1. Investment Snapshot
2. Thesis
3. Valuation & Price Target
4. Business & Product Moat
5. People & Governance
6. Market & Macro
7. Financial Quality
8. Risk Register
9. Prediction Market
10. 𝕏 Posts
Discussion
1. Investment Snapshot
2. Thesis
3. Valuation & Price Target
4. Business & Product Moat
5. People & Governance
6. Market & Macro
7. Financial Quality
8. Risk Register
9. Prediction Market
10. 𝕏 Posts
Discussion
1. Investment Snapshot
2. Valuation
Discussion
Symbol
TRXB
Sector
Health Care
Subsector
Biotechnology
Offer Range
—
Shares Offered
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Implied Upside vs Midpoint
Description
We are a clinical-stage biopharmaceutical company focused on tissue Treg biology for the discovery and development of immunoregulatory medicines designed to restore immune balance and promote tissue repair to address unmet needs of patients with autoimmune and inflammatory diseases. TRexBio was built on a pivotal scientific insight: that regulatory T cells (“Tregs”) in human tissue are not merely passive suppressors of inflammation, but active orchestrators of tissue immune homeostasis and repair. Leveraging our Deep Biology drug discovery and design platform, we integrate tissue-level insights into human biology and Treg function to identify and characterize novel targets and approaches for therapeutic intervention. Our tissue-first conviction and unique insights in Treg biology are the foundation of our pipeline of therapeutic candidates aimed at restoring immune balance and promoting tissue repair for more durable disease control. Our pipeline is focused on augmenting tissue Tregs to address critical treatment gaps in autoimmune and inflammatory diseases. Our most advanced wholly-owned product candidate, TRB-061, is an investigational tumor necrosis factor receptor 2 (“TNFR2”) agonist designed to expand and activate Tregs in inflamed tissues. We believe TRB-061 has broad, multi-indication potential, and are currently conducting a Phase 1a/b clinical trial of TRB-061 in healthy volunteers and patients with moderate-to-severe atopic dermatitis (“AD”). We expect to announce topline data from the Phase 1b portion of the TRB-061 trial in patients with moderate-to-severe AD in mid-2027. Our second wholly-owned product candidate, TRB-071, is an investigational TNF receptor superfamily member 8, better known as TNFRSF8 (or “CD30”) agonist designed to both augment tissue Tregs and block immune system inflammatory signaling axes. Genetic studies support the involvement of CD30 and its ligand in inflammatory bowel disease (“IBD”). TRB-071 is currently in IND-enabling studies and, subject to regulatory allowance to proceed, is expected to enter a Phase 1 trial in the first half of 2027. We believe TRB-071 has the potential to address the significant unmet need in IBD by directly targeting the immune system dysfunction in the gut barrier that drives disease pathology. We believe each of our two lead product candidates has the potential to treat a range of autoimmune and inflammatory diseases with high unmet need, including AD, alopecia areata (“AA”) and IBD. Beyond our lead product candidates, we are advancing multiple preclinical-stage programs focused on differentiated aspects of Treg biology with the goal of transforming the lives of patients affected by autoimmune and inflammatory diseases. We believe our Deep Biology platform, built on a proprietary database of healthy and diseased tissue samples, is key to achieving this goal. Our platform is designed to decode Treg functionality in human tissue, mapping key drivers of immune dysregulation and uncovering novel targets and insights that inform our drug discovery and translational efforts. Our approach is to fundamentally rethink the approaches historically utilized in autoimmune disease drug development. Current therapies in this space rely on broad immunosuppression or focus on inhibiting one or more of the pathways that drive inflammation and often leave patients with chronic residual disease or disease progression. Many patients do not achieve lasting, durable remission, and, given these limitations, a significant number of patients remain untreated or fail to continue treatment with current therapeutic options. By moving away from systemic immunosuppression to immunoregulation, we believe Treg augmentation has the potential to represent a transformative shift in treating and maintaining durable remission of immune-mediated diseases. Tregs are master regulators of immune tolerance and mediators of tissue regeneration. The quantitative insufficiency, functional impairment, and phenotypic instability of Tregs in inflamed tissues are increasingly recognized as critical contributors to the pathogenesis of autoimmune and chronic inflammatory diseases. By studying Tregs in human tissues at high resolution, we better understand how those regulatory pathways affect other tissue immune and stromal cells, and how the failure of Treg-mediated tissue homeostasis drives chronic, self-perpetuating inflammatory cycles. Our approach is designed to address disease at its source—in the tissue—by developing medicines focused on tissue immune homeostasis that we believe have the potential to provide a durable clinical benefit. Our most advanced wholly-owned product candidate, TRB-061, is a fragment crystallizable-fusion, or Fc-fusion, protein designed to agonize TNFR2, selectively, without activation of proinflammatory cells. TNFR2 is a member of the TNF receptor superfamily, a family of cytokine receptors that regulate immune responses and inflammation, and is enriched on tissue Tregs, including in the skin and gut. Our platform identified TNFR2 as a key node in tissue Treg regulatory pathways. Evidence from our preclinical and Phase 1a clinical trial in healthy participants has shown activation and expansion of a highly active subpopulation of Tregs in the tissue following administration of TRB-061, which function to promote restoration of immune balance, forkhead box P3 (“FOXP3”) epigenetic stabilization, and a tissue-reparative phenotype that we believe can address barrier dysfunction. TRB-061 is currently in Phase 1b clinical development in patients with moderate-to-severe AD, and we expect to announce topline data in mid-2027. In addition, we are exploring expanding development of TRB-061 into other autoimmune and inflammatory diseases, including AA, based on data from our platform and published evidence supporting TNFR2 agonism or Treg augmentation as a therapeutic strategy in these conditions. We are also developing TRB-071, an investigational monoclonal antibody designed to leverage the biology of the CD30 and its associated ligand (“CD30L”) by agonizing CD30 to drive Treg activation, expansion and enhanced immune-regulatory capacity, while modulating the inflammatory pathway of CD30L. CD30 is a member of the TNF superfamily highly expressed on tissue Tregs. Human genetic studies have associated variants in both CD30 and CD30L with IBD susceptibility. In in vivo colitis models we saw reduced inflammation following treatment with TRB-071, and in our preclinical non-human primate studies, following administration of TRB-071 we observed Treg activation and expansion. We believe this dual mechanism, activating Tregs to restore immune balance while simultaneously modulating inflammatory signaling, has the potential to address underlying immune dysregulation in immune-mediated diseases such as IBD. We are currently conducting a three-month Good Laboratory Practice (“GLP”) toxicology study of TRB-071 in cynomolgus monkeys and, subject to regulatory allowance to proceed, expect to initiate a Phase 1 clinical trial in the first half of 2027. A central principle of our approach is the ability to connect human disease biology to Treg mechanism of action. Leveraging our proprietary Deep Biology platform, we analyze gene expression, pathway activity and cellular states in disease-relevant human tissues to identify where Treg function is disrupted, whether through impaired activation, instability, altered trafficking, or loss of tissue-reparative programs. These insights inform our target selection process and our design of translational strategies to align with the underlying disease biology. By linking target biology, Treg functional programs, and disease-specific immune dysregulation, we aim to establish a coherent framework that enables rational clinical development and early demonstration of biological activity in patients. Our platform is built on three integrated pillars: (1) Deep tissue biology and computational mapping to pinpoint disease-relevant biology with speed and precision; (2) our Treg Atlas, which recreates human tissue-specific Treg states in vitro; and (3) our Functional Assay Cascade, that interrogates multiple dimensions of Treg biology. Together, we believe these capabilities give us unique access to immune-mediated disease pathology, targets, and insights into how to approach the validation and development of therapeutic candidates in relevant target indications. In addition to our own pipeline of product candidates, we believe the translational power and proprietary ability to discover novel ways to augment Treg biology through our Deep Biology platform have been validated through strategic target-discovery collaborations with global pharmaceutical leaders. We have an ongoing collaboration with Lilly which is advancing a clinical product candidate first identified and developed utilizing our platform. --- TRex Bio, Inc. was incorporated on May 24, 2018, as a Delaware corporation. Our business was originally conducted through TRex Bio Limited, a company incorporated under the laws of England and Wales on January 30, 2018 (initially named Cingularity Therapeutics Limited). In November 2021, we completed a corporate reorganization pursuant to which TRex Holdings Inc., a newly formed Delaware corporation, acquired all of the outstanding shares of TRex Bio Limited through a share exchange, and subsequently acquired all of TRex Bio Limited’s assets and liabilities pursuant to a business transfer agreement, in order to consolidate our business and legal entity structure into the United States. On December 31, 2024, TRex Holdings Inc. merged with and into TRex Bio, Inc., its wholly-owned Delaware subsidiary, with TRex Bio, Inc. continuing as the surviving corporation; in connection with the merger, all outstanding shares of capital stock and options of TRex Holdings Inc. were converted on a one-for-one basis into corresponding shares of capital stock and options of TRex Bio, Inc. Our principal executive offices are located at 269 East Grand Avenue, Suite 300, South San Francisco, CA 94080, and our telephone number is (650) 567-5582. Our corporate website address is trex.bio.