The immunology drug market hit roughly $167 billion at list price in 2023—a figure that sounds impressive until you look closer. Demand isn't the problem. Autoimmune diseases affect millions, clinical pipelines hum along, and AbbVie's Skyrizi and Rinvoq alone pulled in a combined $25.9 billion last year. The problem is that everything has started to feel the same. IL-23 inhibitors march across inflammatory bowel disease and dermatology with clinical precision but limited imagination. Biosimilars chip away at yesterday's blockbusters. And somewhere in this landscape of incrementalism, a three-person startup out of Y Combinator's Winter 2026 batch has decided the real answer might be hiding in the proteins that ticks, viruses, and parasitic worms evolved over millions of years to hijack human immunity.
Ditto Bio's premise sounds like the setup to a science fiction pitch: What if the best drugs for autoimmune disease aren't designed by humans at all, but borrowed from parasites that have spent millennia learning to manipulate our immune systems without killing us?
Founded about seven months before its February 2026 YC debut, Ditto is mining parasite genomes for drug scaffolds that "already work in humans." Not human proteins tweaked in a lab. Not synthetic molecules optimized by machine learning. Actual parasite immunomodulators—decoy receptors from poxviruses, chemokine traps from tick saliva, tolerance inducers from helminth worms—mapped to clinically validated immune pathways. The bet is audacious, maybe even a little absurd: that evolution has already done the hard work of target selection, mechanism, stability, and perhaps immunogenicity.
Whether it will work is another question entirely.
Sameness, Biosimilars, and the Search for What's Next
The autoimmune sector is in the middle of a strange moment. IQVIA data from 2023 placed immunology as the third-largest therapy area, with autoimmune indications accounting for roughly 91% of the category's spending. But growth is slowing—projected at just 2-5% net through 2028—as biosimilars reshape the market economics. The first Stelara biosimilar, Wezlana, launched in the U.S. on New Year's Day 2025 via Optum's private label. Additional biosimilars followed, some with steep list-price discounts. Margin pressure intensified. The bar for novel biologics climbed higher.
Still, differentiation pays when you can deliver it. Bristol Myers Squibb's oral TYK2 inhibitor deucravacitinib (Sotyktu) expanded from psoriasis to psoriatic arthritis in March 2026. Eli Lilly's IL-23p19 inhibitor mirikizumab (Omvoh) secured FDA approval for Crohn's disease in January 2025, building on a 2023 ulcerative colitis nod. AbbVie's immunology franchise posted $30.4 billion in revenue last year, with Skyrizi alone hitting $17.562 billion.
The message is clear enough: new mechanisms matter, but only if they can navigate crowded pathways and prove incremental value over entrenched, increasingly affordable options. Which makes Ditto's parasite-mining strategy either visionary or quixotic, depending on what the data eventually shows.
Why Now? Three Technological Shifts
A decade ago, Ditto's approach wouldn't have been feasible at startup scale. Today, three technological tailwinds make it—at least theoretically—possible.
First, the genomic substrate has materialized. Public databases like WormBase ParaSite (which housed 274 genomes across 208 helminth species as of March 2024), VEuPathDB (for eukaryotic pathogen and host omics), and PHI-base (cataloguing 10,614 pathogen genes and 23,497 interactions in its most recent update) have systematized what was once scattered across decades of parasitology literature. Ditto claims it has analyzed over a million parasite proteins spanning viruses, ticks, and helminths. CEO Dennis Sun, a UC Berkeley PhD in computational and evolutionary biology who previously served as chief of staff at a biotech valued around $500 million, calls it a "data moat."
Second, the prediction layer arrived. AlphaFold 3, released by DeepMind in May 2024 with a code addendum the following year, became a standard tool for inferring protein-protein interactions, including host-pathogen complexes. Methods using AF-Multimer and AF3 proliferated through 2024 and 2025. In its first blog post on March 2, 2026, Ditto demonstrated mapping roughly 10,000 viral proteins to human targets, showing that viral protein frequency could improve autoimmune target ranking compared to human-only datasets—and that the structural logic of etanercept, the TNF inhibitor, mirrors viral decoy receptors.
Third, parasite immunology matured into a translational discipline. The field has moved decisively beyond live-organism therapy—most notably, the trichuris suis ova (TSO) program that failed in mid-stage trials back in 2013—toward defined molecules. Reviews published between 2023 and 2025 emphasize helminth-derived exosomes, peptides, and single proteins with mechanistic clarity: Treg induction, TLR4/MyD88/NF-κB modulation, pattern-recognition receptor signaling. A 2023 PNAS Nexus study showed that a helminth egg peptide, SjDX5-53, induced regulatory T cells and alleviated colitis and psoriasis in mouse models.
This trajectory—from worm to molecule—aligns with Ditto's "molecules, not microbes" framing. Whether it can survive contact with real-world drug development is the test.
The Evolutionary Case: Viruses, Ticks, and Worms
The scientific case for parasite-derived therapeutics rests on examples that span viral, tick, and helminth origins. Some are well-established in academic literature. Others remain speculative.
Viral TNF Inhibitors: Poxviruses encode decoy receptors that bind tumor necrosis factor with picomolar affinity, neutralizing host inflammation to prolong infection. A 2006 study by Alejo and colleagues documented these affinities. Ditto's blog draws a direct line to etanercept, a drug that became a $10-billion-plus franchise at its peak. Epstein-Barr virus produces vIL-10, a functional homolog of human IL-10 with immunosuppressive properties that differ subtly from the endogenous cytokine. Academic literature from 1997 through a 2025 MDPI review has explored these differences for potential therapeutic advantage, though translation remains preclinical—and whether subtle differences matter clinically is anyone's guess.
Tick Chemokine Traps: Evasins, proteins from tick saliva, bind and neutralize multiple chemokines (CXCL1, CXCL8, and others) to suppress host immune responses at feeding sites. Preclinical models dating back to 2008 demonstrated anti-inflammatory effects. A 2026 Accounts of Chemical Research review highlights ongoing protein engineering efforts to broaden selectivity and stability. The molecules represent a class of naturally evolved chemokine inhibitors with no direct human counterparts—which could be an advantage or a regulatory nightmare.
Helminth Modulators: ES-62, secreted by the filarial nematode Acanthocheilonema viteae, suppresses collagen-induced arthritis in mice via TLR4/MyD88 pathway interference. Small-molecule analogs were explored over a decade ago (Journal of Medicinal Chemistry, 2013), with a spin-out called Helmedix attempting commercial development. The program's current status is unclear from public records, though the mechanistic foundation—PRR modulation and Treg induction—has only grown more robust in subsequent research.
Ditto's YC Launch post claimed its early binding data sits in the 1-2 nanomolar range, a potency level competitive with approved biologics if validated in functional assays and animal models. If.
The Immunogenicity Problem
Here's the thing that keeps immunologists up at night when they hear about Ditto's approach: humans have been exposed to parasites throughout evolutionary history. Pre-existing immune memory to parasite epitopes could trigger neutralizing antibodies or adverse reactions. It's not a theoretical concern. It's the central scientific and commercial hurdle.
Ditto acknowledges this explicitly, stating in its YC launch materials that it is building a "tissue biobank to map real-world immune memory to parasite proteins." The strategy suggests awareness of the problem, but awareness and solution aren't the same thing.
Regulatory guidance from the EMA (effective 2017 and still current) and FDA (including a 2022 draft on immunogenicity labeling and ongoing moves toward analytics-heavy biosimilar approvals in 2024-2025) places heavy emphasis on immunogenicity assessment for novel biologics. The covariate-adjustment frameworks and dose-optimization paradigms emerging in oncology (Project Optimus) and rare disease approvals suggest agencies are willing to accept mechanism-based evidence in some contexts. But for chronic autoimmune indications with established benchmarks, robust PK, analytics, and immunogenicity packages will be non-negotiable.
CSO Adair Borges—a UCSF PhD, former Miller Fellow at UC Berkeley, and co-inventor of anti-CRISPR systems with over 50 publications including Cell and Science—brings 15 years of host-parasite research to the immunogenicity problem. CTO Emily Weiss, a UCSD PhD with prior roles at Illumina and DuPont, brings computational biology and AI expertise, evidenced by publications in Nature Microbiology and eLife.
Whether the team's internal MoleculeMapper platform and biobank can de-risk immunogenicity at scale will determine whether parasite-derived scaffolds become shelf-stable drug candidates or evolutionary curiosities relegated to academic conferences.
The Competitive Terrain
Ditto enters an autoimmune landscape where mechanism novelty is necessary but insufficient—a lesson learned the hard way by countless biotechs.
Cell therapies are advancing into mid-stage trials for severe autoimmune diseases like systemic lupus erythematosus, systemic sclerosis, and inflammatory myopathies. CAR-T targeting CD19 and BCMA, engineered regulatory T cells—Nature Medicine published multiple basket and Phase 1 studies in 2025, and press coverage floated the possibility of "immune reset" paradigms that could redefine endpoints and reimbursement. Quell Therapeutics paused its liver transplant Treg trial in February 2026 to focus on its preclinical autoimmune candidate QEL-005. Abata Therapeutics secured IND clearance in 2024 for a TCR-Treg therapy in progressive multiple sclerosis.
These modalities target curative outcomes in narrow, high-severity patient subsets. Ditto's parasite-derived proteins, assuming they clear immunogenicity hurdles, would likely compete in the chronic-dosing biologic space against IL-23 inhibitors, TYK2 inhibitors, and future oral mechanisms. The company lists rheumatoid arthritis, eczema, IBD, psoriasis, SLE, asthma, Crohn's, MS, and type 1 diabetes among its focus indications—breadth that signals platform ambition but also highlights just how crowded the terrain is.
No major late-stage programs built around viral or tick immunomodulators have emerged from industry R&D as of early 2026. Tick evasin research remains largely academic, with a 2026 review noting "growing translational interest" but no disclosed corporate assets. Helminth-derived molecules beyond ES-62 have not advanced past preclinical proof-of-concept, and live helminth therapy companies like Tanawisa (which produced TSO) have receded after clinical failures.
This leaves Ditto, at least publicly, as the first attempt to systematize parasite mining at computational scale for autoimmune therapeutics. Whether that makes them first movers or cautionary tales depends entirely on what happens next.
The Long Road From Genome to Clinic
The thesis Ditto is testing has a certain elegance: parasites evolved to modulate human immunity without killing the host, so their molecular solutions may be safer and more durable than synthetic designs. Simple in principle.
In practice, the challenges stack up fast. Immunogenicity could disqualify entire families of parasite proteins. Manufacturability—producing complex, glycosylated, or otherwise post-translationally modified proteins at scale—could prove prohibitive. And even if candidates reach the clinic, they will compete for formulary position against oral TYK2 inhibitors and biosimilar-priced IL-23s in a market where payers demand both differentiation and cost savings.
Yet the underlying scientific logic has traction, perhaps more than it did even five years ago. The field has moved from live worms to defined molecules. Computational infrastructure—AlphaFold 3, parasite genome databases, protein-protein interaction prediction—has matured. Regulatory pathways for novel biologics, while rigorous, are navigable.
If Ditto's MoleculeMapper platform can surface targets and scaffolds that perform in preclinical disease models and clear immunogenicity screens, the company could pioneer a new source category for immunomodulatory biologics—one grounded not in human protein engineering or small-molecule screening, but in millions of years of host-pathogen co-evolution. That's the bet, anyway.
For now, Ditto is a three-person team (per YC's biotech company list) with a blog post, a platform claim, and backing from Y Combinator's Winter 2026 batch. Whether "evolutionary therapies," as the company bills them, can compete with the precision of synthetic biology or the market momentum of IL-23 inhibitors remains an open question.
The answer will hinge on data—binding affinities, functional assays, animal efficacy, and above all, human immunogenicity—that has yet to leave the lab. In biotech, that's where the real work begins. And where most bold ideas meet their end.
