Next-Generation Platforms
Genome- and Transcriptome-Wide Mapping of Alternative Nucleic Acids
We provide the only platforms engineered to map alternative nucleic acid structures that conventional static assays miss, accelerating target validation.
Our Core Technologies
DNA is commonly represented as the canonical right-handed double helix, but genomic DNA and RNA can adopt a diverse range of alternative and non-canonical structures under specific sequence, topological, and cellular conditions.
These structures can emerge transiently throughout the genome and may influence gene regulation, transcription, replication, genome stability, and cellular responses to stress. Because many of these structures are dynamic and short-lived, accurately identifying where and when they form inside cells remains challenging.
Dynoma is developing technologies for the genome- and transcriptome-wide mapping of alternative DNA and RNA conformations in their biological context.
Our goal is to generate high-resolution maps connecting DNA/RNA structural states with genomic function and disease-associated pathways. By integrating molecular recognition technologies with genomic approaches, we aim to reveal how changes in DNA/RNA topology and conformation contribute to cellular regulation.
These platforms may provide new opportunities to identify structure-associated biomarkers, regulatory mechanisms, disease vulnerabilities, and therapeutic targets that cannot be readily discovered through conventional sequence-based genomics alone.
Beyond Mapping
Harnessing the RNA Dynamics to Activate Innate Immunity
Dynoma Biosciences is developing a new class of Z-conformation–stabilizing small molecules designed to stabilize Z-RNA and harness its immunological potential for cancer therapy.
Z-RNA is a transient, left-handed nucleic acid conformation that can function as a powerful danger signal within cells. Our approach aims to selectively increase the stability and persistence of Z-RNA, promoting its recognition by Z-DNA-binding protein 1 (ZBP1), an innate immune sensor capable of initiating inflammatory signaling and programmed cell death.
By pharmacologically enhancing Z-RNA–ZBP1 signaling, we aim to trigger innate immune activation and immunogenic tumor cell death, potentially transforming poorly immunogenic tumors into an environment more favorable for anti-tumor immune responses.
Our goal is to establish Z-RNA stabilization as a new therapeutic strategy in cancer immunotherapy, with the potential to complement existing treatments and provide new options for tumors that respond poorly to current immunotherapies.
Accelerate Your Drug Discovery Pipeline
Request technical specifications or schedule a platform demonstration to see how Dynoma can unlock novel therapeutic targets with unprecedented mechanistic resolution.