Teaching the brain to clean up after itself - clearing Alzheimer's plaques through the body's own machinery, without the inflammation.
Every anti-amyloid drug approved for Alzheimer's shares a stubborn flaw. They strip plaque from the brain, but often at a cost: ARIA - amyloid-related imaging abnormalities, the swelling and micro-bleeds that show up on brain scans and force doctors to monitor patients closely. Illimis Therapeutics, a biotechnology company founded in Seoul in 2021, was built around a different question. What if you could clear the plaque without picking a fight with the immune system?
The answer is a platform the company calls GAIA - short for Gas6-mediated Anti-Inflammatory Adaptor. Rather than flagging amyloid for an inflammatory attack, GAIA hands it to the body's cleanup crew and asks them to digest it quietly, the same way the body disposes of billions of dead cells every day.
That process - efferocytosis - is one of biology's oldest housekeeping tricks. Illimis is trying to turn it into medicine. The company pairs deep science with an unusually global footprint: research headquarters in Seoul, a subsidiary in Boston, an advisory bench that includes a founding figure in TAM-receptor biology, and a collaboration with Eli Lilly, one of the few companies to actually bring an Alzheimer's antibody to market.
In July 2025, Illimis closed a $42 million Series B backed by 18 investors - a notable vote of confidence during a lean stretch for biotech funding, and enough to push its lead candidate toward first-in-human trials.
GAIA is a bispecific fusion protein. One arm grips a disease target - such as amyloid-beta. The other arm is an engineered version of Gas6, the natural ligand of the TAM receptors (Tyro3, Axl, Mer). By binding both at once, GAIA acts as a molecular adaptor that tells nearby immune cells to swallow and dissolve the plaque - quietly.
One arm binds the pathological target - amyloid-beta, tau, or alpha-synuclein - marking it for removal.
The engineered Gas6 arm dimerizes the TAM receptor on microglia and astrocytes, switching on phagocytosis.
The cell engulfs and clears the misfolded protein through efferocytosis, the same anti-inflammatory pathway the body uses for dead cells. No inflammatory cascade means a lower risk of ARIA-style side effects.
"We translate cutting-edge science into innovative medicine."
In preclinical models, Illimis ran its GAIA construct head-to-head against aducanumab - the first FDA-approved anti-amyloid antibody, later withdrawn amid debate over its side effects and benefit.
The company reported greater cognitive improvement alongside markedly lower inflammatory response and reduced ARIA. These are preclinical, animal-model results - not clinical proof - but they define the exact claim Illimis is racing to test in humans by 2027.
Bars below are a schematic illustration of the company's stated preclinical direction, not published trial percentages.
| Program | Target | Indication | Stage |
|---|---|---|---|
| ILM01 | Amyloid-beta | Alzheimer's disease | Preclinical → IND 2027 |
| ILM02 | Tau | Neurodegeneration | Discovery |
| ILM03 | Alpha-synuclein | Synucleinopathies | Discovery |
| GAIA (platform) | TAM receptor / Gas6 | CNS & immune disease | Core technology |
Because GAIA is an engine rather than a single molecule, the same design principle extends beyond the brain. With its Series B, Illimis said it would broaden its targets into immune diseases - the second act for a company that started with neurodegeneration.
On July 14, 2025, Illimis closed a 58 billion KRW ($42 million) Series B - bringing total funding to roughly $65.4 million. Eight existing investors returned; ten new ones joined.
The round is a business-model tell. Pre-commercial biotechs like Illimis run on equity and grants, converting capital into clinical progress and, eventually, into partnering deals with large pharma. The presence of the Korea Development Bank and the Industrial Bank of Korea alongside venture funds signals both institutional and strategic backing.
Led fundraise with 18 investors to advance ILM01 into preclinical development and expand into immune disease.
Cumulative capital raised since the 2021 founding, across seed, Series A, and Series B rounds.
Co-founded Illimis in 2021 and leads the company's scientific and business strategy from Seoul.
Co-founded the company alongside Park, building its TAM-receptor and fusion-protein foundations.
Leads Illimis Therapeutics USA from Boston. 18+ years in drug development, formerly at Codiak Biosciences and hC Bioscience.
TAM-biology pioneer Greg Lemke (Salk Institute) and neuroscientist Morgan Sheng (Broad Institute, ex-Genentech) advise the science.
Collaboration through Lilly's Catalyze360-ExploR&D to apply the GAIA platform to neurodegenerative disease.
Winner of the BMS Innovation Square Challenge - early validation of the platform science.
Member of Johnson & Johnson's global incubator network, extending Illimis's reach across Asia.
Alzheimer's is one of medicine's largest unmet needs, and the anti-amyloid field is crowded at the top: Eisai and Biogen's lecanemab (Leqembi) and Eli Lilly's donanemab (Kisunla) are on the market, both carrying ARIA warnings.
Illimis is not trying to build a slightly better antibody. It is competing on mechanism - clearance via phagocytosis instead of inflammatory tagging. That places it near other differentiated neuro-immune approaches, such as TREM2 agonists and microglia-modulating biotechs, rather than in a straight race with the incumbents.
For patients and the physicians who treat them, the promise is simple to state and hard to deliver: the benefit of plaque removal with less of the monitoring burden and risk that comes with today's drugs. For pharma partners, GAIA offers a reusable engine that could be pointed at tau, alpha-synuclein, or immune targets.
The catch, as with all preclinical-stage biotech, is that the story is still unproven in humans. The 2027 IND is the moment the thesis meets the clinic.
"MOONSHOT means the transformation of a huge idea that will change the future of human beings into reality."
Sanghoon Park, Chanhyeok Kim, and Jeong Won Seok launch Illimis around TAM-receptor-driven protein clearance.
Bristol Myers Squibb recognition validates the early platform science.
Signs a Catalyze360-ExploR&D deal with Eli Lilly and joins J&J's JLABS network.
Closes an 18-investor Series B, publishes GAIA efferocytosis data, and moves ILM01 into preclinical development.
Aims to file for first-in-human trials of its lead Alzheimer's candidate.
It develops protein-based medicines for CNS and immune diseases using its GAIA platform, which clears misfolded proteins like amyloid-beta through the body's own phagocytic cleanup - without triggering inflammation.
A bispecific fusion protein that binds a disease target on one arm and engineered Gas6 on the other, dimerizing TAM receptors to trigger inflammation-free clearance via efferocytosis.
Conventional anti-amyloid antibodies can cause ARIA from inflammation. Illimis clears amyloid via phagocytosis without inflammation, and in preclinical work showed better cognition and reduced ARIA versus aducanumab.
About $65.4 million total, including a $42 million (58B KRW) Series B closed in July 2025 backed by 18 investors.
ILM01 entered preclinical development in H2 2025, with an IND submission targeted by the end of 2027.