Four innovative programs spanning IND-cleared, preclinical, and discovery-stage development.
Pendred syndrome is a genetic disorder associated with congenital hearing loss and SLC26A4 mutations. ARBM-301 is an early-stage small-molecule corrector designed to improve trafficking and cell-surface expression of mutant pendrin in inner-ear epithelial cells.
ARBM-301 is designed as a pharmacological chaperone (corrector) for H723R mutant pendrin. The misfolded mutant protein is retained in the endoplasmic reticulum; ARBM-301 is designed to promote its correct folding so that pendrin can traffic through the Golgi to the plasma membrane and resume anion exchange.
In H723R pendrin-expressing cells, ARBM-301 restored cell-surface localization of mutant pendrin and recovered Cl⁻/HCO₃⁻ exchange in a dose-dependent manner. Cell-surface pendrin also increased in primary epithelial cells from a Pendred syndrome patient.
In vivo studies in a dox-inducible H723R transgenic mouse model are ongoing to support preclinical candidate selection. No clinical efficacy has been established.
Mechanism of pendrin correction and in vitro evidence in H723R mutant and patient-derived cells. No clinical efficacy has been established.

Panc1 cells expressing human WT or H723R pendrin · ARBM-301 3 µM · Immunocytochemistry
H723R mutant pendrin, retained in the ER, was restored localization on the cell surface (membrane) by ARBM-301 — a distribution similar to wild-type pendrin.

H723R pendrin-expressing cells · Western blotting (surface biotinylation) and anion (Cl⁻/HCO₃⁻) exchange assay
Western blots showed restored cell surface expression of mature pendrin (C form) with ARBM-301, and Cl⁻/HCO₃⁻ exchange was significantly recovered at 3 and 10 µM.

