Parasites have spent millions of years perfecting the art of hijacking human immunity. They evade detection, dampen inflammation, manipulate host biology with a molecular precision that would make any drug designer envious. A three-person team in San Francisco thinks they can steal evolution's playbook.
Ditto Biosciences is mining proteins from viruses, ticks, and worms to build drugs for inflammatory bowel disease, rheumatoid arthritis, and a roster of conditions where the immune system turns traitor. The pitch—that parasites are "the world's best immunologists"—sounds almost flip until you look at what the founders have done in seven months: screened over 1 million proteins, flagged thousands with predicted activity against validated immune targets, and generated early binders hitting 1–2 nanomolar affinity. That's potency competitive with approved monoclonal antibodies, for those keeping score.
Whether this works at scale is another question entirely.
The company emerged from Y Combinator's Winter 2026 cohort, and the approach is unconventional even in a field that's lately embraced CAR-T cell therapies and "inverse vaccines." But the autoimmune market is vast—projected to climb from $168.6 billion in 2025 to $226.2 billion by 2035, according to industry analyses—and still leaves patients stranded when first- and second-line therapies fail. Roughly 15 million Americans live with at least one of 105 recognized autoimmune diseases, per a January 2025 Mayo Clinic study. There's room, in theory, for another approach.
The question is whether parasites can deliver.
A Market in Flux
Immunology is the heavyweight champion of specialty pharma. In 2024, specialty medicines crossed 52% of U.S. pharmaceutical sales, with immunology claiming 36% of that segment—the largest slice by therapeutic category. AbbVie's Skyrizi pulled in $7.85 billion in the first half of 2025; Rinvoq added $3.75 billion. These blockbusters are offsetting the slow-motion collapse of Humira, which slid to $2.3 billion in the same period as adalimumab biosimilars chewed into market share. Sanofi's Dupixent, meanwhile, is on track for $17 billion this year.
But the ground is shifting beneath all of them. Biosimilars for ustekinumab (Stelara) hit the U.S. market in January 2025, with multiple entrants arriving by March. Net prices are compressing. The Inflation Reduction Act's drug price negotiations took effect January 1, 2026, targeting high-cost immunology assets like Enbrel and Stelara. A third round of negotiations, announced late last month, will pull another 15 drugs into the fold by 2028. Payers are tightening formularies. The era of unchecked pricing power for biologics is over, or nearly so.
At the same time, the science is accelerating. The NIH launched a five-year strategic plan for autoimmune disease research in July 2025, prioritizing AI, computational biology, and translational pipelines. Earlier this year, the agency flagged autoimmune research as a "Highlighted Topic," explicitly encouraging proposals that weave together genetics, environment, and immunology. Academic labs and startups are responding—some with more resources than others.
The Parasite Hypothesis
The idea that parasites might hold therapeutic secrets isn't new. Scientists have known for decades that helminths—parasitic worms—secrete proteins that modulate host immunity, often dampening inflammatory responses to ensure their own survival. H. polygyrus AIP-2, for instance, induces regulatory T cells and suppresses airway inflammation in mouse models. Tick salivary evasins bind and neutralize chemokines, the signaling molecules that recruit immune cells to sites of inflammation.
The trick has always been translating that biology into something you can dose to humans.
Whole-organism approaches stumbled badly. Trials of Trichuris suis ova—pig whipworm eggs, if you're wondering—showed transient symptom improvement in a small 2005 ulcerative colitis study. But larger randomized trials in Crohn's disease (2016) and ulcerative colitis (2024) found no superiority over placebo after 24 weeks. The takeaway, as a parasitology journal review put it in 2024, is clear: molecules, not microbes.
That's where AI enters the picture. Tools like AlphaFold 3, released in May 2024, can now predict protein-ligand interactions with startling accuracy. Frameworks like MIT's FragFold, published in February 2025, design computationally validated protein fragments that bind and inhibit specific targets. Ditto is layering these advances onto older structural biology—ingesting millions of parasite protein sequences, running structural predictions, screening for matches against validated drug targets, then validating binders experimentally.
Adair Borges, one of the cofounders, describes the strategy as systematic. She holds a PhD from UCSF and previously served as a Miller Fellow; her earlier work on proteome-wide mimicry screens in malaria offers a methodological blueprint for detecting when parasite proteins structurally or functionally mimic human immune regulators. Dennis Sun, trained at Harvard and UC Berkeley in evolutionary developmental biology and genomics, handles computational work. Emily Weiss, who has a PhD in microbiology and stints at Illumina and DuPont on her résumé, brings industrial-scale biology expertise.
The team is also building something less glamorous but perhaps more critical: a human tissue biobank across multiple organ systems. The goal is to proactively map immunogenicity risk. Therapeutic proteins derived from non-human species face a brutal bar—even highly effective biologics can trigger anti-drug antibodies that neutralize efficacy or cause safety issues. The FDA's 2014 guidance on immunogenicity assessment remains foundational, but 2025 publications in journals like AAPS and Genome Medicine show improved T-cell epitope prediction tools that integrate patient genetics and clinical factors.
Ditto's bet is that preemptive de-immunization—editing out predicted epitopes before clinical development—can turn exotic scaffolds into viable drugs. Whether that works in practice is, well, the whole game.
Precedents and Parallels
Ditto isn't exactly pioneering this territory. Akari Therapeutics' nomacopan, a dual C5/LTB4 inhibitor derived from a tick protein, has been in development for years. In July 2024, the company received positive pre-IND feedback from the FDA for a long-acting version targeting geographic atrophy; an IND filing was expected sometime in 2025, though recent updates are hard to come by. The asset previously advanced to Phase 3 in pediatric hematopoietic stem cell transplant-associated thrombotic microangiopathy, proof that a tick-derived molecule can clear major regulatory hurdles. The path has been slow and capital-intensive, though—a cautionary tale as much as a success story.
Smaller efforts have come and gone. Dalazatide (ShK-186), a peptide from sea anemone venom that blocks the Kv1.3 potassium channel, passed through multiple corporate hands and now sits with TEKv Therapeutics. Recent clinical updates? Scarce. Meanwhile, in October 2025, selectION reported Phase 1b proof-of-concept data for si-544, a small-molecule Kv1.3 blocker in psoriasis. The target remains attractive; the natural-product route has stalled.
The broader autoimmune space is seeing innovation along different axes. COUR Pharmaceuticals secured FDA IND clearance in February 2025 for CNP-103, a liver-targeted tolerogenic nanoparticle for type 1 diabetes, and has partnered with Takeda on a celiac disease program. Anokion is testing KAN-101, another liver-targeted tolerance platform, in celiac disease, with Phase 2 registry updates logged through December 2025. These "inverse vaccines" aim to teach the immune system to tolerate specific antigens rather than suppress it broadly—a conceptual cousin to parasite-derived immunomodulation, though the mechanisms diverge.
Then there's CAR-T, which is generating some of the field's most dramatic results. Long-term follow-up data from German trials, published in 2025, show durable remissions in systemic lupus erythematosus after CD19-targeted CAR-T—without severe neurotoxicity. Quell Therapeutics and Sonoma Biotherapeutics are engineering regulatory T cells with chimeric antigen receptors to selectively suppress autoimmunity. Quell's program in liver transplant advanced to an efficacy cohort in 2024, and this past March the company initiated a Phase I/II trial for rheumatoid arthritis and systemic sclerosis. CRISPR Therapeutics' zugo-cel, tested in a basket trial for autoimmune diseases, showed early pharmacodynamic signals in December 2025.
The contrast is instructive. CAR-T and Treg therapies are cell-based, expensive to manufacture, and face scalability questions that won't be solved cheaply. Inverse vaccines and nanoparticle platforms are antigen-specific but require deep knowledge of disease-driving epitopes, which vary wildly across patients and conditions. Parasite-derived proteins—if they can be engineered for safety and manufacturability—offer a middle path: biologics with defined mechanisms, potentially broad activity across inflammatory pathways, and the manufacturing infrastructure of conventional antibodies already in place.
That's the pitch, anyway.
What Comes Next
The next few years will test whether Ditto's thesis can move from computational hits to actual patients. Several forces will shape the outcome, not all of them under the company's control.
First, immunogenicity prediction is improving, but it's not solved. The 2025 literature on T-cell epitope modeling shows incremental gains—tools like PredIG, published in Genome Medicine this year, are becoming more interpretable—but no amount of in silico trimming guarantees a clean immunogenicity profile in humans. Ditto's tissue biobank is a hedge. Akari's experience—years of clinical work on a single tick-derived molecule—illustrates the challenge.
Second, the commercial bar is rising fast. Biosimilar competition and IRA pricing negotiations are squeezing gross-to-net spreads for established immunology drugs. Payers will demand clear differentiation: better efficacy, better safety, or access to patient populations that fail on IL-23, IL-4/13, and JAK inhibitors. Niche indications with high unmet need—refractory IBD phenotypes, steroid-dependent conditions, organ-specific autoimmunity—may offer easier entry points than head-to-head trials against Skyrizi or Dupixent. Maybe.
Third, the scientific ecosystem is crowded but not saturated. A January review in Accounts of Chemical Research lays out a roadmap for engineering tick evasins into multi-chemokine inhibitors, conceptually aligned with what Ditto is attempting. Academic labs continue publishing structure-function work on helminth proteins like H. polygyrus TGM-2 (a TGF-β mimic) and viral immune evasion proteins, including SARS-CoV-2 nsp15. The raw material—evolution's archive of immune-modulating molecules—is vast. The tools to mine it are maturing.
What Ditto hasn't disclosed is which targets it's pursuing first, or when a lead program might enter IND-enabling studies. The company's public statements focus on platform capabilities rather than pipeline specifics—typical for an early-stage biotech, but it leaves open questions about whether the million-protein screen has yielded molecules differentiated enough to command investor and pharma attention in a field where clinical validation is everything. And clinical validation, in case anyone's forgotten, takes years and hundreds of millions of dollars.
The opportunity is real. Autoimmune diseases affect millions; existing therapies leave gaps; the regulatory and scientific environment increasingly favors novel mechanisms. If Ditto can demonstrate that parasites' evolutionary toolkit translates into safe, effective, manufacturable drugs, the company will have done more than build a business. It will have validated a new source of therapeutic innovation hiding in plain biological sight.
If not, it joins a long list of nature-inspired platforms that looked elegant on paper but couldn't clear the messy reality of human trials.
For now, the founders are in the lab, screening proteins and building tissue banks. The rest of the industry is watching—skeptically, perhaps, but also with a flicker of curiosity. Because if evolution spent millions of years solving the problem of immune modulation, maybe the pharmaceutical industry should be paying closer attention. Or at least taking notes.
