Drug intelligence / Profile preview

RD-23

Development stage
Preclinical
Lead developer
University of Minnesota
Modality
PROTACs (E3 ligase recruitment) → Targeted Protein Degraders (TPDs) → Small Molecules, Bivalent/Multivalent Binders → Multivalent & Scaffold-Based Small Molecules → Small Molecules
01

Overview

RD-23 is a proteolysis-targeting chimera (PROTAC) designed to induce the degradation of the RET (Rearranged during Transfection) receptor tyrosine kinase. It is chemically derived from the selective RET inhibitor selpercatinib. RD-23 is being investigated for its potential to overcome resistance mechanisms associated with traditional RET kinase inhibitors, particularly in aggressive cancers like neuroendocrine prostate cancer (NEPC) and small cell lung cancer (SCLC), where RET expression is often driven by the transcription factor ASCL1. By utilizing a catalytic mechanism to eliminate the entire RET protein rather than just inhibiting its enzymatic activity, RD-23 aims to provide more durable suppression of RET signaling compared to occupancy-based inhibitors.

02

Targets

RET (Rearranged during transfection receptor tyrosine kinase)

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