UCSF, Annogen Announce Collaboration to Identify Superior Treg-Specific Promoters

UCSF, Annogen Announce Collaboration to Identify Superior Treg-Specific Promoters

Annogen, a leader in gene expression engineering, and the prestigious labs of Qizhi Tang and Brian Shy at University of California, San Francisco (UCSF) today announced a collaboration to identify and characterize promoters specific for regulatory T cells (Treg). This partnership aims to set a new benchmark for precision gene expression in Treg cell therapies.

Tregs are a specialized subset of T-cells that help prevent autoimmune diseases by suppressing excessive immune responses, ensuring the body doesn’t attack its own tissues. The unique function of Tregs makes them a promising target for therapies aimed at treating autoimmune conditions and enhancing transplant success, with many companies developing Treg-based treatments. The Tang lab has previously shown that Treg-infusions can reverse type 1 diabetes and prevent rejection of transplanted organs by establishing immune tolerance.

Many labs and companies are developing genetically engineered Tregs to targeting to specific tissue and to enhance their persistence.  A challenge in Treg cell therapy is that it is difficult to avoid a few contaminating non-Tregs and Tregs can lose their lineage identity after infusion and become exTregs.  Expressing targeting or persistent genes in non-Tregs or exTregs could potentially cause tissue damages rather than protecting the tissue from immune aggression. Therefore, finding a way to selectively engineer Tregs would hugely improve the efficacy and safety of Treg therapies.

Annogen’s SuRE™ platform will be used to exhaustively screen the entire human genome for Treg-specific promoters and enhancers, combinations of which will subsequently be tested to identify the optimal Treg-specific promoter. 

We’re thrilled to partner with the labs of Dr. Tang and Dr. Shy, both considered leading experts in Treg biology and Treg therapy development“, said Dr. Martijn Kelder, Chief Strategy Officer at Annogen. “Their expertise combined with our ability to discover and develop the most optimal promoters will hopefully allow for the future development of safer and more effective therapies.

We are excited to partner with the outstanding team at Annogen and leverage their innovative SuRE platform to identify context-specific regulatory elements that will help drive the next-generation of advanced Treg therapies.“, concludes Dr. Shy.

Academic partnership regulatory T cell synthetic promoter
Why promoter design is no longer just an expression checkbox, it’s the key to therapeutic endurance.

Why promoter design is no longer just an expression checkbox, it’s the key to therapeutic endurance.

Promoter design is becoming central to durable cell and gene therapy, as the field moves beyond delivery and toward precise expression control. Standard promoters like CMV or PGK often fail to solve key clinical challenges: off-target activity, “always-on” expression that can drive cellular exhaustion, and epigenetic silencing that shuts therapies down in vivo. Annogen’s SuRE™ platform addresses these bottlenecks by experimentally screening millions of non-coding DNA fragments in relevant models and refining designs with machine learning. The result is not a generic promoter, but a validated, non-viral promoter tailored for the specific tissue, condition, and therapeutic context.

VectorY’s Clinical Milestone and the Shift Toward Experimentally-Validated Promoters

VectorY’s Clinical Milestone and the Shift Toward Experimentally-Validated Promoters

The first patient dosing in VectorY Therapeutics’ PIONEER-ALS trial marks a definitive shift in gene therapy, moving past the “conservative” reliance on blunt viral promoters and the “digital guesses” of AI. While many rely on algorithms built from incomplete and insensitive data, VTx-002 is powered by an Annogen genome-derived promoter discovered through rigorous, large-scale experimental validation. This milestone proves that true therapeutic precision isn’t predicted in a black box—it is found by interrogating the genome directly to deliver the biological truth required for the clinic.

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