considered druggable, all approved drugs to date work through only 716 distinct targets. Drug hunters knew there was more biology to address but lacked a way to find and prioritize candidates at scale. AI is changing that. By scanning genetic evidence, biological networks and scientific literature at a scale no human team can match, AI is surfacing targets that were previously out of reach and ranking them by the strength of the evidence behind them.

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Another Crack in the RAS Code: The Measurement Story Behind Daraxonrasib

Posted on by Elise Johnson

In late May 2026, a clinical trial result landed in the New England Journal of Medicine and immediately rewrote what oncologists believed was possible for patients with metastatic pancreatic cancer. Before the paper was published, people in the field were already calling it “transformative.” The data, when it came, agreed. In a disease where most second-line treatments offer months at best, a drug called daraxonrasib nearly doubled how long patients lived compared to those who received chemotherapy.¹

RAS proteins, which regulate cell growth and are mutated in more than a third of all human cancers,² had spent forty years resisting every attempt to drug them. The protein’s surface offered no obvious foothold for a small molecule. Once the word “undruggable” attached itself to the RAS protein family, most of the field moved on to more cooperative targets.

Some researchers stayed. And Promega stayed committed to the question that never goes away: does this new compound work inside a living cell? When the next chapter of the RAS story arrived, the tools were ready. Daraxonrasib is one culmination of a much longer story, one that matters for every researcher pursuing a target the field has written off.

The First Answer

To understand what daraxonrasib represents, it helps to see how an earlier chapter of the RAS story faced the same fundamental measurement challenge.

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Screening Disease-Relevant Biology: How the Endo-GeneScreen Platform Uses Endogenous Protein Detection to Drive Drug Discovery 

Posted on by Amy Landreman

Drug discovery has long grappled with a fundamental tension in high-throughput screening: the more biologically relevant your model, the harder it is to scale. Phenotypic assays in primary disease-relevant cells offer rich biological context, but capturing meaningful, target-specific readouts from these complex systems at screening scale has remained a significant challenge.  In contrast, simpler, more scalable systems are easier to deploy but sacrifice the biological fidelity that makes hits meaningful. A recent study by Samowitz et al. in Nature Communications describes an interesting approach to resolve this tension, the Endo-GeneScreen (EGS) platform. A high-throughput screening system designed to enable scalable detection of endogenous protein levels within disease-modeling cellular contexts. 

A Well-Chosen Proof of Concept 

The authors selected Syngap1 as their proof-of-concept target to develop and demonstrate this approach. De novo mutations in this gene that lead to haploinsufficiency are among the most common genetic causes of sporadic neurodevelopmental disorders, including intellectual disability, autism, and epilepsy. Small molecules that boost SynGAP protein levels back toward wildtype would address the root cause of these disorders rather than managing downstream symptoms. Importantly, Syngap1 function is closely tied to cortical excitatory neurons. Well-validated in vitro and in vivo models for these neurons already exist, creating an integrated system for both discovering new compounds and validating them in the same biological context. That continuity is an important step toward improving the translational relevance of lead molecules coming out of the screen. 

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Your Media Choice Might Be Designing Your T-Cell Fate

Posted on by Simon Moe

Why Metabolism Matters in T-Cell Expansion

Adoptive T-cell therapies rely on generating metabolically fit, functional cells during ex vivo expansion—but this process often pushes T cells toward highly glycolytic, terminally differentiated states that limit their persistence and therapeutic potential. These metabolic programs begin shifting within hours of activation, therefore understanding early metabolic remodeling is essential for designing culture conditions that support durable, cytotoxic, and memory-enriched T-cell populations.

Researchers at Promega set out to address this challenge by systematically mapping how media composition and activation strength shape T-cell metabolism during the first 72 hours after stimulation. Using a suite of bioluminescent assays, they profiled intracellular energy cofactors, redox balance, and extracellular metabolites across several conditions. This approach revealed distinct, media-driven metabolic states that not only emerged early but also predicted downstream expansion, proliferation, and cytotoxic function.

Their work demonstrates how integrating metabolic profiling into in vitro expansion workflows can provide a more informed framework for optimizing T-cell manufacturing strategies.

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CRISPR/Cas9 Endogenous Tagging in Drug Discovery

Posted on by Teresa Simon

Limitations of Traditional Protein Study Methods 

Studying proteins in their native biological context has long been a major challenge in molecular biology. Traditional methods, although widely used, often distort the actual cellular environment and limit functional interpretation. Techniques like antibody-based detection or plasmid-driven overexpression can introduce artifacts and do not allow real-time analysis in living cells. 

In this context, the need for tools that enable the observation of proteins as they naturally occur, under physiological conditions, and within live cells is becoming increasingly evident in molecular biology. 

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Accelerating Drug Discovery at Grove Biopharma with MyGlo® and ProNect®

Posted on by Promega

At Grove Biopharma, the R&D team is advancing a rational design approach to drug discovery. Their Bionic Biologics™ Platform assembles custom-engineered peptides to target intracellular protein-protein interactions into stable, potent, cell permeable therapeutics. By combining the precision of biologics with the efficiency of synthesizing small molecules, Grove accelerates lead generation and optimization.

Grove’s technology enables targeting key proteins involved in cancer and neurodegenerative diseases for which effective therapeutics have historically been difficult to develop. Their candidate molecules focus on important targets such as the Androgen Receptor splice variant, SHOC2 within the RAS/RAF pathway, the MYC-regulator WDR5, a Tau isoform relevant to Alzheimer’s Disease, and the Keap1-Nrf2 interaction associated with neurodegeneration. These programs have made significant progress and now represent some of the most advanced agents in their pipeline.

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CRISPR/Cas9 Knock-In Tagging: Simplifying the Study of Endogenous Biology

Posted on by Ken Doyle

Understanding the expression, function and dynamics of proteins in their native environment is a fundamental goal that’s common to diverse aspects of molecular and cell biology. To study a protein, it must first be labeled—either directly or indirectly—with a “tag” that allows specific and sensitive detection.

Using a labeled antibody to the protein of interest is a common method to study native proteins. However, antibody-based assays, such as ELISAs and Western blots, are not suitable for use in live cells. These techniques are also limited by throughput and sensitivity. Further, suitable antibodies may not be available for the target protein of interest.

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