Remix Therapeutics Receives FDA Fast Track Designation For REM-422, a First-In-Class MYB mRNA Degrader For MYB-Driven Adenoid Cystic Carcinoma

Remix Therapeutics, a clinical-stage biotechnology company developing small molecule therapies that modulate RNA processing, announced that the U.S. Food and Drug Administration has granted Fast Track designation to its first-in-class MYB mRNA degrader, REM-422. The designation applies to patients with recurrent, metastatic, or unresectable adenoid cystic carcinoma (ACC) whose tumors express MYB transcripts containing a poison exon.

Peter Smith, Ph.D., Co-Founder and Chief Executive Officer of Remix Therapeutics, said the designation highlights the urgent need for new therapies for patients with ACC. Peter Smith noted that REM-422 is designed to target MYB—a key oncogenic driver in ACC that has historically been challenging to inhibit—and emphasized that Fast Track status will support efforts to advance the therapy efficiently through clinical development.

REM-422 is an oral, first-in-class small molecule MYB mRNA degrader engineered to reduce MYB expression by promoting incorporation of a poison exon into the MYB transcript. This triggers degradation of the mRNA and suppresses production of the MYB protein. MYB dysregulation is a well-recognized disease driver in ACC as well as several hematologic malignancies.

The therapy is currently being evaluated in the Phase 1/2 ARIA study, which is assessing safety, pharmacokinetics, and early signals of anti-tumor activity in patients with recurrent, metastatic, or unresectable ACC. Early Phase 1 data demonstrated proof-of-mechanism and proof-of-concept, showing reduction of MYB expression along with a favorable safety profile and meaningful anti-tumor activity in patients whose tumors express MYB transcripts containing a poison exon.

The FDA’s Fast Track program is intended to accelerate development and review of therapies addressing serious conditions with unmet medical needs. According to Remix Therapeutics, the new designation reflects encouraging early clinical results and supports the potential of REM-422 as a novel therapeutic option for patients with MYB-driven ACC.