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Kickstarting an
Immune System Reboot.

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Tr1X's cells work the same way as naturally occurring Tr1 cells by homing to sites of inflammation, suppressing unwanted activity, and boosting production of antigen-specific Tr1 cells to reset the immune system and restore balance.

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Timeline

Backed by decades of research in immunology and T-cell biology.

Tr1X was established to translate key academic discoveries in T-regulatory type 1 (Tr1) cell function and biology into commercially available treatments.

2009

Tr1 Cells

Tr1 Cells are found in patients with tolerance following allogeneic stem cell transplantation.
(Serafini et al. Haematologica. 2009;94(10):1415-1426.)
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2010

Tr1 Cells

Tr1 Cells are differentiated in vitro using tolerogenic dendritic cells.
(Gregori et al. Blood. 2010;116(6):935-44)
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2012

First demonstration

First demonstration that IL-10 engineered human CD4+ T cells acquire Tr1 cell functions.
(Andolfi et al. Mol Ther. 2012; 20(9): 1778–1790)
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2013

Naturally occurring

Naturally occurring Tr1 cell marker expression characterized.
(Gagliani et al. Nat Med. 2013; 19, 739–746)
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2014

Results from first

Results from first in human trial with in vitro differentiated Tr1 cells.
(Bacchetta et al. Front Immunol. 2014;5:16)
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2017

Proof about IL-10

Proof that IL-10 engineered human CD4+ Tr1 cells prevent GvHD in preclinical models.
(Locafaro et al. Mol Ther. 2017 ;25(10):2254-2269)
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2019

Preliminary results

Preliminary results from second generation in vitro differentiated Tr1 cell trial in patients undergoing Hematopoietic Stem Cell Transplantation.
(Agarwal et al. ASTCT 2019; 411:26(3), S272-S273)
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2021

Evidence

Evidence that in vitro generated Tr1 cells persist long term in patients following their administration.
(Chen et al. Sci Transl Med. 2021;13(617):eabf5264)
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2024

First engineered Tr1 cells dosed in human subjects.

First engineered Tr1 cells dosed in human subjects.
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Foundational
Science

A scalable, modular platform that leverages unique Tr1 cell biology.

Master Regulators of Immune Homeostasis.

Tr1 cells prevent and downregulate undesired immune responses to pathogenic and non-pathogenic antigens and are associated with long-term tolerance across many different conditions.
M.G. Roncarolo et al. Immunity 49,1004-1019 (2018).

Natural Homing to Sites of Inflammation

Tr1 cells express a series of chemokine receptors that enable them to traffic to the sites of inflammation in the body, allowing for local, targeted delivery of desired cytokines.
H. Yu et al. PNAS 114, 10443-10448(2017).

Capable of Tackling the NLRP3 Inflammasome

Tr1 cells, unlike Foxp3+ Tregs, inhibit the transcription of pro–IL-1β mRNA, inflammasome-mediated activation of caspase-1, and secretion of mature IL-1β.
Y. Yao et al. J Immunol 195, 488-497(2015).

Stable and Long Lived, Even Under Inflammatory Conditions

Tr1 cells were detectable in the peripheral blood of stem cell transplant patients up to 1 year after administration, proving their longevity and stability.
P. P. Chen et al. Sci Trans Med 13,eabf5264 (2021).

First engineered Tr1 cells dosed in human subjects.

2024

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Evidence

2021

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Preliminary results

2019

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Proof about IL-10

2017

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Results from first

2014

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Naturally occurring

2013

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First demonstration

2012

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Tr1 Cells

2010

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Tr1 Cells

2009

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The Platform

Removing bottlenecks and pitfalls of Treg-based therapeutics.

Tr1X is leveraging a unique population of regulatory T cells that overcome many of the current limitations with other Treg-based products. This includes several characteristics that are exclusively tied to Tr1 cells, which underpin all of our products.

Scalable Production

Our cells are produced using a highly scalable and modular production process, allowing for the generation of multiple products at high purity levels and high dose quantities.

Tr1-like components

Our cells have a localized suppression feature-set, which includes high IL-10 production, expression of co-inhibitory receptors, inflammasome downregulation, tissue healing & wound repair.

Homing & Stability

Our cells home to sites of inflammation thanks to their array of chemokine receptors. They are highly stable and do not revert to effector cells even under inflammatory conditions.