ai3Bio, a biotechnology company targeting autoimmune disease at its root source, today announced its launch with $48 million in Series A funding. ai3Bio’s proprietary antibody and lipid nanoparticle-based technologies offer complementary innovations to reset the immune system by directly targeting and eliminating disease-causing Th17 cells in vivo, in a single step. The capital will be used to advance both of ai3Bio’s platforms, including IND-enabling studies that advance to first-in-human trials in autoimmune disease.

The round is led by founding investors UPMC Enterprises and Ziff Capital Partners, who backed the complementary and foundational technology innovations that were combined to create ai3Bio. The round includes support from Cockrell Interests and Tanis Ventures.

“Despite billions of dollars of investment, no therapeutic on the market today delivers lasting remission for the more than 15 million Americans who live with autoimmune diseases,” said Steven Altschuler, M.D., Chief Executive Officer of ai3Bio. “We founded ai3Bio to reimagine autoimmune care, shifting the focus from broadly suppressing inflammation to precisely removing the underlying cause of disease — with a goal of providing patients with a one-step treatment.”

The global market for autoimmune disease treatment has surpassed $130 billion, yet patients remain trapped in a frustrating cycle, often moving from drug to drug while enduring difficult side effects without lasting relief. Current therapies suppress the immune system broadly to calm symptoms, leaving underlying disease-causing cells untouched, and patients to relapse once treatment ends. Newer in vivo therapies reprogram cells inside the body, but most target B cells through indirect, multi-step processes. In contrast, ai3Bio’s proprietary and next-generation platforms reset the immune system by directly targeting and eliminating disease-causing Th17 cells in vivo, offering a one-step solution to autoimmune disease.

“The newest generation of cytokine inhibitors have proven the importance of IL-17 in autoimmune disease. Yet, these drugs leave the cells that produce this dangerous cytokine — Th17 cells — untouched. In order to reset the immune system, the Th17 cells that produce these cytokines need to be eliminated,” said Jonathan Kagan, Ph.D., Scientific Co-founder and Distinguished Scientist, ai3Bio; the Marian R. Neutra, Ph.D. Professor of Pediatrics at Harvard Medical School; and the Director of Basic Research and Shwachman Chair in Gastroenterology at Boston Children’s Hospital. “By combining our AI discovery platform with a deeper understanding of the immune system, we are focused on selectively removing pathogenic Th17 cells in vivo while preserving the function of the rest of the immune system. We believe this unique mechanism will allow for a true, first-of-its-kind T cell immune system reset.”

ai3Bio is advancing two platforms built on this approach: STARx and T Deplete. STARx uses a lipid nanoparticle to deliver mRNA that triggers a targeted, anti-inflammatory self-destruct process in disease-causing Th17 cells. T Deplete is a complementary approach that uses a targeting antibody to recruit the body’s own immune cells to clear the same cells. Preclinical testing of blood samples from patients with autoimmune disease demonstrated that the LNP technology effectively removed disease-causing Th17 cells. ai3Bio’s antibody platform demonstrated potent efficacy in a non-human primate model, with IND-enabling safety studies underway.

ai3Bio is led by a team with deep experience across biotechnology and drug discovery. The company’s leadership team includes CEO Steven Altschuler, Scientific Co-founder Jonathan Kagan, Chief Technology Officer Michael Lyman, Ph.D., and Chief Financial and Business Officer Nick Seaver.

The company’s distinguished Scientific Advisory Board includes strategic advisor John Maraganore, Ph.D., founding CEO of Alnylam Pharmaceuticals, alongside world-renowned immunologists Vijay Kuchroo, DVM, Ph.D. — recognized for his pioneering work defining Th17 cells — and National Academy of Sciences members Ruslan Medzhitov, Ph.D., Alexander Rudensky, Ph.D., and Arlene Sharpe, M.D., Ph.D.

“I am very careful about where I commit my time, and I truly believe ai3Bio has the potential to revolutionize autoimmune disease treatment,” said Vijay Kuchroo, DVM, Ph.D., Samuel L. Wasserstrom Professor of Neurology at Harvard Medical School; Director of The Gene Lay Institute of Immunology and Inflammation at Mass General Brigham and Harvard Medical School; and Senior Scientist at Brigham and Women’s Hospital. “By targeting Th17 cells with a highly innovative approach, the company is positioned to address massive unmet needs in immunology. I look forward to working closely with the board and leadership team to help unlock the full clinical and strategic value of their platforms.”

“ai3Bio represents a fundamentally new approach to autoimmune disease, targeting the pathogenic cells that drive disease, rather than suppressing symptoms,” said Fabian Tenenbaum, Executive Vice President, UPMC Enterprises and Board Chair, ai3Bio. “Pairing AI-enabled discovery with precise in vivo biology gives this platform the potential to deliver disease-modifying therapies across a broad range of autoimmune conditions and improve the lives of millions of patients. We are excited to partner with the ai3Bio team as they advance this vision.”

About ai3Bio

ai3Bio is a biotechnology company resetting the immune system at its root. The company’s name nods to three disciplines that make this possible: advanced immunology, autoimmunity, and artificial intelligence. ai3Bio aims to move autoimmune care from a lifetime of management toward lasting remission for millions of patients. Its proprietary STARx and T Deplete platforms combine an AI discovery platform with technology engineered to directly target and eliminate disease-causing Th17 cells in vivo, in one step. The company is backed by more than $48 million from investors including UPMC Enterprises and Ziff Capital Partners. For more information, visit ai3.Bio.

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