RNA–Protein Interaction Therapeutics

We are developing decoys designed to out-compete LIN28's natural RNA targets for binding.

RNAissance is developing a new class of therapeutics that directly modulate disease-driving RNA–protein interactions.

Lead program: LIN28 Decoy Oligonucleotides (LDOs) · Stage: Discovery / preclinical validation

See the lead program → Partner with us
Two states, one strand, LIN28 and its decoy.
Why Now

Beyond RNA silencing

Advances in structural biology, oligonucleotide chemistry, and RNA therapeutic development now make previously inaccessible RNA–protein interactions increasingly tractable as drug targets.

The first generation of RNA medicines showed that RNA can be a therapeutic modality. RNAissance is extending that paradigm to the proteins and molecular interactions that control RNA biology.

Approach

Why RNA–protein interactions?

Conventional RNA therapeutics are sequence-driven: they degrade a transcript or block its translation. RNAissance's approach is structure-driven, with an LDO designed as a fold, not a sequence, engineered to occupy the binding site a target protein already recognizes.

Chemistry

β-L-ribose backbone

A proprietary β-L-ribose chemistry designed to improve the stability and molecular properties of therapeutic oligonucleotides.

Mechanism

Sequestration, not degradation

An LDO is designed to occupy a target protein's native binding site, holding it rather than destroying it, so the protein's natural substrate is left free to act. The molecule can engage its target through its designed molecular structure, rather than being recognized as natural genetic material.

Design

Structure-guided

Each decoy is designed from the structural biology of its target interaction, informed by structural and biophysical characterization of the target axis.

The sequence is not the therapeutic recognition code; molecular structure is.

We are developing a new class of therapeutics that directly modulate disease-driving RNA–protein interactions.

01

Structure

02

Design

03

Chemistry

04

Biology

05

Medicine

Pipeline

LDO-101: LIN28B / Hepatoblastoma

Our lead program targets hepatoblastoma, the most common pediatric liver cancer, in the LIN28B-high subtype where the LIN28/let-7 axis is a validated driver of tumor growth.

Target
LIN28B
Indication
LIN28B-high hepatoblastoma
Mechanism
LIN28 sequestration → let-7 restoration → tumor suppression
Modality
Decoy oligonucleotide
Stage
Discovery / preclinical validation
Patient population
LIN28B-high / C2 embryonal subtype
A pediatric indication with potential access to FDA rare pediatric disease incentives.
Current objective: Establish biochemical and cellular proof-of-concept for LDO-101 and advance toward in vivo validation.

Current validation

Biochemical

LIN28–LDO binding and competitive interaction

Cellular

LIN28 pathway engagement and let-7 restoration

Functional

Tumor-suppressive activity

Design
We are hereBiochemical validation
Cellular PoC
In vivo PoC
Candidate selection
IND-enabling
Science

How LDOs work

The LIN28/let-7 axis, and how a structured decoy oligonucleotide is designed to release it.

01

Disease state

LIN28 over-expression traps pre-let-7 and blocks its maturation.

LIN28 binding pre-let-7, blocking maturation
LIN28LIN28let-7 blocked
  • LIN28
  • let-7
  • Oncogenic programs
→
02

LDO intervention

A structured decoy oligonucleotide is designed to out-compete LIN28 for the native binding site.

LDO decoy binding LIN28 in place of pre-let-7
LIN28LDO
  • LDO binds LIN28
  • Protein sequestered, not degraded
  • Native binding site left free
→
03

Therapeutic hypothesis

With LIN28 occupied, pre-let-7 matures and native suppression resumes.

pre-let-7 maturing into mature let-7
  • LIN28 activity
  • let-7 processing restored
  • Tumor-suppressive signaling

Structure-driven engagement rather than sequence-complementary targeting. Hypothesis figure, not to scale.

01

Conventional RNA therapeutics

Sequence-driven. One node, two outcomes.

RNA payload
┄┄>
Degradation
Translation modulation

Knock a transcript down or nudge its output. The RNA is a message to be silenced.

VERSUS
02

RNAissance

Structure-driven. A cascade the cell already knows.

STEP 01

LDO

A let-7 decoy oligonucleotide, designed as a fold, not a sequence.

›
STEP 02

LIN28 sequestration

The RNA-binding protein is occupied and held, not destroyed.

›
STEP 03

let-7 restoration

The tumor-suppressive miRNA matures again on its own.

›
OUTCOME

Tumor suppression

Native regulation returns rather than being replaced.

LIN28 / let-7 biology
Decoy mechanism
β-L-ribose chemistry
Structure-guided design
IP & Publications

Intellectual property

RNAissance's intellectual property is designed to protect two layers: the underlying LDO platform chemistry itself, and its therapeutic application in LIN28-driven disease, not a single narrow filing.

Patent Application

Application No.U.S. Provisional Patent Application No. 63/901,790
FiledOctober 19, 2025
TitleLIN28 Decoy Oligonucleotides (LDOs) with Novel β-L-Ribose and Modular Therapeutic Design
Composition-of-Matter / Platform

Claims directed to the β-L-ribose LDO chemistry itself, intended to protect the underlying platform across future decoy designs, not just LDO-101.

Therapeutic Application

Claims directed to the use of LIN28 decoy oligonucleotides in LIN28-driven disease, including LDO-101 in hepatoblastoma.

Selected Publications

Manuscripts in preparation, to be added as they're submitted.

Scientific Advisors

To be announced.

Non-Confidential Overview

A non-confidential summary deck is available on request. Get in touch.

Team

The team

Structural biologists and chemists working on the problem RNAissance is solving now.

YC

Young-Jin Cho, PhD

Founder & CEO
Structural Biology · RNA Biology · Drug Discovery
  • PhD, structural biology
  • Background spanning RNA therapeutics and biophysics
  • Prior industry experience at Wave Life Sciences, Warp Drive Bio, Arrakis Therapeutics, and NextRNA Therapeutics
YL

Young-Tae Lee, PhD

Chief Scientific Officer
Structural Biology

Leads structural biology. Co-inventor on core IP.

JS

Jarnail Singh, PhD

Head of Biology
Molecular Biology

Leads molecular biology.

Company

Mission & vision

Mission

To turn structure-guided RNA–protein interaction biology into medicines, starting where the biology is clearest.

Vision

A pipeline of decoy oligonucleotide therapeutics addressing RNA-binding proteins that conventional modalities can't reach.

Why RNAissance

Across my academic training in DNA, RNA, and protein structure, and later in industry, working across small molecules, antisense oligonucleotides, and other macromolecular therapeutics, I kept arriving at the same tension: the most potent interventions were often the most disruptive ones, degrading or silencing biology outright, with real risk of downstream consequences.

RNAissance started from a different premise: what if a therapeutic could work with the body's own regulatory logic instead of against it? Let-7 is a tumor suppressor the body already makes. We didn't need to invent a new biological effector, just restore one that disease had silenced. And by building that decoy from L-ribose, a mirror-image sugar the body's own enzymes don't recognize, the molecule can engage its target by shape alone, without being read, processed, or reacted with as natural genetic material.

That combination, a natural tumor suppressor delivered through a chemistry the body can't mistake for its own, is what RNAissance is built on.

Young-Jin Cho, Founder & CEO