Today, we’re announcing an open call for guest investigators in life sciences. Over 8–12 weeks, guest investigators will work directly with my team and other Anthropic researchers to produce analyses and tools for their work. We’ll run our models and harnesses, at no cost to them. We’ll work together to open-source the resulting data, artifacts, and code, and write preprints about what we find. We want humans to remain at the center of scientific discovery, deciding what questions to pursue, and how to pursue them. Those decisions are not ours to make alone. This open call is part of our ongoing efforts at Anthropic to support researchers and accelerate scientific discovery. I’m looking for principal investigators and their research groups at academic institutions, nonprofits, or government labs, working in causal human biology, structural and computational molecular biology, medicinal chemistry, drug discovery, and clinical science. Applications are open for about 14 days: anthropic.com/news/open-call…

Our newest book is finally here! Making the Modern Laboratory is a spectacular 504-page hardcover that tells the story of everything in the research laboratory and how it came to be, from pipettes to heat-resistant glass to microscopes and more. It features dozens of articles (most of which will never appear in print), 100+ full-color images, and original writing from 36 authors. It's printed on Arena Natural Rough paper from Fedrigoni. These books are THICC and would make a great gift for both the science-curious and the working scientist. :) We have spent the last year working on this project. It has been an insane labor of love. The best way to support our independent science journalism is to buy a copy. <3 Pre-order for $49, with free shipping: press.asimov.com/articles/mo…

Co-sign

In the AI era, I expect to see many new modalities emerge in biotech. These will be therapeutics in unusual shapes and sizes, not the legacy small molecule drugs that our IP laws, tech transfer departments and biopharma term sheets were designed to bring to market. CRISPR was a practice run. It was an experiment to see how well the existing biotech ecosystem is set up to commercialize new modalities. 14 years after the CRISPR patent wars, it should be seen as a failure and motivate significant reform. Imo the failure of CRISPR reveals two needs: 1) We need better legal and financial tools for nonexclusive foundational IP licenses. If a new modality has 100 applications, we can't assign exclusive rights to 3 companies who then spend the next decade suing each other. 2) We need better infrastructure for modality-wide safety trials and re-use of clinical data. If a new modality has 100 applications, we shouldn't demand that each use build a new portfolio of clinical evidence from scratch. I believe the AI era will deliver dozens of CRISPR-scale new medical innovations. Let's not allow the CRISPR fiasco to happen again. statnews.com/2026/10/07/cari…

Big pharma committed about $6.6 billion to in vivo CAR-T in roughly seven months last year. @abbvie bought @capstantx for $2.1B. @AstraZeneca bought EsoBiotec for up to $1B. @bmsnews paid $1.5B for Orbital. @KitePharma picked up Interius for $350M. EsoBiotec and Interius both run on lentiviral vectors. So does @UmojaBiopharma, which AbbVie partnered with before buying Capstan. Which is why today's news from @AsimovBio and @LonzaGroup caught my attention. In ex vivo cell therapy, the lentivirus is a tool. You use it in a lab to engineer a patient's cells and you're done with it. In vivo flips that. The vector goes into the patient. As @alectricity put it, the vector becomes the drug. That makes manufacturing the hard part. Most lentivirus is still made by transfecting cells with multiple plasmids, batch after batch. It's expensive, variable, and tough to scale. Asimov's LV Edge Producer lines build all the lentiviral genes into the host cell itself. No transient transfection, no GMP plasmid bill, and titers above 1E9 TU/mL for CAR constructs, about 10x what they saw before. Lonza brings the process development, analytics, scale-up and GMP manufacturing. Putting the two together at the cell line stage means manufacturability gets designed in early, before a program hits scale-up and finds out the hard way. If in vivo CAR-T works the way pharma is betting, the bottleneck moves to making enough clean, consistent vector at a cost that works for big indications. That's the problem this collaboration is going after. Alec first spoke at @SynBioBeta in 2018, back when Asimov was a genetic circuits startup. Soren Flygenring Basset from Lonza joined us on stage in San Jose this May. Fun to see these two worlds connect. Congrats to @alectricity, Imroz Ghangas and the @AsimovBio team, and to Daniel Palmacci, Thomas Fellner and Soren at @LonzaGroup.

big news for asimov today: we're partnering with lonza on in vivo lentiviral vector manufacturing. i'm pretty excited about this one for a lot of reasons. ex vivo CAR-T has now treated tens of thousands of patients, and many of them have been cured of their cancer. but it requires extracting and engineering human cells outside the body, which means every dose is its own batch. it's an impressive manufacturing effort, but it's hard to scale. in vivo approaches skip the cell extraction step. you dose the gene delivery vector directly into the patient, and it engineers the target cells inside their body. this means one drug product can serve many patients, but the catch is that the vector is now the actual drug, not just a reagent, so consistency and a well-defined product profile matter a lot more. traditionally, lentiviral vectors are made by large-scale transient transfection of a production host cell line, which is plagued by scalability and consistency problems. every cell in the bioreactor can receive a different number of plasmids, anywhere from zero to thousands. stable producer cell lines take a different approach. they're clonal engineered lines with the production genetics integrated into the genome, so no transfection is needed during manufacturing. the whole process starts to look more like antibody manufacturing, which is highly controllable and scalable. (as an aside, refactoring the lentivirus genome to gain tight control over the multi-step molecular process it encodes is one of the most technically impressive feats i've seen since starting asimov) we're seeing order of magnitude higher titers and infectivity with our stable producer systems compared to transient transfection. with lonza, we're pairing that with their process development, analytics, and GMP manufacturing expertise to support drug developers. we think in vivo cell and gene therapies are the future, and that they'll bring many more drugs to patients in the years to come.

I love living in the future

When you go skiing in the winter, and see those big machines spitting out snow, know that they are spitting out purified proteins made from dead bacteria. I didn’t realize this until recently! Basically, they take Pseudomonas syringae cells — not engineered; a natural microbe found on plants — and grow them up in huge bioreactors. The cells make ice-nucleating proteins, which sit on their outer membranes and help ice crystals form. The cells are concentrated, freeze-dried, and sterilized until only these proteins remain. The reason these proteins are useful is because they help water molecules form ice more quickly. Water can remain liquid even below 0°C, and only freezes when enough molecules form into a crystal. The proteins have, on their surfaces, repeating snippets of amino acids that help water molecules organize into that shape. So these snow machines just blast super cold water with these proteins, and the two hit the air, mix together, and immediately freeze into snow.

v1 gene therapy

I’ve expected this for a while but it still hurts. The “Life Sciences Verification Program.” It breaks my heart to know that biological knowledge will be locked down and gatekept like this. I want to take a moment to mourn, because I believe this marks an end for open science as I knew it. I think back to my education. I owe so much to the open-access literature. I'm so deeply thankful to the culture of transparency among scientists. All the free knowledge I've been given. The free GenBank sequences. The free PDB structures. The education and know-show that my colleagues shared with me for the pure love of learning. The Life Sciences Verification Program will kill that spirit. The most important biology tools of the next decade will be locked down and controlled. Some fragments of the old literature will remain free, but the real heart of where science happens will not be free. Frontier knowledge will belong only to people who the authorities decide deserve it. I want to fight this, but I don’t think I can. I don’t believe bioterrorism is a serious threat, but convincing people of that is not realistic. The fear is embedded too deep in the psyche. If I tried, there are armies of internet trolls eager to accuse me of evil things. It would become my entire online life. There is a growing and well funded fear-industrial complex dedicated to the idea that Bio-AI is a terrible risk and the people who practice it need to be monitored and policed. Hundreds of full-time professionals whose salary depends on their belief that biology presents a dire threat. What hope do I have of arguing with them? On the other side, the traditional defenders of free information are historically weak. Biology professors are struggling just to keep the lights on. The last thing they want is to be called reckless enemies of national security. They aren’t going to fight this - I’m sure many of them are already signing up to ask for permission to be on the list. So I’m writing this to bear witness. This is how it ended. Biology isn’t going to be free going forward. That was an idea of the pre-AI era and it is over now. The fight now isn’t over free access to information. It’s over who gets verified access to the closed information. Big pharma companies get permission, of course. So do professors at elite universities. But we can petition Anthropic to expand that list. Maybe they might allow access for high school teachers, medical students and nurses? I hope they will approve farmers, iGEM teams, community biolabs, birdwatchers, park rangers and community gardens. Will Anthropic allow those people to study biology at the frontier? As of today, the power officially belongs to them. We can only ask.

Today, there's a strong focus on fast-follows of existing drugs. The drug programs that inspire me look different – the target is known, but we don't know how to build the drug, often requiring the dev of new tech that paves the path for more drugs.

CAR-T therapies engineer patients’ immune cells to kill cancer and they have achieved remarkable results in blood cancers that resist other treatments. Solid tumors (e.g. liver, breast cancer) have proved much harder -- until now. This new report of one patient in a Phase I trial offers a very promising example of progress: a three-year-old with chemotherapy-resistant metastatic liver cancer achieved complete remission lasting at least a year -- a truly breakthrough result considering the severity of this cancer. The history of how this results came about shows how CAR-T progress depends on repeated cycles of engineering, testing in patients and learning from the results. Most of this iterative learning happens in Phase I trials like the current one, which shows how important such studies are for driving medical progress forward. One additional difficulty for solid tumors is that they suppress immune activity, which in turn makes it difficult for CAR-T cells to sustain an attack. So to extend CAR-T’s success in blood cancers to solid tumors, researchers had to help the engineered cells survive in this more hostile territory. In 2020, the team’s earlier clinical work across 4 Phase I trials tested CAR-T cells targeting glypican-3, a protein on certain solid tumors. In 12 patients, these cells produced no objective tumor responses. Another 12 received cells engineered to also produce IL-15, a naturally occurring immune signaling protein that helps T cells survive and multiply. Although 4 patients responded, none achieved complete remission. But the responses were promising and revealed that there was value in giving CAR-Ts their own survival signals. So the researchers doubled down on this lesson. In this new Phase I study, built on the learnings from the previous one, researchers engineered the expression of two different cytokines – IL-15 and IL-21. They also added an emergency off switch that allows doctors to destroy the engineered cells if necessary to reduce toxicity. Remarkably, a first infusion shrank the cancer of the 3 year old patient and a after a second, the remaining tumor disappeared. A year later the patient remained disease-free. There is an obvious caveat here: one patient cannot definitively establish how reliably the treatment works. But the results are striking enough to offer real hope that this would work in at least a subset of patients. I believe this development beautifully illustrates why Phase I trials matter: they let researchers observe how engineered cells behave inside patients and carry those lessons into further development. I am committed to making these studies easier to run in order to accelerate this cycle of iterative learning.

1. >10M people die of infectious diseases per year today. AI is already helping us get better at tackling that. 2. Many ways to create very dangerous bioweapons without any AI/synbio (and it was true for the last 50-75 years). The delta on risk is quite small imo.

don’t forget you can now safely vortex the shit out of this guy

navier-stokes drama is like the crispr battle but for fluid dynamicists

wow so much drama about navier stokes. had no idea things could blow up so infinitely in such a finite time.

wake up babe asimov press is back

Everyone goes through AI psychosis once where you heavily using AI. Then (hopefully) you become enlightened and don't use it for writing/creative work. But it's hard to tell when someone sends work without slop if they're pre-psychosis or post-enlightenment.

I'm starting a new series: 30 Days of Biology History Day #1: Penicillin manufacturing during WWII was only made possible because of a moldy cantaloupe in Illinois. In 1928, Alexander Fleming returned from a holiday to discover a mold on his bacterial plates. The mold made penicillin and killed the bacteria. Fleming published the discovery in 1929. He claimed that — being somewhat "absent-minded" — he had left his laboratory window open, allowing mold to drift in. This is the story taught in schools, but it's likely false: 1. His lab window was rarely, if ever, left open. The window story also wasn't mentioned until a decade-plus after the event. 2. Fleming claimed to find the plate on September 3rd, but his first notebook entry is dated October 30th. That entry doesn't describe a "chance" contamination, but a deliberate experiment where Fleming grew mold on a plate FIRST, then added bacteria. 3. Penicillin only kills bacteria while they're actively growing; it cannot kill mature colonies. Every attempt to recreate Fleming's experiment as described has failed. It only works if you grow mold first and add bacteria afterward. Chemists who initially tried to purify penicillin failed repeatedly. In the late 1930s, Ernst Chain and Howard Florey figured out how to purify the molecule and showed it could cure mice of infections. By 1941, penicillin was given to the first human patient, a policeman named Albert Alexander, whose symptoms abated but who died when supplies ran out. Scientists still couldn't isolate penicillin in large amounts, so they tried extracting it from patients' urine. (In 1942, a single patient consumed half of the United States' entire experimental supply. That's how little was available.) Around this time, Florey went to Peoria, Illinois to visit an agriculture laboratory and try to scale manufacturing. Fleming's mold only grew as a thin mat on the surface of a liquid, so scaling up meant thousands of shallow vessels stacked on shelves. It took about 2,000 liters of culture fluid to treat a single patient! The Peoria scientists solved this. They swapped the growth medium for corn steep liquor, a corn starch byproduct, and put the mold into 300-gallon tanks while blowing in air from the bottom. The mold circulated throughout the whole tank, growing in a larger volume. This boosted yields 500-fold. Still, Fleming's original mold was bad at making penicillin! So the Peoria team put out a public call for mold samples. Surprisingly, the best strain was discovered by Mary Hunt, a research assistant in the laboratory, on a rotting cantaloupe at a local market. It made about six-times more penicillin than Fleming's. This combination (better fermentation + a better strain) meant that, by D-Day in 1944, US companies scaled penicillin manufacturing to 2.3 million doses. The cantaloupe strain, dubbed Penicillium rubens NRRL 1951, is still the ancestor to all the mold strains used to make penicillin today.

Our @AsimovPress book on the history of the molecular biology lab is nearly finished. It's currently 455 pages, with 100+ images. Some previews below. We've spent the last 6+ months making this book as beautiful, and detailed, as possible. And we're excited for you to hold it.